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Gene Information
Gene symbol: NFKB1
Gene name: nuclear factor of kappa light polypeptide gene enhancer in B-cells 1
HGNC ID: 7794
Synonyms: KBF1, p105, NFKB-p50, p50, NF-kappaB, NFkappaB, NF-kB1
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 8751937 | By using 70Z/3-derived pre-B-cell lines either lacking or expressing human CD14 (the LPS receptor), it was observed that expression of human CD14 imparted responsiveness to LPS but not to OspA or spirochetal lipopeptides (assessed by induction of NF-kappa B and expression of surface immunoglobulin M). |
| 2 | 8906837 | OspA also rapidly up-regulated endothelial cell production of several proteins whose transcription is dependent on NF-kappa B: the cytokine IL-6; the chemokine IL-8; and the adhesion molecules E-selectin, VCAM-1, and ICAM-1. |
| 3 | 9597145 | Recent findings in B lymphocytes have clearly illustrated that these external inputs affect the magnitude and duration of the intracellular calcium response, which in turn contributes to differential triggering of the transcriptional regulators NF kappa B, JNK, NFAT, and ERK. |
| 4 | 9597145 | The regulation of calcium responses involves a network of tyrosine kinases (e.g. lyn, syk), tyrosine or lipid phosphatases (CD45, SHP-1, SHIP), and accessory molecules (CD21/CD19, CD22, FcR gamma 2b). |
| 5 | 9643372 | HIV viral load and type 1 (IL-2 and IFN-gamma) and type 2 (IL-4 and IL-10) cytokine production were evaluated before and 7, 14, and 28 days after vaccination. |
| 6 | 9643372 | Because polysaccharides of the bacterial cell wall stimulate TNF-alpha production by monocyte-macrophages and TNF-alpha was shown to stimulate HIV replication directly on activation of NF-kappa b after binding the long terminal repeat (LTR) sequences of HIV, we measured TNF-alpha production and observed a significant increase in both groups of vaccines. |
| 7 | 9890416 | The expression of intercellular adhesion molecule 1 (ICAM-1) by endothelial cells is important for the regulation of adhesion and transendothelial migration of a variety of leukocytes that express the integrins lymphocyte function-associated antigen 1 (LFA-1) and/or Mac-1. |
| 8 | 9890416 | Strain-specific differences in the ability of Mor and CAM-70 to induce ICAM-1 correlated with their ability to activate the latent transcription factor NF-kappaB. |
| 9 | 9890416 | These studies suggest a preexisting component of MV particles that leads to strain-specific differences in the activation of NF-kappaB and the induction of ICAM-1 gene expression. |
| 10 | 9890416 | The expression of intercellular adhesion molecule 1 (ICAM-1) by endothelial cells is important for the regulation of adhesion and transendothelial migration of a variety of leukocytes that express the integrins lymphocyte function-associated antigen 1 (LFA-1) and/or Mac-1. |
| 11 | 9890416 | Strain-specific differences in the ability of Mor and CAM-70 to induce ICAM-1 correlated with their ability to activate the latent transcription factor NF-kappaB. |
| 12 | 9890416 | These studies suggest a preexisting component of MV particles that leads to strain-specific differences in the activation of NF-kappaB and the induction of ICAM-1 gene expression. |
| 13 | 10452971 | Transfection of TLR2 into cell lines conferred responsiveness to lipoproteins, lipopeptides, and sonicated B. burgdorferi, as measured by nuclear translocation of NF-kappaB and cytokine production. |
| 14 | 10452971 | Futhermore, TLR2-dependent signaling by lipoproteins was facilitated by CD14. |
| 15 | 10464164 | Rel, a haemopoietic cell-restricted member of the NF-kappaB/Rel family of transcription factors, has recently been shown to be important in the function of B and T lymphocytes. |
| 16 | 10464164 | These findings establish that during the response to influenza virus, Rel function allows optimal development of humoral immunity, a role that apparently cannot be fulfilled by other NF-kappaB/Rel proteins. |
| 17 | 10464164 | Rel, a haemopoietic cell-restricted member of the NF-kappaB/Rel family of transcription factors, has recently been shown to be important in the function of B and T lymphocytes. |
| 18 | 10464164 | These findings establish that during the response to influenza virus, Rel function allows optimal development of humoral immunity, a role that apparently cannot be fulfilled by other NF-kappaB/Rel proteins. |
| 19 | 10542221 | Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide inhibit interleukin-12 transcription by regulating nuclear factor kappaB and Ets activation. |
| 20 | 10542221 | The vasoactive intestinal peptide (VIP) and the structurally related neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) act as "macrophage-deactivating factors". |
| 21 | 10542221 | We showed previously that VIP and PACAP inhibit the production of macrophage-derived tumor necrosis factor-alpha, interleukin (IL)-6, nitric oxide, and IL-12. |
| 22 | 10542221 | This study examines the molecular mechanisms involved in the VIP/PACAP inhibition of IL-12 production. |
| 23 | 10542221 | VIP and PACAP inhibit IL-12 (p40) gene expression by affecting both NF-kappaB binding and the composition of the Ets-2 binding complex. |
| 24 | 10542221 | Both neuropeptides prevent the activation-induced nuclear translocation of the NF-kappaB components p65 and c-Rel by inhibiting the reduction in cytoplasmic IkappaBalpha. |
| 25 | 10542221 | Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide inhibit interleukin-12 transcription by regulating nuclear factor kappaB and Ets activation. |
| 26 | 10542221 | The vasoactive intestinal peptide (VIP) and the structurally related neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) act as "macrophage-deactivating factors". |
| 27 | 10542221 | We showed previously that VIP and PACAP inhibit the production of macrophage-derived tumor necrosis factor-alpha, interleukin (IL)-6, nitric oxide, and IL-12. |
| 28 | 10542221 | This study examines the molecular mechanisms involved in the VIP/PACAP inhibition of IL-12 production. |
| 29 | 10542221 | VIP and PACAP inhibit IL-12 (p40) gene expression by affecting both NF-kappaB binding and the composition of the Ets-2 binding complex. |
| 30 | 10542221 | Both neuropeptides prevent the activation-induced nuclear translocation of the NF-kappaB components p65 and c-Rel by inhibiting the reduction in cytoplasmic IkappaBalpha. |
| 31 | 10753705 | In mutant LTRs, which lack NF-kappaB and Sp1 binding sites, TATA box motifs, and the 5' half of the U3 region, promoter activity was stringently controlled by doxycycline (Dox). |
| 32 | 10769064 | Interleukin-18 (IL-18) is a proinflammatory cytokine that plays a key role in the activation of natural killer and T helper 1 cell responses principally by inducing interferon-gamma (IFN-gamma). |
| 33 | 10769064 | The ectromelia virus protein was found to block NF-kappaB activation and induction of IFN-gamma in response to IL-18. |
| 34 | 11015437 | B lymphocyte stimulator (BLyS) is a newly identified monocyte-specific TNF family cytokine. |
| 35 | 11015437 | BLyS acts on primary splenic B cells autonomously, and directly cooperates with CD40 ligand (CD40L) in B cell activation in vitro by protecting replicating B cells from apoptosis. |
| 36 | 11015437 | Attenuation of apoptosis by BLyS correlates with changes in the ratios between Bcl-2 family proteins in favor of cell survival, predominantly by reducing the proapoptotic Bak and increasing its prosurvival partners, Bcl-2 and Bcl-xL. |
| 37 | 11015437 | In either resting or CD40L-activated B cells, the NF-kappaB transcription factors RelB and p50 are specifically activated, suggesting that they may mediate BLyS signals for B cell survival. |
| 38 | 11015437 | The ability of BLyS to increase B cell survival indiscriminately, at either a resting or activated state, and to cooperate with CD40L, further suggests that attenuation of apoptosis underlies BLyS enhancement of polyclonal autoimmunity as well as the physiologic humoral immune response. |
| 39 | 11029527 | The growth rates of both vaccines in murine macrophages were the same, however, Onco-BCG induced stronger and longer-lasting secretion of TNF-alpha, IL-6 and nitric oxide. |
| 40 | 11029527 | Onco-vaccine was also more potent in inducing NF-kappaB p65/p50 DNA-binding activity whilst in ID-BCG-infected cells the activity was transient and then gradually replaced by the transcriptionally inactive homodimer p50/p50. |
| 41 | 11325600 | Influenza A virus infection results in the production of chemotactic (RANTES, MIP-1 alpha, MCP-1, MCP-3, and IP-10), pro-inflammatory (IL-1 beta, IL-6, IL-18, and TNF-alpha), and antiviral (IFN-alpha/beta) cytokines. |
| 42 | 11325600 | Cytokine gene expression is associated with the activation of NF-kappa B, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. |
| 43 | 11325600 | IFN-alpha/beta also prolongs T cell survival, upregulates IL-12 and IL-18 receptor gene expression and together with IL-18 stimulates NK and T cell IFN-gamma production and the development of Th1-type immune response. |
| 44 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 45 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 46 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 47 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 48 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 49 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 50 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 51 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 52 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 53 | 11441107 | Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. |
| 54 | 11441107 | Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate immune responses to various microbial agents. |
| 55 | 11441107 | We have previously shown that human dermal endothelial cells (HMEC) express TLR4, but very little TLR2, and respond to LPS, but not to Mycobacterium tuberculosis 19-kDa lipoprotein, unless transfected with TLR2. |
| 56 | 11441107 | We further characterized the signaling pathway in response to STF, OspA-L, and PSM in TLR2-transfected HMEC. |
| 57 | 11441107 | The TLR2 signaling pathway for NF-kappaB trans-activation shares the IL-1R signaling molecules. |
| 58 | 11441107 | Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the concept of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands. |
| 59 | 11441107 | Moreover, we show that Toll-interacting protein (Tollip) coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and overexpression of Tollip inhibits NF-kappaB activation in response to TLR2 and TLR4 signaling. |
| 60 | 11441107 | Collectively, these findings suggest that there is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addition to S. epidermidis (PSM) Ags, and that engagement of TLR2 triggers a signaling cascade, which shares the IL-1R signaling molecules, similar to the TLR4-LPS signaling cascade. |
| 61 | 11441107 | Our data also suggest that Tollip may be an important constituent of both the TLR2 and TLR4 signaling pathways. |
| 62 | 11585920 | Human T-cell lymphotropic virus type 1 Tax represses c-Myb-dependent transcription through activation of the NF-kappaB pathway and modulation of coactivator usage. |
| 63 | 11585920 | Here we demonstrate that activation of the NF-kappaB pathway by the HTLV-1 Tax protein leads to transcriptional inactivation of c-Myb. |
| 64 | 11585920 | This conclusion was supported by the fact that Tax mutants unable to stimulate the NF-kappaB pathway could not inhibit c-Myb transactivating functions. |
| 65 | 11585920 | In addition, inhibition of Tax-mediated NF-kappaB activation by coexpression of IkappaBalpha restored c-Myb transcription, and Tax was unable to block c-Myb transcription in a NEMO knockout cell line. |
| 66 | 11585920 | Importantly, physiological stimuli, such as signaling with the cellular cytokines tumor necrosis factor alpha, interleukin 1 beta (IL-1beta), and lipopolysaccharide, also inhibited c-Myb transcription. |
| 67 | 11585920 | Interestingly, an amino-terminal deletion form of p300 lacking the C/H1 and KIX domains and unable to bind RelA retained the ability to stimulate c-Myb transcription and prevented NF-kappaB-mediated repression. |
| 68 | 11585920 | Human T-cell lymphotropic virus type 1 Tax represses c-Myb-dependent transcription through activation of the NF-kappaB pathway and modulation of coactivator usage. |
| 69 | 11585920 | Here we demonstrate that activation of the NF-kappaB pathway by the HTLV-1 Tax protein leads to transcriptional inactivation of c-Myb. |
| 70 | 11585920 | This conclusion was supported by the fact that Tax mutants unable to stimulate the NF-kappaB pathway could not inhibit c-Myb transactivating functions. |
| 71 | 11585920 | In addition, inhibition of Tax-mediated NF-kappaB activation by coexpression of IkappaBalpha restored c-Myb transcription, and Tax was unable to block c-Myb transcription in a NEMO knockout cell line. |
| 72 | 11585920 | Importantly, physiological stimuli, such as signaling with the cellular cytokines tumor necrosis factor alpha, interleukin 1 beta (IL-1beta), and lipopolysaccharide, also inhibited c-Myb transcription. |
| 73 | 11585920 | Interestingly, an amino-terminal deletion form of p300 lacking the C/H1 and KIX domains and unable to bind RelA retained the ability to stimulate c-Myb transcription and prevented NF-kappaB-mediated repression. |
| 74 | 11585920 | Human T-cell lymphotropic virus type 1 Tax represses c-Myb-dependent transcription through activation of the NF-kappaB pathway and modulation of coactivator usage. |
| 75 | 11585920 | Here we demonstrate that activation of the NF-kappaB pathway by the HTLV-1 Tax protein leads to transcriptional inactivation of c-Myb. |
| 76 | 11585920 | This conclusion was supported by the fact that Tax mutants unable to stimulate the NF-kappaB pathway could not inhibit c-Myb transactivating functions. |
| 77 | 11585920 | In addition, inhibition of Tax-mediated NF-kappaB activation by coexpression of IkappaBalpha restored c-Myb transcription, and Tax was unable to block c-Myb transcription in a NEMO knockout cell line. |
| 78 | 11585920 | Importantly, physiological stimuli, such as signaling with the cellular cytokines tumor necrosis factor alpha, interleukin 1 beta (IL-1beta), and lipopolysaccharide, also inhibited c-Myb transcription. |
| 79 | 11585920 | Interestingly, an amino-terminal deletion form of p300 lacking the C/H1 and KIX domains and unable to bind RelA retained the ability to stimulate c-Myb transcription and prevented NF-kappaB-mediated repression. |
| 80 | 11585920 | Human T-cell lymphotropic virus type 1 Tax represses c-Myb-dependent transcription through activation of the NF-kappaB pathway and modulation of coactivator usage. |
| 81 | 11585920 | Here we demonstrate that activation of the NF-kappaB pathway by the HTLV-1 Tax protein leads to transcriptional inactivation of c-Myb. |
| 82 | 11585920 | This conclusion was supported by the fact that Tax mutants unable to stimulate the NF-kappaB pathway could not inhibit c-Myb transactivating functions. |
| 83 | 11585920 | In addition, inhibition of Tax-mediated NF-kappaB activation by coexpression of IkappaBalpha restored c-Myb transcription, and Tax was unable to block c-Myb transcription in a NEMO knockout cell line. |
| 84 | 11585920 | Importantly, physiological stimuli, such as signaling with the cellular cytokines tumor necrosis factor alpha, interleukin 1 beta (IL-1beta), and lipopolysaccharide, also inhibited c-Myb transcription. |
| 85 | 11585920 | Interestingly, an amino-terminal deletion form of p300 lacking the C/H1 and KIX domains and unable to bind RelA retained the ability to stimulate c-Myb transcription and prevented NF-kappaB-mediated repression. |
| 86 | 11585920 | Human T-cell lymphotropic virus type 1 Tax represses c-Myb-dependent transcription through activation of the NF-kappaB pathway and modulation of coactivator usage. |
| 87 | 11585920 | Here we demonstrate that activation of the NF-kappaB pathway by the HTLV-1 Tax protein leads to transcriptional inactivation of c-Myb. |
| 88 | 11585920 | This conclusion was supported by the fact that Tax mutants unable to stimulate the NF-kappaB pathway could not inhibit c-Myb transactivating functions. |
| 89 | 11585920 | In addition, inhibition of Tax-mediated NF-kappaB activation by coexpression of IkappaBalpha restored c-Myb transcription, and Tax was unable to block c-Myb transcription in a NEMO knockout cell line. |
| 90 | 11585920 | Importantly, physiological stimuli, such as signaling with the cellular cytokines tumor necrosis factor alpha, interleukin 1 beta (IL-1beta), and lipopolysaccharide, also inhibited c-Myb transcription. |
| 91 | 11585920 | Interestingly, an amino-terminal deletion form of p300 lacking the C/H1 and KIX domains and unable to bind RelA retained the ability to stimulate c-Myb transcription and prevented NF-kappaB-mediated repression. |
| 92 | 11823477 | This ability is dependent on MyD88 and Toll-like receptor (TLR)2 expression, as demonstrated by a lack of a response by B cells from MyD88 or TLR2 knockout mice to the porins. |
| 93 | 11823477 | Using previously described TLR2-dependent reporter constructs, these results were confirmed and were shown to be due to induction of NF-kappaB nuclear translocation. |
| 94 | 11861616 | The recognition of CpG motifs requires Toll-like receptor (TLR) 9, which triggers alterations in cellular redox balance and the induction of cell signaling pathways including the mitogen activated protein kinases (MAPKs) and NF kappa B. |
| 95 | 11861616 | Cells that express TLR-9, which include plasmacytoid dendritic cells (PDCs) and B cells, produce Th1-like proinflammatory cytokines, interferons, and chemokines. |
| 96 | 11991987 | Among the proinflammatory cytokines and their mRNAs measured (IL-6, IL-1 beta, IL-8, and tumor necrosis factor alpha), IL-8 showed the greatest change following D2V infection. |
| 97 | 11991987 | Nuclear factor kappa B (NF-kappa B) and nuclear factor IL-6 (NFIL-6) are primary mediators of IL-8 expression. |
| 98 | 11991987 | We studied the transcriptional regulation of IL-8 in the ECV304 and 293T cell lines and found that the induction of IL-8 gene expression involved the activation of NF-kappa B (P = 0.001) and, to a lesser extent, the activation of NFIL-6 in ECV304 cells only. |
| 99 | 11991987 | IL-8 produced by infected monocytes and also IL-8 that may be produced by endothelial or other epithelial cells is associated with the hyperacetylation of histones bound to the IL-8 promoter in addition to the activation of transcription by NF-kappa B. |
| 100 | 11991987 | Among the proinflammatory cytokines and their mRNAs measured (IL-6, IL-1 beta, IL-8, and tumor necrosis factor alpha), IL-8 showed the greatest change following D2V infection. |
| 101 | 11991987 | Nuclear factor kappa B (NF-kappa B) and nuclear factor IL-6 (NFIL-6) are primary mediators of IL-8 expression. |
| 102 | 11991987 | We studied the transcriptional regulation of IL-8 in the ECV304 and 293T cell lines and found that the induction of IL-8 gene expression involved the activation of NF-kappa B (P = 0.001) and, to a lesser extent, the activation of NFIL-6 in ECV304 cells only. |
| 103 | 11991987 | IL-8 produced by infected monocytes and also IL-8 that may be produced by endothelial or other epithelial cells is associated with the hyperacetylation of histones bound to the IL-8 promoter in addition to the activation of transcription by NF-kappa B. |
| 104 | 11991987 | Among the proinflammatory cytokines and their mRNAs measured (IL-6, IL-1 beta, IL-8, and tumor necrosis factor alpha), IL-8 showed the greatest change following D2V infection. |
| 105 | 11991987 | Nuclear factor kappa B (NF-kappa B) and nuclear factor IL-6 (NFIL-6) are primary mediators of IL-8 expression. |
| 106 | 11991987 | We studied the transcriptional regulation of IL-8 in the ECV304 and 293T cell lines and found that the induction of IL-8 gene expression involved the activation of NF-kappa B (P = 0.001) and, to a lesser extent, the activation of NFIL-6 in ECV304 cells only. |
| 107 | 11991987 | IL-8 produced by infected monocytes and also IL-8 that may be produced by endothelial or other epithelial cells is associated with the hyperacetylation of histones bound to the IL-8 promoter in addition to the activation of transcription by NF-kappa B. |
| 108 | 12203103 | The role of NF-kappaB in enhancement of TNF-alpha production was confirmed in experiments in which MG132, an inhibitor of NF-kappaB activation, reversed the effect of AdAMP. |
| 109 | 12203103 | AdAMP-induced augmentation of TNF-alpha production by B78/TNF cells was accompanied by morphological changes in the treated cells and a decrease in their adherence to fibrinogen and collagen IV. |
| 110 | 12349944 | P3CSK4 activates the expression of tumor suppressor protein p53 (p53), c-rel, inhibitor of nuclear factor kappa B (NFkappaB) alpha (IkappaB alpha), type 2 (inducible) nitric oxide (NO) synthase (iNOS), CD40-LR, intercellular adhesion molecule-1 (ICAM-1) and interleukin 1/6/15 (IL-1/6/15). |
| 111 | 12349944 | We detected no activation of heat shock protein (HSP) 27, 60, 84 and 86, osmotic stress protein 94 (Osp 94), IL-12, extracellular signal-regulated protein kinase 1 (ERK1), p38 mitogen activated protein (MAP)-kinase (p38), c-Jun NH2-terminal kinase (JNK), signal transducer and activator of transcription 1 (STAT1), CD14 and caspase genes. |
| 112 | 12349944 | Furthermore, we monitored inhibition of STAT6, Janus kinase 3 (Jak3) and cyclin D1/D3 gene transcription after stimulating bone marrow-derived macrophages (BMDM) with lipopeptide. |
| 113 | 12385032 | In experiments designed to get insights into the interactions between PTX and circulating immune cells, we first observed that addition of PTX to adult whole blood induced the release of IL-12 and TNF-alpha as well as maturation of myeloid dendritic cells (DC). |
| 114 | 12385032 | Secondly, studies on DC generated in vitro by culturing monocytes with IL-4 and GM-CSF showed that PTX directly stimulates MHC class II and costimulatory molecules up-regulation, cytokine synthesis and NF-kappa B activation. |
| 115 | 12391201 | CD28, TNF receptor, and IL-12 are critical for CD4-independent cross-priming of therapeutic antitumor CD8+ T cells. |
| 116 | 12391201 | Previously, we have shown that priming of therapeutic CD8(+) T cells in tumor vaccine-draining lymph nodes of mice vaccinated with GM-CSF secreting B16BL6 melanoma cells occurs independent of CD4 T cell help. |
| 117 | 12391201 | In this study, we examined the contribution of the major costimulatory molecules, CD40 ligand (CD40L), CD80, and CD86, in the priming of CD8(+) T cells. |
| 118 | 12391201 | Priming of therapeutic CD8(+) T cells by a GM-CSF-transduced tumor vaccine did not require CD40 and CD40L interactions, as therapeutic T cells could be generated from mice injected with anti-CD40L Ab and from CD40L knockout mice. |
| 119 | 12391201 | However, costimulation via either CD80 or CD86 was required, as therapeutic T cells could be generated from mice injected with either anti-CD80 or anti-CD86 Ab alone, but administration of both Abs completely inhibited the priming of therapeutic T cells. |
| 120 | 12391201 | Blocking experiments also identified that priming of therapeutic T cells in MHC class II-deficient mice required TNFR and IL-12 signaling, but signaling through CD40, lymphotoxin-betaR, or receptor activator of NF-kappaB was not essential. |
| 121 | 12391201 | Thus, cross-priming of therapeutic CD8(+) T cells by a tumor vaccine transduced with GM-CSF requires TNFR, IL-12, and CD28 signaling. |
| 122 | 12396612 | These activities include inhibition of cell proliferation, inhibition of NF-kappaB activation, inhibition of CD4 T-cell proliferation, and induction of apoptosis in tissue culture. |
| 123 | 12532177 | Researchers also discussed the role of IL1 gene family and TNF gene polymorphisms in gastric pathology and various immune mechanisms involved in gastric cancer, such as down-regulation of NF kappa B, IL-1 and IL-1RA, cyclooxygenase signalling, and identification of MGAg antibodies. |
| 124 | 12547609 | We report here the in vivo activity of a series of fully synthetic LPS receptor agonists that have been shown to activate NF-kappaB signaling through the Toll-like receptor 4 (TLR4). |
| 125 | 12595472 | The mutant was found to be severely defective in inducing leukocyte signaling, as shown by failure to (i) trigger caspase 3-mediated CD8(+)-T-cell apoptosis, (ii) activate nuclear translocation of NF-kappaB in Jurkat T cells, (iii) induce a potent anti-B-subunit response in mice, or (iv) serve as a mucosal adjuvant. |
| 126 | 12626542 | Members of the TNF ligand superfamily and the TNFR superfamily contribute to this costimulatory molecule signaling. |
| 127 | 12626542 | Coexpression of 4-1BBL in these E7-expressing DCs increased effector and memory CTL responses when they were used for immunization. 4-1BBL expression up-regulated CD80 and CD86 second signaling molecules in DCs. |
| 128 | 12626542 | We also report an additive effect of 4-1BBL and receptor activator of NF-kappa B/receptor activator of NF-kappa B ligand coexpression in E7-transduced DC immunogens on E7-directed effector and memory CTL responses and on MHC class II and CD80/86 expression in DCs. |
| 129 | 12641655 | Peripheral blood monocytes were differentiated into immature DCs with interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor, and pulsed with an immunogenic tetanus toxoid peptide. |
| 130 | 12641655 | However, stimulation with antigen-pulsed DCs overexpressing IotakappaBetaalpha, the endogenous inhibitor of NF-kappaB, led to a significant reduction in T-cell proliferation, and decreased production of interferon-gamma, IL-4 and IL-10, whereas transforming growth factor-beta production was low throughout. |
| 131 | 12654840 | Similarly, in vitro experiments using a human fetal intestinal epithelial cell line (INT 407) demonstrated that, although significantly (P < 0.05) fewer S. enterica serovar Infantis than S. enterica serovar Typhimurium organisms invaded the monolayers, S. enterica serovar Infantis induced an NF-kappaB response and significantly (P < 0.05) raised interleukin 8 levels and transmigration of porcine PMN. |
| 132 | 12686724 | Among those signaling pathways, activation of NF-kappaB leads to up-regulation of IL-1beta, IL-8 and TNF-alpha, mucin MUC2 and Toll-like receptor 2 (TLR2), whereas activation of p38 MAP kinase mediates not only up-regulation of inflammatory mediators and mucin MUC5AC but also down-regulation of TLR2. |
| 133 | 12686724 | Interestingly, NTHi-induced activation of the PI3K-Akt pathway, however, leads to inhibition of p38 mitogen-activated protein (MAP) kinase. |
| 134 | 12686724 | Moreover, the TGF-beta-Smad signaling pathway cooperates with NF-kappaB to mediate up-regulation of mucin MUC2. |
| 135 | 12686724 | Finally, glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAP kinase phosphatase-1 that, in turn, leads to inactivation of p38 MAP kinase, the negative regulator for TLR2 expression. |
| 136 | 12686724 | Among those signaling pathways, activation of NF-kappaB leads to up-regulation of IL-1beta, IL-8 and TNF-alpha, mucin MUC2 and Toll-like receptor 2 (TLR2), whereas activation of p38 MAP kinase mediates not only up-regulation of inflammatory mediators and mucin MUC5AC but also down-regulation of TLR2. |
| 137 | 12686724 | Interestingly, NTHi-induced activation of the PI3K-Akt pathway, however, leads to inhibition of p38 mitogen-activated protein (MAP) kinase. |
| 138 | 12686724 | Moreover, the TGF-beta-Smad signaling pathway cooperates with NF-kappaB to mediate up-regulation of mucin MUC2. |
| 139 | 12686724 | Finally, glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAP kinase phosphatase-1 that, in turn, leads to inactivation of p38 MAP kinase, the negative regulator for TLR2 expression. |
| 140 | 14530334 | Enhanced effector and memory CTL responses generated by incorporation of receptor activator of NF-kappa B (RANK)/RANK ligand costimulatory molecules into dendritic cell immunogens expressing a human tumor-specific antigen. |
| 141 | 14530334 | In this study, we used adenoviral vectors to express a model tumor Ag (the E7 oncoprotein of human papillomavirus 16) with or without coexpression of receptor activator of NF-kappaB (RANK)/RANK ligand (RANKL) or CD40/CD40L costimulatory molecules, and used these transgenic DCs to immunize mice for the generation of E7-directed CD8(+) T cell responses. |
| 142 | 14530334 | We show that coexpression of RANK/RANKL, but not CD40/CD40L, in E7-expressing DCs augmented E7-specific IFN-gamma-secreting effector and memory T cells and E7-specific CTLs. |
| 143 | 14530334 | These responses were also augmented by coexpression of T cell costimulatory molecules (RANKL and CD40L) or DC costimulatory molecules (RANK and CD40) in the E7-expressing DC immunogens. |
| 144 | 14530334 | Augmentation of CTL responses correlated with up-regulation of CD80 and CD86 expression in DCs transduced with costimulatory molecules, suggesting a mechanism for enhanced T cell activation/survival. |
| 145 | 14530334 | Enhanced effector and memory CTL responses generated by incorporation of receptor activator of NF-kappa B (RANK)/RANK ligand costimulatory molecules into dendritic cell immunogens expressing a human tumor-specific antigen. |
| 146 | 14530334 | In this study, we used adenoviral vectors to express a model tumor Ag (the E7 oncoprotein of human papillomavirus 16) with or without coexpression of receptor activator of NF-kappaB (RANK)/RANK ligand (RANKL) or CD40/CD40L costimulatory molecules, and used these transgenic DCs to immunize mice for the generation of E7-directed CD8(+) T cell responses. |
| 147 | 14530334 | We show that coexpression of RANK/RANKL, but not CD40/CD40L, in E7-expressing DCs augmented E7-specific IFN-gamma-secreting effector and memory T cells and E7-specific CTLs. |
| 148 | 14530334 | These responses were also augmented by coexpression of T cell costimulatory molecules (RANKL and CD40L) or DC costimulatory molecules (RANK and CD40) in the E7-expressing DC immunogens. |
| 149 | 14530334 | Augmentation of CTL responses correlated with up-regulation of CD80 and CD86 expression in DCs transduced with costimulatory molecules, suggesting a mechanism for enhanced T cell activation/survival. |
| 150 | 14593121 | Here, we demonstrate that the p50/p65 NF-kappaB transcription factors enhanced the Tat-mediated transcriptional activation of SIVmac239. |
| 151 | 14627128 | Immature monocyte-derived dendritic cells (imMo-DCs) isolated from human peripheral blood monocytes stimulated with granulocyte-macrophage colony stimulating factor and interleukin-4 were exposed to maturation factors, i.e., lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF-alpha) plus prostaglandin E2 (PGE2), and OK-432 for 2 days. |
| 152 | 14627128 | OK-432 increased expression of activation- and maturation-related molecules such as HLA-DR, CD80, CD83, and CD86 in imMo-DCs at levels similar to that of TNF-alpha plus PGE2, and higher than that of LPS. |
| 153 | 14627128 | Only OK-432 caused significant production of interleukin-12 (IL-12) p70 and interferon gamma (IFN-gamma) at both the mRNA and protein levels in imMo-DCs. |
| 154 | 14627128 | Neutralizing antibody against IL-12 p70 blocked IFN-gamma secretion from OK-432-stimulated Mo-DCs. |
| 155 | 14627128 | IL-12 p70 produced by OK-432-stimulated imMo-DCs induced secretion of IFN-gamma by CD4+ T cells. |
| 156 | 14627128 | Both secretion of IL-12 p70 and IFN-gamma and activation of NF-kappaB induced by OK-432 were suppressed when imMo-DCs were pretreated with cytochalasin B. |
| 157 | 14627128 | These results indicate that uptake of OK-432 by imMo-DCs is an early critical event for IL-12 p70 production and that NF-kappaB activation induced by OK-432 also contributes partially to IL-12 p70 production. |
| 158 | 14627128 | Immature monocyte-derived dendritic cells (imMo-DCs) isolated from human peripheral blood monocytes stimulated with granulocyte-macrophage colony stimulating factor and interleukin-4 were exposed to maturation factors, i.e., lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF-alpha) plus prostaglandin E2 (PGE2), and OK-432 for 2 days. |
| 159 | 14627128 | OK-432 increased expression of activation- and maturation-related molecules such as HLA-DR, CD80, CD83, and CD86 in imMo-DCs at levels similar to that of TNF-alpha plus PGE2, and higher than that of LPS. |
| 160 | 14627128 | Only OK-432 caused significant production of interleukin-12 (IL-12) p70 and interferon gamma (IFN-gamma) at both the mRNA and protein levels in imMo-DCs. |
| 161 | 14627128 | Neutralizing antibody against IL-12 p70 blocked IFN-gamma secretion from OK-432-stimulated Mo-DCs. |
| 162 | 14627128 | IL-12 p70 produced by OK-432-stimulated imMo-DCs induced secretion of IFN-gamma by CD4+ T cells. |
| 163 | 14627128 | Both secretion of IL-12 p70 and IFN-gamma and activation of NF-kappaB induced by OK-432 were suppressed when imMo-DCs were pretreated with cytochalasin B. |
| 164 | 14627128 | These results indicate that uptake of OK-432 by imMo-DCs is an early critical event for IL-12 p70 production and that NF-kappaB activation induced by OK-432 also contributes partially to IL-12 p70 production. |
| 165 | 14630697 | Moreover, cells pretreated with an inhibitor of p38 kinase (SB 208530) inhibited Gal-lectin induced TLR-2 mRNA expression by 40%. |
| 166 | 14630697 | We conclude that the Gal-lectin activates NF-kappaB and MAP kinase-signaling pathways in macrophages culminating in the induction of several genes including TLR-2 and hypothesize that this could have a significant impact on macrophage activation and contribute to amoebic pathogenesis. |
| 167 | 14662831 | Cutting edge: a potent adjuvant effect of ligand to receptor activator of NF-kappa B gene for inducing antigen-specific CD8+ T cell response by DNA and viral vector vaccination. |
| 168 | 14662831 | The ligand to receptor activator of NF-kappaB (RANK-L)/RANK interaction has been implicated in CD40 ligand/CD40-independent T cell priming by dendritic cells. |
| 169 | 14662831 | In this report, we show that the coadministration of the RANK-L gene with a Trypanosoma cruzi gene markedly enhances the induction of Trypanosoma Ag-specific CD8(+) T cells and improves the DNA vaccine efficacy. |
| 170 | 14662831 | A similarly potent adjuvant effect of the RANK-L gene on the induction of Ag-specific CD8(+) T cells was also observed when recombinant influenza virus expressing murine malaria Ag was used as an immunogen. |
| 171 | 14662831 | Our results demonstrated, for the first time, the potent immunostimulatory effect of the RANK-L gene to improve the CD8(+) T cell-mediated immunity against infectious agents. |
| 172 | 14662831 | Cutting edge: a potent adjuvant effect of ligand to receptor activator of NF-kappa B gene for inducing antigen-specific CD8+ T cell response by DNA and viral vector vaccination. |
| 173 | 14662831 | The ligand to receptor activator of NF-kappaB (RANK-L)/RANK interaction has been implicated in CD40 ligand/CD40-independent T cell priming by dendritic cells. |
| 174 | 14662831 | In this report, we show that the coadministration of the RANK-L gene with a Trypanosoma cruzi gene markedly enhances the induction of Trypanosoma Ag-specific CD8(+) T cells and improves the DNA vaccine efficacy. |
| 175 | 14662831 | A similarly potent adjuvant effect of the RANK-L gene on the induction of Ag-specific CD8(+) T cells was also observed when recombinant influenza virus expressing murine malaria Ag was used as an immunogen. |
| 176 | 14662831 | Our results demonstrated, for the first time, the potent immunostimulatory effect of the RANK-L gene to improve the CD8(+) T cell-mediated immunity against infectious agents. |
| 177 | 14685242 | The gene product Murr1 restricts HIV-1 replication in resting CD4+ lymphocytes. |
| 178 | 14685242 | Here we show that Murr1, a gene product known previously for its involvement in copper regulation, inhibits HIV-1 growth in unstimulated CD4+ T cells. |
| 179 | 14685242 | Knockdown of Murr1 increased NF-kappaB activity and decreased IkappaB-alpha concentrations by facilitating phospho-IkappaB-alpha degradation by the proteasome. |
| 180 | 14685242 | Murr1 was detected in CD4+ T cells, and RNA-mediated interference of Murr1 in primary resting CD4+ lymphocytes increased HIV-1 replication. |
| 181 | 14722263 | The core enhancer and promoter sequences of the SIV macaque 239nefstop strain (NF-kappaB/Sp1 region from -114 bp to mRNA start) have been exchanged for those of the human cytomegalovirus immediate-early promoter (CMV-IE; from -525 bp to mRNA start). |
| 182 | 14963119 | Mice treated intranasally with interleukin-10 or with a specific cell-permeable peptide that blocks the association of the catalytic subunit IKKbeta with the regulatory protein NEMO showed a striking reduction of lung NF-kappaB DNA binding activity, chemokine gene expression, and airway inflammation in response to RSV infection. |
| 183 | 14975502 | Chloroquine and related anti-malarial drugs appear to promote apoptosis in T-cells by suppressing NF-kappa-B, which enhances the expression of anti-apoptotic proteins (e.g., Bcl-2). |
| 184 | 14975502 | It appears that in the case of HIV, the increased resistance to apoptosis is provided by expression of Bcl-2 and suppression of p53. |
| 185 | 14975502 | Hence, drugs that suppresses Bcl-2 or restore p53 function might be effective in restoring the parity of resistance to apoptosis between infected and uninfected cells. |
| 186 | 15162438 | RNA interference technology has been used to modulate dendritic cell (DC) function by targeting the expression of genes such as IL-12 and NF-kappa B. |
| 187 | 15162438 | Inhibition of IL-10 by siRNA was accompanied by increased CD40 expression and IL-12 production after maturation, which endowed DC with the ability to significantly enhance allogeneic T cell proliferation. |
| 188 | 15162438 | IL-10 siRNA transfection did not affect MHC class II, CD86, CD83, or CD54 expression in mature DC. |
| 189 | 15162438 | To further test the ability of IL-10 siRNA-treated DC to induce a T cell response, naive CD4 T cells were stimulated by autologous DC pulsed with KLH. |
| 190 | 15162438 | The results indicated that IL-10 siRNA-transfected DC enhanced Th1 responses by increasing IFN-gamma and decreasing IL-4 production. |
| 191 | 15181282 | CD137 (4-1BB), is an inducible T-cell costimulatory receptor and a member of the tumor necrosis factor receptor (TNFR) superfamily. |
| 192 | 15181282 | The natural counter receptor for CD137 is 4-1BB ligand, a member of the TNF superfamily that is weakly expressed on naïve or resting B cells, macrophages, and DCs. |
| 193 | 15181282 | In T cells CD137-induced signals lead to the recruitment of TRAF family members and activation of several kinases, including ASK-1, MKK, MAPK3/ MAPK4, p38, and JNK/SAPK. |
| 194 | 15181282 | Kinase activation is then followed by the activation and nuclear translocation of several transcription factors, including ATF-2, Jun, and NF-kappaB. |
| 195 | 15181282 | In addition to augmenting suboptimal TCR-induced proliferation, CD137-mediated signaling protects T cells, and in particular, CD8+ T cells from activation-induced cell death (AICD). |
| 196 | 15189567 | NF-kappaB p50 facilitates neutrophil accumulation during LPS-induced pulmonary inflammation. |
| 197 | 15331713 | IFN synthesis is regulated by specific transcription factors, including interferon regulatory factor (IRF-3), NF-kappaB, and AP-1. |
| 198 | 15331713 | Likewise, NF-kappaB and AP-1 were activated normally, as shown in electrophoretic mobility shift assays. |
| 199 | 15331713 | IFN synthesis is regulated by specific transcription factors, including interferon regulatory factor (IRF-3), NF-kappaB, and AP-1. |
| 200 | 15331713 | Likewise, NF-kappaB and AP-1 were activated normally, as shown in electrophoretic mobility shift assays. |
| 201 | 15353589 | CD26 up-regulates expression of CD86 on antigen-presenting cells by means of caveolin-1. |
| 202 | 15353589 | We now demonstrate that CD26 binds Caveolin-1 on antigen-presenting cells, and that residues 201-211 of CD26 along with the serine catalytic site at residue 630 contribute to binding to caveolin-1 scaffolding domain. |
| 203 | 15353589 | In addition, after CD26-caveolin-1 interaction on TT-loaded monocytes, caveolin-1 is phosphorylated, which links to activate NF-kappaB, followed by up-regulation of CD86. |
| 204 | 15353589 | Finally, reduced caveolin-1 expression on monocytes inhibits CD26-mediated CD86 up-regulation and abrogates CD26 effect on TT-induced T cell proliferation. |
| 205 | 15353589 | Taken together, these results strongly suggest that CD26-caveolin-1 interaction plays a role in the up-regulation of CD86 on TT-loaded monocytes and subsequent engagement with CD28 on T cells, leading to antigen-specific T cell activation. |
| 206 | 15482852 | Porin of Shigella dysenteriae type 1 increased the mRNA levels for Toll-like receptor (TLR) 2 and TLR6 by 1.5- and 2.9-fold respectively, of peritoneal cavity B-1a and B-1b cells, implicating that coexpression of TLR2 and TLR6 is essential as a combinatorial repertoire for recognition of porin by the B-1 cells. |
| 207 | 15482852 | Among the two key TLRs, TLR2 and TLR4, which are primarily responsible for recognizing majority of the bacterial products, TLR2 and not TLR4, participates in porin recognition. |
| 208 | 15482852 | TLR2 got increased on both the B-1 cell populations whereas the TLR4 expression remained unaffected. |
| 209 | 15482852 | Both of the B-1 cell populations expressed strongly the mRNA for NF-kappaB in the presence of porin, that was 2.4-fold more than untreated control, conforming to the earlier finding that coexpression of TLR2 and TLR6, resulted in robust NF-kappaB activation for signaling. |
| 210 | 15482852 | CD80 expression got enhanced on the B-1a cells whereas CD86 got solely expressed on B-1b cells. |
| 211 | 15482852 | The porin-mediated induction of IgA was augmented by interleukin-6 on B-1a and B-1b cells, by 2.4- and 2.6-fold, respectively. |
| 212 | 15585831 | Cutting edge: CD28-mediated transcriptional and posttranscriptional regulation of IL-2 expression are controlled through different signaling pathways. |
| 213 | 15585831 | PI3K was identified early as a candidate for CD28 signaling, but conflicting data during the past decade has left the role of PI3K unresolved. |
| 214 | 15585831 | We show that mutation of the PI3K interaction site in the cytosolic tail of CD28 site disrupts the ability of CD28 to recruit protein kinase C-theta; to the central supramolecular activation cluster (c-SMAC) region of the immunological synapse, promote NF-kappaB nuclear translocation, and enhance IL-2 gene transcription. |
| 215 | 15585831 | In contrast, mutation of the PI3K interaction site had no effect on the ability of CD28 to enhance IL-2 mRNA stability. |
| 216 | 15585831 | These results suggest that two distinct pathways mediate CD28-induced up-regulation of IL-2 expression, a PI3K-dependent pathway that may function through the immunological synapse to enhance IL-2 transcription and a PI3K-independent pathway that induces IL-2 mRNA stability. |
| 217 | 15653568 | Nod1 gene silencing by small interfering RNA reduced C pneumoniae-induced IL-8 release markedly. |
| 218 | 15653568 | Moreover, in HEK293 cells, overexpressed Nod1 or Nod2 amplified the capacity of C pneumoniae to induce nuclear factor kappaB (NF-kappaB) activation. |
| 219 | 15661045 | Activation of dendritic cells by human papillomavirus-like particles through TLR4 and NF-kappaB-mediated signalling, moderated by TGF-beta. |
| 220 | 15661045 | VLP-induced induction of costimulatory molecule expression, RelB activation and cytokine secretion by DC was blocked by inhibition of NF-kappaB activation, heparin or TLR4 mAb. |
| 221 | 15661045 | The data provide evidence that HPV-VLP signal DC through a pathway involving proteoglycan receptors, TLR4 and NF-kappaB, and shed light on the mechanism by which VLP stimulate immunity in the absence of adjuvants in vivo. |
| 222 | 15661045 | Activation of dendritic cells by human papillomavirus-like particles through TLR4 and NF-kappaB-mediated signalling, moderated by TGF-beta. |
| 223 | 15661045 | VLP-induced induction of costimulatory molecule expression, RelB activation and cytokine secretion by DC was blocked by inhibition of NF-kappaB activation, heparin or TLR4 mAb. |
| 224 | 15661045 | The data provide evidence that HPV-VLP signal DC through a pathway involving proteoglycan receptors, TLR4 and NF-kappaB, and shed light on the mechanism by which VLP stimulate immunity in the absence of adjuvants in vivo. |
| 225 | 15661045 | Activation of dendritic cells by human papillomavirus-like particles through TLR4 and NF-kappaB-mediated signalling, moderated by TGF-beta. |
| 226 | 15661045 | VLP-induced induction of costimulatory molecule expression, RelB activation and cytokine secretion by DC was blocked by inhibition of NF-kappaB activation, heparin or TLR4 mAb. |
| 227 | 15661045 | The data provide evidence that HPV-VLP signal DC through a pathway involving proteoglycan receptors, TLR4 and NF-kappaB, and shed light on the mechanism by which VLP stimulate immunity in the absence of adjuvants in vivo. |
| 228 | 15663361 | And, finally, we show that there is no change in NF-kappaB or Blimp-1 in old vs young stimulated B cells. |
| 229 | 15699162 | CpG RNA: identification of novel single-stranded RNA that stimulates human CD14+CD11c+ monocytes. |
| 230 | 15699162 | The current study identifies a novel class of single-stranded oligoribonucleotides (ORN) containing unmethylated CpG motifs and a poly(G) run at the 3' end (CpG ORN) that directly stimulate human CD14+CD11c+ monocytes but not dendritic cells or B cells. |
| 231 | 15699162 | CpG ORN activate NF-kappaB and p38 MAPK, resulting in IL-6 and IL-12 production and costimulatory molecule up-regulation but not IFNalpha. |
| 232 | 15809303 | Furthermore, we show that whereas mycobacterial heat shock protein 65 signals exclusively through Toll-like receptor 4, heat shock protein 70 also signals through Toll-like receptor 2. |
| 233 | 15809303 | Mycobacterial heat shock protein 65-induced NF-kappaB activation was MyD88-, TIRAP-, TRIF-, and TRAM-dependent and required the presence of MD-2. |
| 234 | 15827150 | Effects of nonstructural proteins NS1 and NS2 of human respiratory syncytial virus on interferon regulatory factor 3, NF-kappaB, and proinflammatory cytokines. |
| 235 | 15827150 | It has been shown previously that HRSV nonstructural proteins 1 and 2 (NS1 and NS2) inhibit the induction of alpha/beta interferon (IFN-alpha/beta) in A549 cells and human macrophages. |
| 236 | 15827150 | Two principal transcription factors for the early IFN-beta and -alpha1 response are interferon regulatory factor 3 (IRF-3) and nuclear factor kappaB (NF-kappaB). |
| 237 | 15827150 | At early times postinfection, wild-type HRSV and the NS1/NS2 deletion mutants were very similar in the ability to activate IRF-3. |
| 238 | 15827150 | However, once NS1 and NS2 were expressed significantly, they acted cooperatively to suppress activation and nuclear translocation of IRF-3. |
| 239 | 15827150 | Since these viruses differed greatly in the induction of IFN-alpha/beta, NF-kappaB activation was evaluated in Vero cells, which lack the structural genes for IFN-alpha/beta and would preclude confounding effects of IFN-alpha/beta. |
| 240 | 15827150 | Since recombinant HRSVs from which the NS1 or NS2 genes have been deleted are being developed as vaccine candidates, we investigated whether the changes in activation of host transcription factors and increased IFN-alpha/beta production had an effect on the epithelial production of proinflammatory factors. |
| 241 | 15827150 | Viruses lacking NS1 and/or NS2 stimulated modestly lower production of RANTES (Regulated on Activation Normal T-cell Expressed and Secreted), interleukin 8, and tumor necrosis factor alpha compared to wild-type recombinant RSV, supporting their use as attenuated vaccine candidates. |
| 242 | 15827150 | Effects of nonstructural proteins NS1 and NS2 of human respiratory syncytial virus on interferon regulatory factor 3, NF-kappaB, and proinflammatory cytokines. |
| 243 | 15827150 | It has been shown previously that HRSV nonstructural proteins 1 and 2 (NS1 and NS2) inhibit the induction of alpha/beta interferon (IFN-alpha/beta) in A549 cells and human macrophages. |
| 244 | 15827150 | Two principal transcription factors for the early IFN-beta and -alpha1 response are interferon regulatory factor 3 (IRF-3) and nuclear factor kappaB (NF-kappaB). |
| 245 | 15827150 | At early times postinfection, wild-type HRSV and the NS1/NS2 deletion mutants were very similar in the ability to activate IRF-3. |
| 246 | 15827150 | However, once NS1 and NS2 were expressed significantly, they acted cooperatively to suppress activation and nuclear translocation of IRF-3. |
| 247 | 15827150 | Since these viruses differed greatly in the induction of IFN-alpha/beta, NF-kappaB activation was evaluated in Vero cells, which lack the structural genes for IFN-alpha/beta and would preclude confounding effects of IFN-alpha/beta. |
| 248 | 15827150 | Since recombinant HRSVs from which the NS1 or NS2 genes have been deleted are being developed as vaccine candidates, we investigated whether the changes in activation of host transcription factors and increased IFN-alpha/beta production had an effect on the epithelial production of proinflammatory factors. |
| 249 | 15827150 | Viruses lacking NS1 and/or NS2 stimulated modestly lower production of RANTES (Regulated on Activation Normal T-cell Expressed and Secreted), interleukin 8, and tumor necrosis factor alpha compared to wild-type recombinant RSV, supporting their use as attenuated vaccine candidates. |
| 250 | 15827150 | Effects of nonstructural proteins NS1 and NS2 of human respiratory syncytial virus on interferon regulatory factor 3, NF-kappaB, and proinflammatory cytokines. |
| 251 | 15827150 | It has been shown previously that HRSV nonstructural proteins 1 and 2 (NS1 and NS2) inhibit the induction of alpha/beta interferon (IFN-alpha/beta) in A549 cells and human macrophages. |
| 252 | 15827150 | Two principal transcription factors for the early IFN-beta and -alpha1 response are interferon regulatory factor 3 (IRF-3) and nuclear factor kappaB (NF-kappaB). |
| 253 | 15827150 | At early times postinfection, wild-type HRSV and the NS1/NS2 deletion mutants were very similar in the ability to activate IRF-3. |
| 254 | 15827150 | However, once NS1 and NS2 were expressed significantly, they acted cooperatively to suppress activation and nuclear translocation of IRF-3. |
| 255 | 15827150 | Since these viruses differed greatly in the induction of IFN-alpha/beta, NF-kappaB activation was evaluated in Vero cells, which lack the structural genes for IFN-alpha/beta and would preclude confounding effects of IFN-alpha/beta. |
| 256 | 15827150 | Since recombinant HRSVs from which the NS1 or NS2 genes have been deleted are being developed as vaccine candidates, we investigated whether the changes in activation of host transcription factors and increased IFN-alpha/beta production had an effect on the epithelial production of proinflammatory factors. |
| 257 | 15827150 | Viruses lacking NS1 and/or NS2 stimulated modestly lower production of RANTES (Regulated on Activation Normal T-cell Expressed and Secreted), interleukin 8, and tumor necrosis factor alpha compared to wild-type recombinant RSV, supporting their use as attenuated vaccine candidates. |
| 258 | 15858025 | Immediately upon entry, viruses activate interferon-regulatory factor 3 (IRF3), as well as nuclear factor kappaB (NF-kappaB), which transactivate a subset of ISGs, proinflammatory genes, as well as IFN genes. |
| 259 | 15858025 | Since infection during inhibition of protein expression by cycloheximide or inactivation of viral gene expression by UV treatment did not trigger IRF3 activation or ISG expression by RhCMV, we conclude that RhCMV virions contain a novel inhibitor of IFN-independent viral induction of ISG expression by IRF3. |
| 260 | 15925273 | The recognition leads to activation of intracellular pathways involving nuclear factor kappa B (NF-kappaB) and mitogen-activated protein kinases (MAPK), such as the c-Jun NH2-terminal kinase (JNK), and p38. |
| 261 | 15925273 | We show that in vitro infection with Francisella tularensis results in activation of NF-kappaB, phosphorylation of p38 and c-Jun, and secretion of TNF-alpha in adherent mouse peritoneal cells, in the mouse macrophage-like cell line J774A.1, in the human macrophage cell line THP-1, and in human peripheral blood monocytic cells. |
| 262 | 15925273 | The recognition leads to activation of intracellular pathways involving nuclear factor kappa B (NF-kappaB) and mitogen-activated protein kinases (MAPK), such as the c-Jun NH2-terminal kinase (JNK), and p38. |
| 263 | 15925273 | We show that in vitro infection with Francisella tularensis results in activation of NF-kappaB, phosphorylation of p38 and c-Jun, and secretion of TNF-alpha in adherent mouse peritoneal cells, in the mouse macrophage-like cell line J774A.1, in the human macrophage cell line THP-1, and in human peripheral blood monocytic cells. |
| 264 | 16103156 | Dengue virus nonstructural protein NS5 induces interleukin-8 transcription and secretion. |
| 265 | 16103156 | DEN2V infection of HepG2 and primary dendritic cells induced the production of interleukin-8 (IL-8), RANTES, MIP-1alpha, and MIP-1beta, whereas only IL-8 and RANTES were induced following dengue virus infection of HEK293 cells. |
| 266 | 16103156 | Transfection of a plasmid expressing NS5 or a dengue virus replicon induced IL-8 gene expression and secretion. |
| 267 | 16103156 | Reporter assays showed that IL-8 induction by NS5 was principally through CAAT/enhancer binding protein, whereas DEN2V infection also induced NF-kappaB. |
| 268 | 16103156 | These results indicate a role for the dengue virus NS5 protein in the induction of IL-8 by DEN2V infection. |
| 269 | 16107720 | CD26 mediates dissociation of Tollip and IRAK-1 from caveolin-1 and induces upregulation of CD86 on antigen-presenting cells. |
| 270 | 16107720 | We have previously reported that the addition of recombinant soluble CD26 resulted in enhanced proliferation of human T lymphocytes induced by the recall antigen tetanus toxoid (TT) via upregulation of CD86 on monocytes and that caveolin-1 was a binding protein of CD26, and the CD26-caveolin-1 interaction resulted in caveolin-1 phosphorylation (p-cav-1) as well as TT-mediated T-cell proliferation. |
| 271 | 16107720 | Through proteomic analysis, we identify Tollip (Toll-interacting protein) and IRAK-1 (interleukin-1 receptor-associated serine/threonine kinase 1) as caveolin-1-interacting proteins in monocytes. |
| 272 | 16107720 | We also demonstrate that following stimulation by exogenous CD26, Tollip and IRAK-1 dissociate from caveolin-1, and IRAK-1 is then phosphorylated in the cytosol, leading to the upregulation of CD86 via activation of NF-kappaB. |
| 273 | 16107720 | Binding of CD26 to caveolin-1 therefore regulates signaling pathways in antigen-presenting cells to induce antigen-specific T-cell proliferation. |
| 274 | 16139443 | These results suggest that Trp-P-1 induces NO production mediated by an increased intracellular ROS, NF-kappaB activation, and subsequent iNOS gene expression. |
| 275 | 16168555 | Reverse transcription-polymerase chain reaction (RT-PCR) analysis demonstrated that PhIP attenuated IL-2 mRNA expression in the thymocytes and EL4 cells stimulated with phytohemagglutinin (PHA) plus phorbol 12-myristate 13-acetate (PMA). |
| 276 | 16168555 | Furthermore, an electrophoretic mobility shift assay showed that PhIP inhibited DNA binding activity of nuclear factor for immunoglobulin kappa chain in B cells (NF-kappaB), activator protein-1 (AP-1) and nuclear factor of activated T cells (NF-AT), which are known to be responsible for IL-2 transcriptional activation. |
| 277 | 16168555 | These results suggest that PhIP has potential immunosuppressive effects by inhibiting T-cell proliferation and IL-2 expression through down regulation of ROS generation and thereby inhibiting NF-kappaB, AP-1 and NF-AT activation. |
| 278 | 16168555 | Reverse transcription-polymerase chain reaction (RT-PCR) analysis demonstrated that PhIP attenuated IL-2 mRNA expression in the thymocytes and EL4 cells stimulated with phytohemagglutinin (PHA) plus phorbol 12-myristate 13-acetate (PMA). |
| 279 | 16168555 | Furthermore, an electrophoretic mobility shift assay showed that PhIP inhibited DNA binding activity of nuclear factor for immunoglobulin kappa chain in B cells (NF-kappaB), activator protein-1 (AP-1) and nuclear factor of activated T cells (NF-AT), which are known to be responsible for IL-2 transcriptional activation. |
| 280 | 16168555 | These results suggest that PhIP has potential immunosuppressive effects by inhibiting T-cell proliferation and IL-2 expression through down regulation of ROS generation and thereby inhibiting NF-kappaB, AP-1 and NF-AT activation. |
| 281 | 16256245 | Modification of cysteine by introducing either a methyl or t-butyl group in the free sulfhydryl group and replacing the guanidine group with a urea linkage in the side chain of arginine in the cysteine-rich and arginine-rich Tat peptide sequences completely blocked the ability of these peptides to induce HIV replication, chemokine receptor CCR-5 expression, and NF-kappaB activity in monocytes. |
| 282 | 16275627 | Chlorophyllin attenuates IFN-gamma expression in lipopolysaccharide-stimulated murine splenic mononuclear cells via suppressing IL-12 production. |
| 283 | 16275627 | RT-PCR analysis showed that LPS-activated IFN-gamma expression gradually declined by CHL treatment in a dose dependent manner while mRNA production of TNF-alpha, IL-2, and FasL was not changed. |
| 284 | 16275627 | CHL also suppressed IL-12 production (p70, a heterodimer of p40 and p35) and the mRNA expression of IL-12 p40 and IL-12 receptors (both IL-12Rbeta1 and IL-12Rbeta2), which are involved in the induction of IFN-gamma expression. |
| 285 | 16275627 | Furthermore, an electrophoretic mobility shift assay showed that CHL inhibited DNA binding activity of NF-kappaB, STAT-3, and STAT-4 to their cognate DNA recognition motifs, all of which contribute to the IL-12-induced IFN-gamma transcription. |
| 286 | 16275627 | Exogenous addition of recombinant IL-12 abrogated the inhibitory effect of CHL on IFN-gamma and its mRNA expression in LPS-activated splenocytes. |
| 287 | 16275627 | Collectively, these results show that CHL inhibits IFN-gamma production by LPS-stimulated splenic mononuclear cells due to down-regulation of IL-12 production. |
| 288 | 16314010 | These results suggest that the soluble TLR5 serves as an adjuvant augmenting flagellin-TLR5-mediated NF-kappaB activation even in human. |
| 289 | 16339569 | Differential regulation of osteoblast activity by Th cell subsets mediated by parathyroid hormone and IFN-gamma. |
| 290 | 16339569 | In primary osteoblasts cultured in Th2 cell condition medium, the alkaline phosphatase (ALP) activity was maintained at a basal level. |
| 291 | 16339569 | However, antagonizing PTH in the condition medium resulted in a significant reduction of the ALP activity. |
| 292 | 16339569 | Conversely, treatment of osteoblasts with IFN-gamma suppressed the ALP activity. |
| 293 | 16339569 | In addition, the Th2 cytokine environment also regulated to expression of receptor activator of NF-kappaB ligand and osteoprotegerin through both PTH-dependent and -independent mechanisms. |
| 294 | 16369026 | FlaB bound directly to human TLR5 expressed on cultured epithelial cells and consequently induced NF-kappaB and interleukin-8 activation. |
| 295 | 16379000 | Upregulated transcripts correlated with genes implicated in immune responses, including those encoding interleukin-1 receptor 2 (IL-1R2), IL-6, ISG-15, CD-80, and TNFSF7. |
| 296 | 16379000 | NYVAC infection also stimulated the expression of NF-kappaB1 and NF-kappaB2 as well as that of NF-kappaB target genes. |
| 297 | 16399630 | Chlorophyllin suppresses interleukin-1 beta expression in lipopolysaccharide-activated RAW 264.7 cells. |
| 298 | 16399630 | Furthermore, CHL attenuated the activation of NF-kappaB, NF-IL6 and AP-1, which are known to be responsible for IL-1beta gene expression, as determined by an electrophoretic mobility shift assay and an in vitro transfection assay using p(NF-kappaB)3-CAT, p(NF-IL6)3-CAT, and p(AP-1)3-CAT, respectively. |
| 299 | 16399630 | The immunoblot experiment demonstrated that CHL also caused a substantial decrease in the phosphorylation of p38 MAP kinase in LPS-stimulated RAW 264.7. |
| 300 | 16399630 | These results suggest that CHL inhibits IL-1beta production in macrophages stimulated with LPS at transcriptional level by blocking the phosphorylation of p38 and by suppressing the activation of transcription factors, NF-kappaB, NF-IL6, and AP-1. |
| 301 | 16399630 | Chlorophyllin suppresses interleukin-1 beta expression in lipopolysaccharide-activated RAW 264.7 cells. |
| 302 | 16399630 | Furthermore, CHL attenuated the activation of NF-kappaB, NF-IL6 and AP-1, which are known to be responsible for IL-1beta gene expression, as determined by an electrophoretic mobility shift assay and an in vitro transfection assay using p(NF-kappaB)3-CAT, p(NF-IL6)3-CAT, and p(AP-1)3-CAT, respectively. |
| 303 | 16399630 | The immunoblot experiment demonstrated that CHL also caused a substantial decrease in the phosphorylation of p38 MAP kinase in LPS-stimulated RAW 264.7. |
| 304 | 16399630 | These results suggest that CHL inhibits IL-1beta production in macrophages stimulated with LPS at transcriptional level by blocking the phosphorylation of p38 and by suppressing the activation of transcription factors, NF-kappaB, NF-IL6, and AP-1. |
| 305 | 16426002 | Tumor necrosis factor (TNF) production in PBMC supernatants was measured by an enzyme-linked immunosorbent assay after TLR ligand stimulation and was dependent on gene transcription and NF-kappaB activation. |
| 306 | 16426002 | Finally, three patients with a mutation in the IKBKG gene, encoding the NF-kappaB essential modulator (NEMO) protein, were evaluated as disease controls and were almost uniformly below the standard deviation of healthy donors for all ligands tested. |
| 307 | 16426002 | Tumor necrosis factor (TNF) production in PBMC supernatants was measured by an enzyme-linked immunosorbent assay after TLR ligand stimulation and was dependent on gene transcription and NF-kappaB activation. |
| 308 | 16426002 | Finally, three patients with a mutation in the IKBKG gene, encoding the NF-kappaB essential modulator (NEMO) protein, were evaluated as disease controls and were almost uniformly below the standard deviation of healthy donors for all ligands tested. |
| 309 | 16439803 | Apically presented toll-like receptor 5 responds specifically to bacterial flagellin transducing a number of epithelial proinflammatory signaling cascades, including the induction of Ca2+ fluxes; activation of NF-kappaB, IL-8, and matrilysin; and mucin expression. |
| 310 | 16467339 | Protection by anesthesia correlates with a delay in plasma LPS circulation, resulting in a delayed inflammatory response, particularly DNA binding activity of NF-kappaB and serum levels of tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-10. |
| 311 | 16544247 | We studied the mechanisms of IL-8 induction, using luciferase reporter constructs, and the effect of pharmacological inhibitors of either IL-8 secretion or nuclear factor- kappa B (NF-kappa B) activation on IL-8 induction by dengue 2 virus (DEN2V) infection. |
| 312 | 16544247 | IL-8 induction by DEN2V infection was associated with activation of NF- kappa B and activator protein-1 (AP-1) in HEK293A cells but only with activation of AP-1 in HepG2 cells. |
| 313 | 16544247 | We studied the mechanisms of IL-8 induction, using luciferase reporter constructs, and the effect of pharmacological inhibitors of either IL-8 secretion or nuclear factor- kappa B (NF-kappa B) activation on IL-8 induction by dengue 2 virus (DEN2V) infection. |
| 314 | 16544247 | IL-8 induction by DEN2V infection was associated with activation of NF- kappa B and activator protein-1 (AP-1) in HEK293A cells but only with activation of AP-1 in HepG2 cells. |
| 315 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 316 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 317 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 318 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 319 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 320 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 321 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 322 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 323 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 324 | 16585571 | Engagement of CD28 outside of the immunological synapse results in up-regulation of IL-2 mRNA stability but not IL-2 transcription. |
| 325 | 16585571 | During T cell activation by APC, CD28 is colocalized with TCR in the central supramolecular activation cluster (cSMAC) region of the immunological synapse. |
| 326 | 16585571 | CD28 signaling through PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and induction of IL-2 transcription. |
| 327 | 16585571 | To test this model we have examined the mechanism of CD28-mediated induction of IL-2 secretion when CD28 is engaged outside of the immunological synapse. |
| 328 | 16585571 | CD4 T cells were stimulated with Ag presented by B7-negative APC and CD28 costimulation was provided in trans by anti-CD28-coated beads or by class II-negative, B7-positive cells. |
| 329 | 16585571 | We show that induction of IL-2 secretion under these conditions did not require expression of PKCtheta and did not induce NF-kappaB activation or IL-2 transcription. |
| 330 | 16585571 | In contrast, CD28 costimulation in trans did induce IL-2 mRNA stability, accounting for the up-regulation of IL-2 secretion. |
| 331 | 16585571 | These data indicate that the ability of CD28 to up-regulate IL-2 transcription requires colocalization of TCR and CD28 at the plasma membrane, possibly within the cSMAC of the immunological synapse. |
| 332 | 16585571 | In contrast, the ability of CD28 to promote IL-2 mRNA stability can be transduced from a distal site from the TCR, suggesting that signal integration occurs downstream from the plasma membrane. |
| 333 | 16648481 | Although some family members, PRMT1 and PRMT4, have been implicated in transcriptional modulation or intracellular signaling, the roles of other PRMTs in diverse cellular processes have not been fully established. |
| 334 | 16648481 | Here, we report that PRMT2 inhibits NF-kappaB-dependent transcription and promotes apoptosis. |
| 335 | 16648481 | PRMT2 exerted this effect by blocking nuclear export of IkappaB-alpha through a leptomycin-sensitive pathway, increasing nuclear IkappaB-alpha and decreasing NF-kappaB DNA binding. |
| 336 | 16648481 | PRMT2 also rendered cells susceptible to apoptosis by cytokines or cytotoxic drugs, likely due to its effects on NF-kappaB. |
| 337 | 16648481 | Mouse embryo fibroblasts from PRMT2 genetic knockouts showed elevated NF-kappaB activity and decreased susceptibility to apoptosis compared to wild-type or complemented cells. |
| 338 | 16648481 | Taken together, these data suggest that PRMT2 inhibits cell activation and promotes programmed cell death through this NF-kappaB-dependent mechanism. |
| 339 | 16648481 | Although some family members, PRMT1 and PRMT4, have been implicated in transcriptional modulation or intracellular signaling, the roles of other PRMTs in diverse cellular processes have not been fully established. |
| 340 | 16648481 | Here, we report that PRMT2 inhibits NF-kappaB-dependent transcription and promotes apoptosis. |
| 341 | 16648481 | PRMT2 exerted this effect by blocking nuclear export of IkappaB-alpha through a leptomycin-sensitive pathway, increasing nuclear IkappaB-alpha and decreasing NF-kappaB DNA binding. |
| 342 | 16648481 | PRMT2 also rendered cells susceptible to apoptosis by cytokines or cytotoxic drugs, likely due to its effects on NF-kappaB. |
| 343 | 16648481 | Mouse embryo fibroblasts from PRMT2 genetic knockouts showed elevated NF-kappaB activity and decreased susceptibility to apoptosis compared to wild-type or complemented cells. |
| 344 | 16648481 | Taken together, these data suggest that PRMT2 inhibits cell activation and promotes programmed cell death through this NF-kappaB-dependent mechanism. |
| 345 | 16648481 | Although some family members, PRMT1 and PRMT4, have been implicated in transcriptional modulation or intracellular signaling, the roles of other PRMTs in diverse cellular processes have not been fully established. |
| 346 | 16648481 | Here, we report that PRMT2 inhibits NF-kappaB-dependent transcription and promotes apoptosis. |
| 347 | 16648481 | PRMT2 exerted this effect by blocking nuclear export of IkappaB-alpha through a leptomycin-sensitive pathway, increasing nuclear IkappaB-alpha and decreasing NF-kappaB DNA binding. |
| 348 | 16648481 | PRMT2 also rendered cells susceptible to apoptosis by cytokines or cytotoxic drugs, likely due to its effects on NF-kappaB. |
| 349 | 16648481 | Mouse embryo fibroblasts from PRMT2 genetic knockouts showed elevated NF-kappaB activity and decreased susceptibility to apoptosis compared to wild-type or complemented cells. |
| 350 | 16648481 | Taken together, these data suggest that PRMT2 inhibits cell activation and promotes programmed cell death through this NF-kappaB-dependent mechanism. |
| 351 | 16648481 | Although some family members, PRMT1 and PRMT4, have been implicated in transcriptional modulation or intracellular signaling, the roles of other PRMTs in diverse cellular processes have not been fully established. |
| 352 | 16648481 | Here, we report that PRMT2 inhibits NF-kappaB-dependent transcription and promotes apoptosis. |
| 353 | 16648481 | PRMT2 exerted this effect by blocking nuclear export of IkappaB-alpha through a leptomycin-sensitive pathway, increasing nuclear IkappaB-alpha and decreasing NF-kappaB DNA binding. |
| 354 | 16648481 | PRMT2 also rendered cells susceptible to apoptosis by cytokines or cytotoxic drugs, likely due to its effects on NF-kappaB. |
| 355 | 16648481 | Mouse embryo fibroblasts from PRMT2 genetic knockouts showed elevated NF-kappaB activity and decreased susceptibility to apoptosis compared to wild-type or complemented cells. |
| 356 | 16648481 | Taken together, these data suggest that PRMT2 inhibits cell activation and promotes programmed cell death through this NF-kappaB-dependent mechanism. |
| 357 | 16648481 | Although some family members, PRMT1 and PRMT4, have been implicated in transcriptional modulation or intracellular signaling, the roles of other PRMTs in diverse cellular processes have not been fully established. |
| 358 | 16648481 | Here, we report that PRMT2 inhibits NF-kappaB-dependent transcription and promotes apoptosis. |
| 359 | 16648481 | PRMT2 exerted this effect by blocking nuclear export of IkappaB-alpha through a leptomycin-sensitive pathway, increasing nuclear IkappaB-alpha and decreasing NF-kappaB DNA binding. |
| 360 | 16648481 | PRMT2 also rendered cells susceptible to apoptosis by cytokines or cytotoxic drugs, likely due to its effects on NF-kappaB. |
| 361 | 16648481 | Mouse embryo fibroblasts from PRMT2 genetic knockouts showed elevated NF-kappaB activity and decreased susceptibility to apoptosis compared to wild-type or complemented cells. |
| 362 | 16648481 | Taken together, these data suggest that PRMT2 inhibits cell activation and promotes programmed cell death through this NF-kappaB-dependent mechanism. |
| 363 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 364 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 365 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 366 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 367 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 368 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 369 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 370 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 371 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 372 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 373 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 374 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 375 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 376 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 377 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 378 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 379 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 380 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 381 | 16699040 | Human cytomegalovirus attenuates interleukin-1beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation. |
| 382 | 16699040 | Viral infection is associated with a vigorous inflammatory response characterized by cellular infiltration and release of the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha). |
| 383 | 16699040 | In the present study, we identified a novel function of human cytomegalovirus (HCMV) that results in inhibition of IL-1 and TNF-alpha signaling pathways. |
| 384 | 16699040 | IL-1 and TNF-alpha signaling pathways converge at a point upstream of NF-kappaB activation and involve phosphorylation and degradation of the NF-kappaB inhibitory molecule IkappaBalpha. |
| 385 | 16699040 | The HCMV inhibition of IL-1 and TNF-alpha pathways corresponded to a suppression of NF-kappaB activation. |
| 386 | 16699040 | Analysis of IkappaBalpha phosphorylation and degradation suggested that HCMV induced two independent blocks in NF-kappaB activation, which occurred upstream from the point of convergence of the IL-1 and TNF-alpha pathways. |
| 387 | 16750567 | Besides TLRs, mRNA for MyD88 and TRAF6, and nuclear translocation of NF-kappaB were enhanced that indicate their involvement in tandem in the activity of porin. |
| 388 | 16750567 | The protein selectively up-regulated CD80 on the activated MPhi together with MHC class II molecule and CD40, and had no effect on CD86 expression. |
| 389 | 16750567 | The porin-induced profile of MIP-1alpha, MIP-1beta and RANTES showed strong bias for chemokines correlated with M1 polarization. |
| 390 | 16750567 | Intracellular expression and release of TNF-alpha and IL-12 in presence of porin was found to be TLR2 and NF-kappaB dependent. |
| 391 | 16750567 | Induction of TNF-alpha and IL-12 along with the chemokine profile suggests type I polarization of the MPhi that would influence Th1-type response. |
| 392 | 16750567 | Besides TLRs, mRNA for MyD88 and TRAF6, and nuclear translocation of NF-kappaB were enhanced that indicate their involvement in tandem in the activity of porin. |
| 393 | 16750567 | The protein selectively up-regulated CD80 on the activated MPhi together with MHC class II molecule and CD40, and had no effect on CD86 expression. |
| 394 | 16750567 | The porin-induced profile of MIP-1alpha, MIP-1beta and RANTES showed strong bias for chemokines correlated with M1 polarization. |
| 395 | 16750567 | Intracellular expression and release of TNF-alpha and IL-12 in presence of porin was found to be TLR2 and NF-kappaB dependent. |
| 396 | 16750567 | Induction of TNF-alpha and IL-12 along with the chemokine profile suggests type I polarization of the MPhi that would influence Th1-type response. |
| 397 | 16790806 | Both events require binding of Inv to beta1 integrins, which initiates signaling cascades including activation of focal adhesion complexes, Rac1, mitogen-activated protein kinase, and NF-kappaB. |
| 398 | 16790806 | OVA-specific CD4 T cells produced both gamma interferon (IFN-gamma) and IL-4 as determined by enzyme-linked immunosorbent assay. |
| 399 | 16790806 | Likewise, pronounced OVA-specific CD8 T-cell responses associated with IFN-gamma production were observed. |
| 400 | 16790806 | Together, these results suggest that Inv might be an attractive tool in vaccination as it confers both host cell uptake and adjuvant activity by engagement of beta1 integrins of host cells, which leads to CD4 as well as CD8 T-cell responses. |
| 401 | 16810633 | A role for the transcription factor RelB in IFN-alpha production and in IFN-alpha-stimulated cross-priming. |
| 402 | 16810633 | Although plasmacytoid dendritic cell numbers were similar, serum interferon (IFN)-alpha levels in RelB(-/-) and RelB(+/-) chimeras were markedly lower than in RelB(+/+) chimeras during early LCMV infection. |
| 403 | 16810633 | Further, both RelB(-/-) and RelB(+/-) chimeras mounted a lower-magnitude LCMV-specific CD8(+) T cell response than their RelB(+/+) counterparts, although the LCMV-specific CD8(+) T cells present were differentiated into functional cytotoxic cells. |
| 404 | 16810633 | In LCMV-infected RelB(-/-) mice, induction of cross-priming to an independently injected soluble protein, which depends on the IFN-alpha/beta made during the viral infection, was also impaired. |
| 405 | 16810633 | Notably, provision of exogenous IFN-alpha did not restore the ability of RelB(-/-) mice to cross-prime. |
| 406 | 16810633 | In summary, these results show that the RelB/NF-kappaB pathway is required for optimal IFN-alpha production after LCMV infection and suggest a crucial role for RelB in IFN-alpha-stimulated cross-priming of CD8(+) T cell responses. |
| 407 | 16893987 | Regulation of lipopolysaccharide-induced interleukin-12 production by activation of repressor element GA-12 through hyperactivation of the ERK pathway. |
| 408 | 16893987 | In response to LPS, peritoneal macrophages produced bioactive IL-12 p70, a heterodimer (p40/p35) of subunits, but macrophage lines such as J774.1 and RAW264.7 did not. |
| 409 | 16893987 | Induction of the p35 subunit was impaired in both cell lines, and additional impairment of p40 induction was observed in RAW264.7 cells. |
| 410 | 16893987 | These results suggest that some negative regulatory mechanisms against LPS-induced IL-12 p40 production are constitutively functioning in RAW264.7 cells but not in the other types of cells. |
| 411 | 16893987 | Activation of GA-12 (a repressor element of IL-12 p40), rather than suppression of promoter elements, such as binding sites for NF-kappaB, AP-1, and IRF-1, was detected in LPS-stimulated RAW264.7 cells, accompanying hyperactivation of extracellular signal-related kinase (ERK). |
| 412 | 16893987 | Taken together, these results demonstrate that hyperactivation of the ERK pathway plays a role in upstream signaling for the activation of GA-12, leading to the repression of IL-12 p40 production in mouse macrophages. |
| 413 | 16968658 | These purified recombinant fusion proteins demonstrated potent TLR5-specific NF-kappaB dependent activity in vitro. |
| 414 | 16971487 | Here, we describe an approach to enhance immunogenicity that involves the activation of NF-kappaB by the transgenic expression of an intracellular signaling molecule, NF-kappaB-inducing kinase (NIK). |
| 415 | 16971487 | In vitro, NIK increases dendritic cell antigen presentation in allogeneic and antigen-specific T cell proliferation assays by potently activating NF-kappaB and consequently up-regulating the expression of cytokines (TNF-alpha, IL-6, IL-12, IL-15, and IL-18), chemokines [IL-8, RANTES (regulated on activation, normal T cell expressed and secreted), macrophage inflammatory protein-1alpha, monocyte chemoattractant protein-1, and monocyte chemoattractant protein-3], MHC antigen-presenting molecules (class I and II), and costimulatory molecules (CD80 and CD86). |
| 416 | 16971487 | In vivo, NIK enhances immune responses against a vector-encoded antigen and shifts them toward a T helper 1 immune response with increased IgG2a levels, T cell proliferation, IFN-gamma production, and cytotoxic T lymphocyte responses more potently than complete Freund's adjuvant, a very efficacious T helper 1-inducing adjuvant. |
| 417 | 16971487 | These findings define NIK, and possibly other inducers of NF-kappaB activation, as a potent adjuvant strategy that offers great potential for genetic vaccine development. |
| 418 | 16971487 | Here, we describe an approach to enhance immunogenicity that involves the activation of NF-kappaB by the transgenic expression of an intracellular signaling molecule, NF-kappaB-inducing kinase (NIK). |
| 419 | 16971487 | In vitro, NIK increases dendritic cell antigen presentation in allogeneic and antigen-specific T cell proliferation assays by potently activating NF-kappaB and consequently up-regulating the expression of cytokines (TNF-alpha, IL-6, IL-12, IL-15, and IL-18), chemokines [IL-8, RANTES (regulated on activation, normal T cell expressed and secreted), macrophage inflammatory protein-1alpha, monocyte chemoattractant protein-1, and monocyte chemoattractant protein-3], MHC antigen-presenting molecules (class I and II), and costimulatory molecules (CD80 and CD86). |
| 420 | 16971487 | In vivo, NIK enhances immune responses against a vector-encoded antigen and shifts them toward a T helper 1 immune response with increased IgG2a levels, T cell proliferation, IFN-gamma production, and cytotoxic T lymphocyte responses more potently than complete Freund's adjuvant, a very efficacious T helper 1-inducing adjuvant. |
| 421 | 16971487 | These findings define NIK, and possibly other inducers of NF-kappaB activation, as a potent adjuvant strategy that offers great potential for genetic vaccine development. |
| 422 | 16971487 | Here, we describe an approach to enhance immunogenicity that involves the activation of NF-kappaB by the transgenic expression of an intracellular signaling molecule, NF-kappaB-inducing kinase (NIK). |
| 423 | 16971487 | In vitro, NIK increases dendritic cell antigen presentation in allogeneic and antigen-specific T cell proliferation assays by potently activating NF-kappaB and consequently up-regulating the expression of cytokines (TNF-alpha, IL-6, IL-12, IL-15, and IL-18), chemokines [IL-8, RANTES (regulated on activation, normal T cell expressed and secreted), macrophage inflammatory protein-1alpha, monocyte chemoattractant protein-1, and monocyte chemoattractant protein-3], MHC antigen-presenting molecules (class I and II), and costimulatory molecules (CD80 and CD86). |
| 424 | 16971487 | In vivo, NIK enhances immune responses against a vector-encoded antigen and shifts them toward a T helper 1 immune response with increased IgG2a levels, T cell proliferation, IFN-gamma production, and cytotoxic T lymphocyte responses more potently than complete Freund's adjuvant, a very efficacious T helper 1-inducing adjuvant. |
| 425 | 16971487 | These findings define NIK, and possibly other inducers of NF-kappaB activation, as a potent adjuvant strategy that offers great potential for genetic vaccine development. |
| 426 | 17055123 | Furthermore, the C16 lipopeptide was the most effective in activating dendritic cells, measured by up regulation of surface MHC Class II molecules, and also in activating NF-kappaB in a Toll-like receptor-2 (TLR2)-dependent manner. |
| 427 | 17092436 | IgE levels in serum and IL-4/IL-13 levels in BALF were determined by ELISA. |
| 428 | 17092436 | Expressions of STAT6 and NF-kappaB in lung were determined by immunohistochemistry staining. |
| 429 | 17092436 | Significant reductions of eosinophil infiltration and levels of IL-4 and IL-13 in BALF were observed after vaccination. |
| 430 | 17092436 | Further more, DNA vaccination inhibited STAT6 and NF-kappaB expression in lung tissue in Der p 2-immunized mice. |
| 431 | 17092436 | IgE levels in serum and IL-4/IL-13 levels in BALF were determined by ELISA. |
| 432 | 17092436 | Expressions of STAT6 and NF-kappaB in lung were determined by immunohistochemistry staining. |
| 433 | 17092436 | Significant reductions of eosinophil infiltration and levels of IL-4 and IL-13 in BALF were observed after vaccination. |
| 434 | 17092436 | Further more, DNA vaccination inhibited STAT6 and NF-kappaB expression in lung tissue in Der p 2-immunized mice. |
| 435 | 17100625 | We also discuss the contribution of specific host immune/inflammatory responses to atherogenesis, and describe cellular signaling pathways (lipopolysaccharide-binding protein [LBP], CD14, MD-2, TLR4, MyD88, and NF-kappaB, among others) that play key roles in innate immune signaling. |
| 436 | 17108047 | While the majority of serotypes utilize coxsackievirus-adenovirus receptor (CAR) as their primary attachment receptor, subgroup B and subgroup D Ad37 serotypes use CD46. |
| 437 | 17108047 | We found that CD46 Ads were capable of alpha interferon (IFN-alpha) induction by peripheral blood mononuclear cells and that plasmacytoid dendritic cells (pDCs) were the principal producers of this cytokine. |
| 438 | 17108047 | IFN-alpha induction correlated with the permissivity of pDCs to CD46- but not CAR-utilizing Ad serotypes. |
| 439 | 17108047 | A role for Toll-like receptor 9 (TLR9) recognition of Ad was supported by the requirement for viral DNA and efficient endosomal acidification and by the ability of a TLR9-inhibitory oligonucleotide to attenuate IFN-alpha induction. |
| 440 | 17108047 | Cell lines expressing TLR9 that are permissive to infection by both CAR- and CD46-utilizing serotypes showed a preferential induction of TLR9-mediated events by CD46-utilizing Ads. |
| 441 | 17108047 | Specifically, the latter virus types induced higher levels of cytokine expression and NF-kappaB activation in HeLa cells than CAR-dependent Ad types, despite equivalent infection rates. |
| 442 | 17143781 | Of the genes tested, 21 genes (IRF-1, IFN 1-2 promoter, IFNAR-1, IRF-10, IFN-gamma, 2',5'-OAS, IAP-1, caspase 8, TRAIL-like, STAT-3, IL-6, IL-8, MIP-3 alpha, MHC-I, MHC-II, TVB, GLVR-1, OTF, IL-13R alpha, ST3GAL-VI and PGK) showed an increased expression. |
| 443 | 17143781 | The remaining seven genes (IFNAR-2, IFN-alpha, NF-kappaB subunit p65, BLRcp38, DDX1, G6PDH and UB) showed a constant expression or only slight alteration. |
| 444 | 17219364 | FACS analysis demonstrated an up-regulation of DC maturation markers CD80, CD86, CD40 and MHC class II upon exposure to Gal-lectin. |
| 445 | 17219364 | The activation of DC by Gal-lectin was mediated by MAPK and NF-kappaB. |
| 446 | 17257568 | Although the mechanisms responsible for induction of these chemokines and cytokines are unclear, studies on the closely related human (H)RSV suggest that activation of NF-kappaB via TLR4 and TLR3 signalling pathways is involved. |
| 447 | 17312143 | These maturational changes of DCs involved the MyD88-mediated NF-kappaB signaling pathway. |
| 448 | 17515202 | Synthetic oligonucleotides containing one of four kinds of cis-acting elements, binding sites for activating protein-1 (AP-1), nuclear factor kappaB (NF-kappaB), CArG binding factor A (CBF-A), and nuclear factor Y (NF-Y), were randomly ligated to construct DNA fragments. |
| 449 | 17517865 | We reported previously that F. tularensis live vaccine strain (LVS) elicited strong, dose-dependent NF-kappaB reporter activity in Toll-like receptor 2 (TLR2)-expressing HEK293T cells and proinflammatory gene expression in primary murine macrophages. |
| 450 | 17517865 | Colocalization of intracellular F. tularensis LVS, TLR2, and MyD88 was visualized by confocal microscopy. |
| 451 | 17517865 | F. tularensis LVS replicates in macrophages; however, bacterial replication was not required for TLR2 signaling because LVSDeltaguaA, an F. tularensis LVS guanine auxotroph that fails to replicate in the absence of exogenous guanine, activated NF-kappaB in TLR2-transfected HEK293T cells and induced cytokine expression in wild-type macrophages comparably to wild-type F. tularensis LVS. |
| 452 | 17517865 | We reported previously that F. tularensis live vaccine strain (LVS) elicited strong, dose-dependent NF-kappaB reporter activity in Toll-like receptor 2 (TLR2)-expressing HEK293T cells and proinflammatory gene expression in primary murine macrophages. |
| 453 | 17517865 | Colocalization of intracellular F. tularensis LVS, TLR2, and MyD88 was visualized by confocal microscopy. |
| 454 | 17517865 | F. tularensis LVS replicates in macrophages; however, bacterial replication was not required for TLR2 signaling because LVSDeltaguaA, an F. tularensis LVS guanine auxotroph that fails to replicate in the absence of exogenous guanine, activated NF-kappaB in TLR2-transfected HEK293T cells and induced cytokine expression in wild-type macrophages comparably to wild-type F. tularensis LVS. |
| 455 | 17537851 | The expression profiles of transcription factors such as NF-kappaB/Rel and STAT were regulated similarly by both viruses; in contrast, OASL, MDA5, and IRIG-I expression increased only during MVA infection. |
| 456 | 17565687 | Expression of PAdV-3 E1Blarge inhibited the NF-kappaB dependent transcription of luciferase from IL-8 promoter. |
| 457 | 17565687 | These results suggest that E1Blarge interacts with NF-kappaB to prevent transcription and down regulate proinflammatory cytokine IL-8 production. |
| 458 | 17565687 | Expression of PAdV-3 E1Blarge inhibited the NF-kappaB dependent transcription of luciferase from IL-8 promoter. |
| 459 | 17565687 | These results suggest that E1Blarge interacts with NF-kappaB to prevent transcription and down regulate proinflammatory cytokine IL-8 production. |
| 460 | 17570527 | HlyA oligomer-treated murine B-1a cells up-regulated TLR2 and involved the signaling molecules MyD88, TRAF6 and NF-kappaB. |
| 461 | 17570527 | Apoptosis was detected in majority of the monomer-treated cells that involved caspase-9 and caspase-3. |
| 462 | 17989335 | Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways. |
| 463 | 17989335 | In this study, we report that stimulation of HEK293 cells expressing human TLR2 with M. bovis BCG resulted in increased CCL2 and CCL5 secretion, as determined by an enzyme-linked immunosorbent assay. |
| 464 | 17989335 | M. bovis BCG infection resulted in the activation of c-Jun N-terminal kinase (JNK), and the inhibition of JNK activity had a significant effect on M. bovis BCG-dependent CCL5 secretion in TLR2-expressing cells but no effect on M. bovis BCG-dependent CCL2 secretion from infected HEK293 cells expressing human TLR2. |
| 465 | 17989335 | The M. bovis BCG-induced CCL5 release was attenuated by sulfasalazine (a well-described inhibitor of NF-kappaB activity), BAY 11-7082 (an IkappaB phosphorylation inhibitor), and ALLN (a well-described inhibitor of NF-kappaB activation that prevents degradation of IkappaB and eventually results in a lack of translocated NF-kappaB in the nucleus). |
| 466 | 17989335 | In addition, stimulation of TLR2-expressing cells with M. bovis BCG resulted in translocation of NF-kappaB subunits from the cytoplasmic to the nuclear fraction, and stimulation of cells with M. bovis BCG activated IkappaB kinase alphabeta. |
| 467 | 17989335 | These findings indicate that M. bovis BCG induces CCL5 production through mechanisms that include a TLR2-dependent component that requires JNK and NF-kappaB activities. |
| 468 | 17989335 | Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways. |
| 469 | 17989335 | In this study, we report that stimulation of HEK293 cells expressing human TLR2 with M. bovis BCG resulted in increased CCL2 and CCL5 secretion, as determined by an enzyme-linked immunosorbent assay. |
| 470 | 17989335 | M. bovis BCG infection resulted in the activation of c-Jun N-terminal kinase (JNK), and the inhibition of JNK activity had a significant effect on M. bovis BCG-dependent CCL5 secretion in TLR2-expressing cells but no effect on M. bovis BCG-dependent CCL2 secretion from infected HEK293 cells expressing human TLR2. |
| 471 | 17989335 | The M. bovis BCG-induced CCL5 release was attenuated by sulfasalazine (a well-described inhibitor of NF-kappaB activity), BAY 11-7082 (an IkappaB phosphorylation inhibitor), and ALLN (a well-described inhibitor of NF-kappaB activation that prevents degradation of IkappaB and eventually results in a lack of translocated NF-kappaB in the nucleus). |
| 472 | 17989335 | In addition, stimulation of TLR2-expressing cells with M. bovis BCG resulted in translocation of NF-kappaB subunits from the cytoplasmic to the nuclear fraction, and stimulation of cells with M. bovis BCG activated IkappaB kinase alphabeta. |
| 473 | 17989335 | These findings indicate that M. bovis BCG induces CCL5 production through mechanisms that include a TLR2-dependent component that requires JNK and NF-kappaB activities. |
| 474 | 17989335 | Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways. |
| 475 | 17989335 | In this study, we report that stimulation of HEK293 cells expressing human TLR2 with M. bovis BCG resulted in increased CCL2 and CCL5 secretion, as determined by an enzyme-linked immunosorbent assay. |
| 476 | 17989335 | M. bovis BCG infection resulted in the activation of c-Jun N-terminal kinase (JNK), and the inhibition of JNK activity had a significant effect on M. bovis BCG-dependent CCL5 secretion in TLR2-expressing cells but no effect on M. bovis BCG-dependent CCL2 secretion from infected HEK293 cells expressing human TLR2. |
| 477 | 17989335 | The M. bovis BCG-induced CCL5 release was attenuated by sulfasalazine (a well-described inhibitor of NF-kappaB activity), BAY 11-7082 (an IkappaB phosphorylation inhibitor), and ALLN (a well-described inhibitor of NF-kappaB activation that prevents degradation of IkappaB and eventually results in a lack of translocated NF-kappaB in the nucleus). |
| 478 | 17989335 | In addition, stimulation of TLR2-expressing cells with M. bovis BCG resulted in translocation of NF-kappaB subunits from the cytoplasmic to the nuclear fraction, and stimulation of cells with M. bovis BCG activated IkappaB kinase alphabeta. |
| 479 | 17989335 | These findings indicate that M. bovis BCG induces CCL5 production through mechanisms that include a TLR2-dependent component that requires JNK and NF-kappaB activities. |
| 480 | 18074095 | Hepatitis C virus non-structural protein-2 activates CXCL-8 transcription through NF-kappaB. |
| 481 | 18074095 | Furthermore, when the kappaB site on the IL-8 promoter was eliminated by mutagenesis or when intracellular NF-kappaB activity was suppressed by an inhibitor, NS2 did not activate the IL-8 promoter, suggesting a role of NF-kappaB in this process. |
| 482 | 18074095 | This hypothesis was tested by determination of NF-kappaB-driven reporter gene expression and NF-kappaB p65 subunit subcellular localization after HCV NS2 expression. |
| 483 | 18074095 | These results demonstrate that HCV NS2 up-regulates IL-8 transcription through NF-kappaB. |
| 484 | 18074095 | Hepatitis C virus non-structural protein-2 activates CXCL-8 transcription through NF-kappaB. |
| 485 | 18074095 | Furthermore, when the kappaB site on the IL-8 promoter was eliminated by mutagenesis or when intracellular NF-kappaB activity was suppressed by an inhibitor, NS2 did not activate the IL-8 promoter, suggesting a role of NF-kappaB in this process. |
| 486 | 18074095 | This hypothesis was tested by determination of NF-kappaB-driven reporter gene expression and NF-kappaB p65 subunit subcellular localization after HCV NS2 expression. |
| 487 | 18074095 | These results demonstrate that HCV NS2 up-regulates IL-8 transcription through NF-kappaB. |
| 488 | 18074095 | Hepatitis C virus non-structural protein-2 activates CXCL-8 transcription through NF-kappaB. |
| 489 | 18074095 | Furthermore, when the kappaB site on the IL-8 promoter was eliminated by mutagenesis or when intracellular NF-kappaB activity was suppressed by an inhibitor, NS2 did not activate the IL-8 promoter, suggesting a role of NF-kappaB in this process. |
| 490 | 18074095 | This hypothesis was tested by determination of NF-kappaB-driven reporter gene expression and NF-kappaB p65 subunit subcellular localization after HCV NS2 expression. |
| 491 | 18074095 | These results demonstrate that HCV NS2 up-regulates IL-8 transcription through NF-kappaB. |
| 492 | 18074095 | Hepatitis C virus non-structural protein-2 activates CXCL-8 transcription through NF-kappaB. |
| 493 | 18074095 | Furthermore, when the kappaB site on the IL-8 promoter was eliminated by mutagenesis or when intracellular NF-kappaB activity was suppressed by an inhibitor, NS2 did not activate the IL-8 promoter, suggesting a role of NF-kappaB in this process. |
| 494 | 18074095 | This hypothesis was tested by determination of NF-kappaB-driven reporter gene expression and NF-kappaB p65 subunit subcellular localization after HCV NS2 expression. |
| 495 | 18074095 | These results demonstrate that HCV NS2 up-regulates IL-8 transcription through NF-kappaB. |
| 496 | 18177634 | Sphingosine kinase, phosphatidylinositol 3-kinase, Akt, NF-kappaB, and p300 are required for CCL5 production in Mycobacterium bovis Bacillus Calmette-Guérin (BCG)-infected epithelial cells. |
| 497 | 18177634 | Although NF-kappaB has been implicated, signaling cascades involved in CCL5 production by epithelial cells following infection with Mycobacterium bovis BCG are still not defined. |
| 498 | 18177634 | Here we show that using pharmacological inhibition of sphingosine kinase (SPK), striking inhibition of M. bovis BCG-induced CCL5 protein was observed. |
| 499 | 18177634 | Phosphatidylinositol 3-kinase (PI3K) and Akt were also important for CCL5 production by epithelial cells infected with M. bovis BCG. |
| 500 | 18177634 | Moreover, there was increased activation of PI3K, IKK/alphabeta and NF-kappaB in A549 cells infected with M. bovis BCG. |
| 501 | 18177634 | Importantly, the PI3K activation was dependent on SPK. |
| 502 | 18177634 | Together, these studies are the first to show that M. bovis BCG-induced CCL5 secretion is dependent on the SPK/PI3K/Akt/NF-kappaB and p300 signaling pathway. |
| 503 | 18177634 | Sphingosine kinase, phosphatidylinositol 3-kinase, Akt, NF-kappaB, and p300 are required for CCL5 production in Mycobacterium bovis Bacillus Calmette-Guérin (BCG)-infected epithelial cells. |
| 504 | 18177634 | Although NF-kappaB has been implicated, signaling cascades involved in CCL5 production by epithelial cells following infection with Mycobacterium bovis BCG are still not defined. |
| 505 | 18177634 | Here we show that using pharmacological inhibition of sphingosine kinase (SPK), striking inhibition of M. bovis BCG-induced CCL5 protein was observed. |
| 506 | 18177634 | Phosphatidylinositol 3-kinase (PI3K) and Akt were also important for CCL5 production by epithelial cells infected with M. bovis BCG. |
| 507 | 18177634 | Moreover, there was increased activation of PI3K, IKK/alphabeta and NF-kappaB in A549 cells infected with M. bovis BCG. |
| 508 | 18177634 | Importantly, the PI3K activation was dependent on SPK. |
| 509 | 18177634 | Together, these studies are the first to show that M. bovis BCG-induced CCL5 secretion is dependent on the SPK/PI3K/Akt/NF-kappaB and p300 signaling pathway. |
| 510 | 18177634 | Sphingosine kinase, phosphatidylinositol 3-kinase, Akt, NF-kappaB, and p300 are required for CCL5 production in Mycobacterium bovis Bacillus Calmette-Guérin (BCG)-infected epithelial cells. |
| 511 | 18177634 | Although NF-kappaB has been implicated, signaling cascades involved in CCL5 production by epithelial cells following infection with Mycobacterium bovis BCG are still not defined. |
| 512 | 18177634 | Here we show that using pharmacological inhibition of sphingosine kinase (SPK), striking inhibition of M. bovis BCG-induced CCL5 protein was observed. |
| 513 | 18177634 | Phosphatidylinositol 3-kinase (PI3K) and Akt were also important for CCL5 production by epithelial cells infected with M. bovis BCG. |
| 514 | 18177634 | Moreover, there was increased activation of PI3K, IKK/alphabeta and NF-kappaB in A549 cells infected with M. bovis BCG. |
| 515 | 18177634 | Importantly, the PI3K activation was dependent on SPK. |
| 516 | 18177634 | Together, these studies are the first to show that M. bovis BCG-induced CCL5 secretion is dependent on the SPK/PI3K/Akt/NF-kappaB and p300 signaling pathway. |
| 517 | 18177634 | Sphingosine kinase, phosphatidylinositol 3-kinase, Akt, NF-kappaB, and p300 are required for CCL5 production in Mycobacterium bovis Bacillus Calmette-Guérin (BCG)-infected epithelial cells. |
| 518 | 18177634 | Although NF-kappaB has been implicated, signaling cascades involved in CCL5 production by epithelial cells following infection with Mycobacterium bovis BCG are still not defined. |
| 519 | 18177634 | Here we show that using pharmacological inhibition of sphingosine kinase (SPK), striking inhibition of M. bovis BCG-induced CCL5 protein was observed. |
| 520 | 18177634 | Phosphatidylinositol 3-kinase (PI3K) and Akt were also important for CCL5 production by epithelial cells infected with M. bovis BCG. |
| 521 | 18177634 | Moreover, there was increased activation of PI3K, IKK/alphabeta and NF-kappaB in A549 cells infected with M. bovis BCG. |
| 522 | 18177634 | Importantly, the PI3K activation was dependent on SPK. |
| 523 | 18177634 | Together, these studies are the first to show that M. bovis BCG-induced CCL5 secretion is dependent on the SPK/PI3K/Akt/NF-kappaB and p300 signaling pathway. |
| 524 | 18178854 | Neither hexaacylated nor pentaacylated synthetic lipid A induced NF-kappaB activity in wild-type transfectants under the identical transfection conditions used for LPS; however, increasing human MD-2 expression rescued responsiveness to hexaacylated lipid A only, while murine MD-2 was required to elicit a response to pentaacylated lipid A. |
| 525 | 18178854 | Adherent PBMC of healthy volunteers were also compared for LPS-induced TNF-alpha, IL-6, IL-1beta, and IL-10 production. |
| 526 | 18287580 | Role of protein tyrosine kinase and Erk1/2 activities in the Toll-like receptor 2-induced cellular activation of murine B cells by neisserial porin. |
| 527 | 18287580 | PorB was able to induce (i) protein tyrosine kinase (PTK) activity, (ii) the phosphorylation of Erk1 and Erk2, and (iii) IkappaB-alpha phosphorylation, leading to NF-kappaB nuclear translocation in B cells in a TLR2-dependent manner. |
| 528 | 18287580 | PorB-induced NF-kappaB nuclear translocation was not dependent on either PTK or Erk1/2 activities. |
| 529 | 18287580 | However, B-cell proliferation and the induction of increased surface expression of CD86 by PorB were dependent on PTK activity and not Erk1/2 activation. |
| 530 | 18287580 | In conclusion, PorB acts through TLR2 as a B-cell mitogen, triggering tyrosine phosphorylation of various cellular proteins that are involved in proliferation and CD86 expression, as well as the phosphorylation of Erk1/2, which is not necessary for CD86 upregulation or the proliferation of B cells. |
| 531 | 18287580 | Role of protein tyrosine kinase and Erk1/2 activities in the Toll-like receptor 2-induced cellular activation of murine B cells by neisserial porin. |
| 532 | 18287580 | PorB was able to induce (i) protein tyrosine kinase (PTK) activity, (ii) the phosphorylation of Erk1 and Erk2, and (iii) IkappaB-alpha phosphorylation, leading to NF-kappaB nuclear translocation in B cells in a TLR2-dependent manner. |
| 533 | 18287580 | PorB-induced NF-kappaB nuclear translocation was not dependent on either PTK or Erk1/2 activities. |
| 534 | 18287580 | However, B-cell proliferation and the induction of increased surface expression of CD86 by PorB were dependent on PTK activity and not Erk1/2 activation. |
| 535 | 18287580 | In conclusion, PorB acts through TLR2 as a B-cell mitogen, triggering tyrosine phosphorylation of various cellular proteins that are involved in proliferation and CD86 expression, as well as the phosphorylation of Erk1/2, which is not necessary for CD86 upregulation or the proliferation of B cells. |
| 536 | 18363879 | Moraxella catarrhalis lipooligosaccharide selectively upregulates ICAM-1 expression on human monocytes and stimulates adjacent naïve monocytes to produce TNF-alpha through cellular cross-talk. |
| 537 | 18363879 | ICAM-1 upregulation on human monocytes by the LOS required surface CD14, TLR4, NF-kappaB p65 and c-Jun N-terminal kinase (JNK) activity. |
| 538 | 18363879 | Our study also revealed that the LOS-induced surface ICAM-1 expression was partially mediated through a TNF-alpha dependent autocrine mechanism and could be further augmented by lipopolysaccharide-binding protein in serum. |
| 539 | 18363879 | In addition, M. catarrhalis LOS also stimulated human monocytes to produce pro-inflammatory cytokines in both TLR4- and CD14-dependent pathways. |
| 540 | 18363879 | Furthermore, the LOS-activated human monocytes secreted a significantly high level of IL-8, and could stimulate adjacent naïve monocytes to produce TNF-alpha which was partially mediated via membrane ICAM-1 and IL-8/IL-8RA. |
| 541 | 18389479 | DiC14-amidine liposomes also activated human DC, as shown by synthesis of IL-12p40 and TNF-alpha, accumulation of IL-6, IFN-beta and CXCL10 mRNA, and up-regulation of membrane expression of CD80 and CD86. |
| 542 | 18389479 | DC stimulation by diC14-amidine liposomes was associated with activation of NF-kappaB, ERK1/2, JNK and p38 MAP kinases. |
| 543 | 18389479 | Finally, we demonstrated in mouse and human cells that diC14-amidine liposomes use Toll-like receptor 4 to elicit both MyD88-dependent and Toll/IL-1R-containing adaptor inducing interferon IFN-beta (TRIF)-dependent responses. |
| 544 | 18439678 | Porcine TLR8 and TLR7 are both activated by a selective TLR7 ligand, imiquimod. |
| 545 | 18439678 | We cloned and characterized porcine TLR7 and TLR8 genes from pig lymph node tissue. |
| 546 | 18439678 | Sequence analysis showed that the aa sequence identities of porcine TLR7 with human, mouse and bovine TLR7 are 85, 78 and 90%, respectively, whereas porcine TLR8 aa sequence identities with human, mouse and bovine TLR8 are 73, 69 and 79%, respectively. |
| 547 | 18439678 | Both porcine TLR7 and TLR8 proteins were expressed in cell lines and were N-glycosylated. |
| 548 | 18439678 | The stimulatory activity of TLR7 and TLR8 ligands to porcine and human TLR7 and TLR8 in transiently transfected Cos-7 and 293T cells were analyzed using a NF-kappaB reporter assay. |
| 549 | 18439678 | Two imidazoquinoline molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands. |
| 550 | 18439678 | We further showed that porcine TLR7 and TLR8 are located intracellularly and are mainly within the endoplasmic reticulum. |
| 551 | 18449425 | We found that DV up-regulates Protease Activated receptor type-1 (inflammation) and TF (coagulation) receptors, via the phosphorylation of p38 and ERK1/2 MAPKs, which favor the activation of NF-kappaB transcription factor. |
| 552 | 18449425 | This induces pro-inflammatory (IL-8) or pro-adhesive (VCAM-1) gene expression which may lead to EVC activation. |
| 553 | 18456818 | Effects on DC maturation and in vivo functions correlate to the ability of rHSP70 to activate IkappaB-alpha/NF-kappaB and ERK1/2 pathways in human DCs. |
| 554 | 18483270 | In this study, we have created a chimeric CD40 molecule that incorporates a single chain Fv (scFv) molecule specific for human ErbB2 antigen and fusing to the membrane spanning and cytosolic domains of murine CD40. |
| 555 | 18483270 | After adenoviral transfer to bone marrow-derived DC, this chimeric receptor (CR) induced nuclear factor-kappaB (NF-kappaB)-dependent DC activation and effector function when cultured with immobilized ErbB2 protein or ErbB2-positive tumor cells in vitro. |
| 556 | 18483270 | In murine ErbB2-positive D2F2/E2 breast tumor (BALB/c) and EL4/E2 thymoma (C57BL/6) models, i.v. injection of 1 x 10(6) scFv-CD40-DC significantly inhibited tumor growth and cured established tumors. |
| 557 | 18495849 | Antibodies to proteinase 3 prime human oral, lung, and kidney epithelial cells to secrete proinflammatory cytokines upon stimulation with agonists to various Toll-like receptors, NOD1, and NOD2. |
| 558 | 18495849 | In this study, anti-PR3 antibodies (Abs) and PR3 ANCA-containing sera from WG patients endowed human oral, lung, and kidney epithelial cells with responsiveness to PAMPs in terms of the production of proinflammatory cytokines, such as interleukin-6 (IL-6), IL-8, monocyte chemoattractant protein-1, and tumor necrosis factor alpha. |
| 559 | 18495849 | Protease-activated receptor-2 (PAR-2) agonist peptides mimicked the priming effects of PR3 ANCA against PAMPs. |
| 560 | 18495849 | Furthermore, the anti-PR3 Ab-mediated cell activation was significantly abolished by RNA interference targeting PAR-2 and NF-kappaB. |
| 561 | 18516301 | Compared to rhMPV-WT, rhMPV-Delta G also increased IRF- and NF-kappaB-dependent gene transcription, which was reversely inhibited by G protein expression. |
| 562 | 18516301 | Since RNA helicases have been shown to play a fundamental role in initiating viral-induced cellular signaling, we investigated whether retinoic induced gene (RIG)-I was the target of G protein inhibitory activity. |
| 563 | 18552348 | For example, aspartylglucosaminidase (AGA), PLA2, SIAT8B, GALNT7, or B3GAT1 metabolize chemical ligands to which the influenza virus, herpes simplex, cytomegalovirus (CMV), rubella, or Toxoplasma gondii bind. |
| 564 | 18552348 | The epidermal growth factor receptor (EGR/EGFR) is used by the CMV to gain entry to cells, and a CMV gene codes for an interleukin (IL-10) mimic that binds the host cognate receptor, IL10R. |
| 565 | 18552348 | The fibroblast growth factor receptor (FGFR1) is used by herpes simplex. |
| 566 | 18552348 | KPNA3 and RANBP5 control the nuclear import of the influenza virus. |
| 567 | 18552348 | Disrupted in schizophrenia 1 (DISC1) controls the microtubule network that is used by viruses as a route to the nucleus, while DTNBP1, MUTED, and BLOC1S3 regulate endosomal to lysosomal routing that is also important in viral traffic. |
| 568 | 18552348 | Neuregulin 1 activates ERBB receptors releasing a factor, EBP1, known to inhibit the influenza virus transcriptase. |
| 569 | 18552348 | Other viral or bacterial components bind to genes or proteins encoded by CALR, FEZ1, FYN, HSPA1B, IL2, HTR2A, KPNA3, MED12, MED15, MICB, NQO2, PAX6, PIK3C3, RANBP5, or TP53, while the cerebral infectivity of the herpes simplex virus is modified by Apolipoprotein E (APOE). |
| 570 | 18552348 | Genes encoding for proteins related to the innate immune response, including cytokine related (CCR5, CSF2RA, CSF2RB, IL1B, IL1RN, IL2, IL3, IL3RA, IL4, IL10, IL10RA, IL18RAP, lymphotoxin-alpha, tumor necrosis factor alpha [TNF]), human leukocyte antigen (HLA) antigens (HLA-A10, HLA-B, HLA-DRB1), and genes involved in antigen processing (angiotensin-converting enzyme and tripeptidyl peptidase 2) are all concerned with defense against invading pathogens. |
| 571 | 18552348 | Human microRNAs (Hsa-mir-198 and Hsa-mir-206) are predicted to bind to influenza, rubella, or poliovirus genes. |
| 572 | 18708593 | DnaK induced the activation of MAPKs and NF-kappaB in DC and the production of the proinflammatory cytokines IL-6, TNF-alpha, and IL-12 p40, as well as low levels of IL-10. |
| 573 | 18708593 | DnaK induced phenotypic maturation of DC, as demonstrated by an up-regulation of costimulatory molecules CD40, CD80, and CD86. |
| 574 | 18708593 | DnaK stimulated DC through TLR4 and the adapters MyD88 and Toll/IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) that mediated differential responses. |
| 575 | 18708593 | DnaK induced activation of MAPKs and NF-kappaB in a MyD88- or TRIF-dependent manner. |
| 576 | 18708593 | In contrast, DnaK induced DC maturation in a TRIF-dependent, MyD88-independent manner. |
| 577 | 18708593 | DnaK induced the activation of MAPKs and NF-kappaB in DC and the production of the proinflammatory cytokines IL-6, TNF-alpha, and IL-12 p40, as well as low levels of IL-10. |
| 578 | 18708593 | DnaK induced phenotypic maturation of DC, as demonstrated by an up-regulation of costimulatory molecules CD40, CD80, and CD86. |
| 579 | 18708593 | DnaK stimulated DC through TLR4 and the adapters MyD88 and Toll/IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) that mediated differential responses. |
| 580 | 18708593 | DnaK induced activation of MAPKs and NF-kappaB in a MyD88- or TRIF-dependent manner. |
| 581 | 18708593 | In contrast, DnaK induced DC maturation in a TRIF-dependent, MyD88-independent manner. |
| 582 | 18723827 | CSC costimulation enhanced RSV-induced activation of interferon regulatory factor (IRF)-1 and IRF-7, which bind to the ISRE site. |
| 583 | 18723827 | CSC also furthered RSV-induced activation of the transcription factor nuclear factor kappa B (NF-kappaB), as shown by increased NF-kappaB DNA binding to its specific site of the IL-8 promoter and increased NF-kappaB-driven gene transcription. |
| 584 | 18784835 | Although human B cells bound both human and murine BLyS, nuclear accumulation of NF-kappaB p52, an indication of the induction of a protective anti-apoptotic response, following stimulation with human BLyS was more robust than that induced with murine BLyS suggesting a fundamental disparity in BLyS receptor signaling. |
| 585 | 18784835 | Efficient engraftment of both human B and T lymphocytes in NOD rag1(-/-) Prf1(-/-) immunodeficient mice treated with recombinant human BLyS is observed after adoptive transfer of human PBL relative to PBS treated controls. |
| 586 | 18809662 | Vibrio cholerae flagellins induce Toll-like receptor 5-mediated interleukin-8 production through mitogen-activated protein kinase and NF-kappaB activation. |
| 587 | 18809662 | Bacterial flagellins are known to induce IL-8 production through Toll-like receptor 5 (TLR5). |
| 588 | 18809662 | Since the V. cholerae genome encodes five distinct flagellin proteins, FlaA to FlaE, with homology to conserved TLR5 recognition regions of Salmonella FliC, we hypothesized that V. cholerae flagellins may contribute to IL-8 induction through TLR5 and mitogen-activated protein kinase (MAPK) signaling. |
| 589 | 18809662 | Each purified recombinant V. cholerae flagellin induced IL-8 production in T84 intestinal epithelial cells and also induced nuclear factor kappa B (NF-kappaB) activation in HEK293T/TLR5 transfectants, which was blocked by cotransfection with a TLR5 dominant-negative construct, demonstrating TLR5 specificity. |
| 590 | 18809662 | Supernatants derived from Delta flaAC and Delta flaEDB mutants induced IL-8 production in HT-29 intestinal epithelial cells and in HEK293T cells overexpressing TLR5, whereas Delta flaABCDE supernatants induced significantly less IL-8 production, demonstrating the contribution of multiple flagellins in IL-8 induction. |
| 591 | 18809662 | Purified recombinant V. cholerae FlaA activated the MAPKs p38, c-jun N-terminal kinase (JNK), and extracellular regulated kinase (ERK) in T84 cells. |
| 592 | 18809662 | FlaA-induced IL-8 production in T84 cells was inhibited by the p38 inhibitor in combination with either the JNK or ERK inhibitors. |
| 593 | 18809662 | Collectively, these data suggest that V. cholerae flagellins are present in culture supernatants and can induce TLR5- and MAPK-dependent IL-8 secretion in host cells. |
| 594 | 18809662 | Vibrio cholerae flagellins induce Toll-like receptor 5-mediated interleukin-8 production through mitogen-activated protein kinase and NF-kappaB activation. |
| 595 | 18809662 | Bacterial flagellins are known to induce IL-8 production through Toll-like receptor 5 (TLR5). |
| 596 | 18809662 | Since the V. cholerae genome encodes five distinct flagellin proteins, FlaA to FlaE, with homology to conserved TLR5 recognition regions of Salmonella FliC, we hypothesized that V. cholerae flagellins may contribute to IL-8 induction through TLR5 and mitogen-activated protein kinase (MAPK) signaling. |
| 597 | 18809662 | Each purified recombinant V. cholerae flagellin induced IL-8 production in T84 intestinal epithelial cells and also induced nuclear factor kappa B (NF-kappaB) activation in HEK293T/TLR5 transfectants, which was blocked by cotransfection with a TLR5 dominant-negative construct, demonstrating TLR5 specificity. |
| 598 | 18809662 | Supernatants derived from Delta flaAC and Delta flaEDB mutants induced IL-8 production in HT-29 intestinal epithelial cells and in HEK293T cells overexpressing TLR5, whereas Delta flaABCDE supernatants induced significantly less IL-8 production, demonstrating the contribution of multiple flagellins in IL-8 induction. |
| 599 | 18809662 | Purified recombinant V. cholerae FlaA activated the MAPKs p38, c-jun N-terminal kinase (JNK), and extracellular regulated kinase (ERK) in T84 cells. |
| 600 | 18809662 | FlaA-induced IL-8 production in T84 cells was inhibited by the p38 inhibitor in combination with either the JNK or ERK inhibitors. |
| 601 | 18809662 | Collectively, these data suggest that V. cholerae flagellins are present in culture supernatants and can induce TLR5- and MAPK-dependent IL-8 secretion in host cells. |
| 602 | 18941233 | DNA-dependent activator of IFN regulatory factors (IRF; DAI, also known as ZBP1 or DLM-1) is a cytosolic DNA sensor that initiates IRF3 and NF-kappaB pathways leading to activation of type I IFNs (IFNalpha, IFNbeta) and other cytokines. |
| 603 | 18941233 | In this study, induction of NF-kappaB is shown to depend on the adaptor receptor-interacting protein kinase (RIP)1, acting via a RIP homotypic interaction motif (RHIM)-dependent interaction with DAI. |
| 604 | 18941233 | DAI binds to and colocalizes with endogenous RIP1 at characteristic cytoplasmic granules. |
| 605 | 18941233 | Suppression of RIP1 expression by RNAi abrogates NF-kappaB activation as well as IFNbeta induction by immunostimulatory DNA. |
| 606 | 18941233 | DAI also interacts with RIP3 and this interaction potentiates DAI-mediated activation of NF-kappaB, implicating RIP3 in regulating this RHIM-dependent pathway. |
| 607 | 18941233 | The role of DAI in activation of NF-kappaB in response to immunostimulatory DNA appears to be analogous to sensing of dsRNA by TLR3 in that both pathways involve RHIM-dependent signaling that is mediated via RIP1, reinforcing a central role for this adaptor in innate sensing of intracellular microbes. |
| 608 | 18941233 | DNA-dependent activator of IFN regulatory factors (IRF; DAI, also known as ZBP1 or DLM-1) is a cytosolic DNA sensor that initiates IRF3 and NF-kappaB pathways leading to activation of type I IFNs (IFNalpha, IFNbeta) and other cytokines. |
| 609 | 18941233 | In this study, induction of NF-kappaB is shown to depend on the adaptor receptor-interacting protein kinase (RIP)1, acting via a RIP homotypic interaction motif (RHIM)-dependent interaction with DAI. |
| 610 | 18941233 | DAI binds to and colocalizes with endogenous RIP1 at characteristic cytoplasmic granules. |
| 611 | 18941233 | Suppression of RIP1 expression by RNAi abrogates NF-kappaB activation as well as IFNbeta induction by immunostimulatory DNA. |
| 612 | 18941233 | DAI also interacts with RIP3 and this interaction potentiates DAI-mediated activation of NF-kappaB, implicating RIP3 in regulating this RHIM-dependent pathway. |
| 613 | 18941233 | The role of DAI in activation of NF-kappaB in response to immunostimulatory DNA appears to be analogous to sensing of dsRNA by TLR3 in that both pathways involve RHIM-dependent signaling that is mediated via RIP1, reinforcing a central role for this adaptor in innate sensing of intracellular microbes. |
| 614 | 18941233 | DNA-dependent activator of IFN regulatory factors (IRF; DAI, also known as ZBP1 or DLM-1) is a cytosolic DNA sensor that initiates IRF3 and NF-kappaB pathways leading to activation of type I IFNs (IFNalpha, IFNbeta) and other cytokines. |
| 615 | 18941233 | In this study, induction of NF-kappaB is shown to depend on the adaptor receptor-interacting protein kinase (RIP)1, acting via a RIP homotypic interaction motif (RHIM)-dependent interaction with DAI. |
| 616 | 18941233 | DAI binds to and colocalizes with endogenous RIP1 at characteristic cytoplasmic granules. |
| 617 | 18941233 | Suppression of RIP1 expression by RNAi abrogates NF-kappaB activation as well as IFNbeta induction by immunostimulatory DNA. |
| 618 | 18941233 | DAI also interacts with RIP3 and this interaction potentiates DAI-mediated activation of NF-kappaB, implicating RIP3 in regulating this RHIM-dependent pathway. |
| 619 | 18941233 | The role of DAI in activation of NF-kappaB in response to immunostimulatory DNA appears to be analogous to sensing of dsRNA by TLR3 in that both pathways involve RHIM-dependent signaling that is mediated via RIP1, reinforcing a central role for this adaptor in innate sensing of intracellular microbes. |
| 620 | 18941233 | DNA-dependent activator of IFN regulatory factors (IRF; DAI, also known as ZBP1 or DLM-1) is a cytosolic DNA sensor that initiates IRF3 and NF-kappaB pathways leading to activation of type I IFNs (IFNalpha, IFNbeta) and other cytokines. |
| 621 | 18941233 | In this study, induction of NF-kappaB is shown to depend on the adaptor receptor-interacting protein kinase (RIP)1, acting via a RIP homotypic interaction motif (RHIM)-dependent interaction with DAI. |
| 622 | 18941233 | DAI binds to and colocalizes with endogenous RIP1 at characteristic cytoplasmic granules. |
| 623 | 18941233 | Suppression of RIP1 expression by RNAi abrogates NF-kappaB activation as well as IFNbeta induction by immunostimulatory DNA. |
| 624 | 18941233 | DAI also interacts with RIP3 and this interaction potentiates DAI-mediated activation of NF-kappaB, implicating RIP3 in regulating this RHIM-dependent pathway. |
| 625 | 18941233 | The role of DAI in activation of NF-kappaB in response to immunostimulatory DNA appears to be analogous to sensing of dsRNA by TLR3 in that both pathways involve RHIM-dependent signaling that is mediated via RIP1, reinforcing a central role for this adaptor in innate sensing of intracellular microbes. |
| 626 | 18941233 | DNA-dependent activator of IFN regulatory factors (IRF; DAI, also known as ZBP1 or DLM-1) is a cytosolic DNA sensor that initiates IRF3 and NF-kappaB pathways leading to activation of type I IFNs (IFNalpha, IFNbeta) and other cytokines. |
| 627 | 18941233 | In this study, induction of NF-kappaB is shown to depend on the adaptor receptor-interacting protein kinase (RIP)1, acting via a RIP homotypic interaction motif (RHIM)-dependent interaction with DAI. |
| 628 | 18941233 | DAI binds to and colocalizes with endogenous RIP1 at characteristic cytoplasmic granules. |
| 629 | 18941233 | Suppression of RIP1 expression by RNAi abrogates NF-kappaB activation as well as IFNbeta induction by immunostimulatory DNA. |
| 630 | 18941233 | DAI also interacts with RIP3 and this interaction potentiates DAI-mediated activation of NF-kappaB, implicating RIP3 in regulating this RHIM-dependent pathway. |
| 631 | 18941233 | The role of DAI in activation of NF-kappaB in response to immunostimulatory DNA appears to be analogous to sensing of dsRNA by TLR3 in that both pathways involve RHIM-dependent signaling that is mediated via RIP1, reinforcing a central role for this adaptor in innate sensing of intracellular microbes. |
| 632 | 18945182 | Induction of CC and CXC chemokines in human antigen-presenting dendritic cells by the pneumococcal proteins pneumolysin and CbpA, and the role played by toll-like receptor 4, NF-kappaB, and mitogen-activated protein kinases. |
| 633 | 19017952 | During T cell interaction with APC, CD28 is recruited to the central region (cSMAC) of the immunological synapse. |
| 634 | 19017952 | CD28-mediated signaling through PI3K results in the recruitment of protein kinase C-theta (PKCtheta) to the cSMAC, activation of NF-kappaB, and up-regulation of IL-2 transcription. |
| 635 | 19017952 | In this report, we show that CD28 recruitment and persistence at the immunological synapse requires TCR signals and CD80 engagement. |
| 636 | 19017952 | Addition of mAb to either MHC class II or CD80 results in the rapid displacement of CD28 from the immunological synapse. |
| 637 | 19017952 | Ligand binding is not sufficient for CD28 localization to the immunological synapse, as truncation of the cytosolic tail of CD28 disrupts synapse localization without effecting the ability of CD28 to bind CD80. |
| 638 | 19017952 | Mutation of tyrosine 188 also results in diminished activation of NF-kappaB, suggesting that CD28-mediated localization of PKCtheta to the cSMAC is important for efficient signal transduction. |
| 639 | 19017952 | During T cell interaction with APC, CD28 is recruited to the central region (cSMAC) of the immunological synapse. |
| 640 | 19017952 | CD28-mediated signaling through PI3K results in the recruitment of protein kinase C-theta (PKCtheta) to the cSMAC, activation of NF-kappaB, and up-regulation of IL-2 transcription. |
| 641 | 19017952 | In this report, we show that CD28 recruitment and persistence at the immunological synapse requires TCR signals and CD80 engagement. |
| 642 | 19017952 | Addition of mAb to either MHC class II or CD80 results in the rapid displacement of CD28 from the immunological synapse. |
| 643 | 19017952 | Ligand binding is not sufficient for CD28 localization to the immunological synapse, as truncation of the cytosolic tail of CD28 disrupts synapse localization without effecting the ability of CD28 to bind CD80. |
| 644 | 19017952 | Mutation of tyrosine 188 also results in diminished activation of NF-kappaB, suggesting that CD28-mediated localization of PKCtheta to the cSMAC is important for efficient signal transduction. |
| 645 | 19020113 | We previously reported that LPS-induced de novo expression of RelB is required for generating tolerance to interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) expression. |
| 646 | 19020113 | RelB represses transcription by binding with heterochromatic protein 1 alpha (HP1alpha) to the proximal promoters of IL-1beta and TNF-alpha. |
| 647 | 19020113 | In contrast, we report herein that RelB is required for sustained expression of anti-inflammatory IkappaBalpha in LPS-tolerant THP-1 cells. |
| 648 | 19020113 | RelB transcription activation requires binding to the IkappaBalpha proximal promoter along with NF-kappaB p50 and is associated with an apparent dimer exchange with p65. |
| 649 | 19036811 | We therefore expressed a viral protein that constitutively activates NF-kappaB, vFLIP from Kaposi's sarcoma-associated herpesvirus (KSHV), in a lentivector to mature DCs. vFLIP activated NF-kappaB in mouse bone marrow-derived DCs in vitro and matured these DCs to a similar extent as lipopolysaccharide; costimulatory markers CD80, CD86, CD40, and ICAM-1 were upregulated and tumor necrosis factor alpha and interleukin-12 secreted. |
| 650 | 19072345 | Targeted agents against important mitogenic pathways, including MEK/ERK, Src, PI3K/Akt, mTOR, Hedgehog and NF-kappaB, as well as agents targeting histone deacetylase, poly(ADP-ribose) polymerase, heat shock protein 90 and other agents such as beta-lapachone, hold considerable interest for further development. |
| 651 | 19124729 | A20 down-regulated DCs showed higher activation of the transcription factors NF-kappaB and activator protein-1, which resulted in increased and sustained production of IL-6, IL-10, and IL-12p70. |
| 652 | 19124729 | We further demonstrated that A20 down-regulated DCs skew naive CD4+ T cells toward IFN-gamma producing Th1 cells, a process which is dependent on IL-12p70 and which is unaffected by IL-10. |
| 653 | 19124729 | Furthermore, A20 and/or IL-10 down-regulated DCs had an enhanced capacity to prime Melan-A/MART-1 specific CD8+ T cells. |
| 654 | 19124729 | Finally, we demonstrated that potent T cell stimulatory DCs are generated by the simultaneous delivery of poly(I:C12U), A20, or A20/IL-10 small interfering RNA and Ag-encoding mRNA, introducing a one step approach to improve DC-based vaccines. |
| 655 | 19124729 | Together these findings demonstrate that A20 negatively regulates NF-kappaB and activator protein-1 in DCs and that down-regulation of A20 results in DCs with enhanced T cell stimulatory capacity. |
| 656 | 19124729 | A20 down-regulated DCs showed higher activation of the transcription factors NF-kappaB and activator protein-1, which resulted in increased and sustained production of IL-6, IL-10, and IL-12p70. |
| 657 | 19124729 | We further demonstrated that A20 down-regulated DCs skew naive CD4+ T cells toward IFN-gamma producing Th1 cells, a process which is dependent on IL-12p70 and which is unaffected by IL-10. |
| 658 | 19124729 | Furthermore, A20 and/or IL-10 down-regulated DCs had an enhanced capacity to prime Melan-A/MART-1 specific CD8+ T cells. |
| 659 | 19124729 | Finally, we demonstrated that potent T cell stimulatory DCs are generated by the simultaneous delivery of poly(I:C12U), A20, or A20/IL-10 small interfering RNA and Ag-encoding mRNA, introducing a one step approach to improve DC-based vaccines. |
| 660 | 19124729 | Together these findings demonstrate that A20 negatively regulates NF-kappaB and activator protein-1 in DCs and that down-regulation of A20 results in DCs with enhanced T cell stimulatory capacity. |
| 661 | 19140872 | Our results demonstrates that Mycobacterium bovis BCG (M. bovis BCG) downregulates tumour necrosis factor-alpha (TNF-alpha)-induced COX-2 gene expression in alveolar epithelial cells by inhibiting the phosphorylations of Raf-1 and p38 kinases. |
| 662 | 19140872 | Further, M. bovis BCG-mediated inhibition of COX-2 or p38 mitogen-activated protein kinase could be reversed by Calyculin A, a selective inhibitor of Ser/Thr phosphatases. |
| 663 | 19140872 | Moreover, M. bovis BCG inhibited the TNF-alpha-triggered NF-kappaB activation following IkappaB degradation. |
| 664 | 19264770 | NF-kappaB p50 plays distinct roles in the establishment and control of murine gammaherpesvirus 68 latency. |
| 665 | 19264770 | Because the confounding impact of the loss of p50 on the host response to MHV68 infection prevented a direct analysis of the role of this NF-kappaB family member on MHV68 latency in B cells, we generated and infected mixed p50(+/+)/p50(-/-) bone marrow chimeric mice. |
| 666 | 19264770 | NF-kappaB p50 plays distinct roles in the establishment and control of murine gammaherpesvirus 68 latency. |
| 667 | 19264770 | Because the confounding impact of the loss of p50 on the host response to MHV68 infection prevented a direct analysis of the role of this NF-kappaB family member on MHV68 latency in B cells, we generated and infected mixed p50(+/+)/p50(-/-) bone marrow chimeric mice. |
| 668 | 19275918 | They are traditionally viewed as the immunologic centerpiece that is able to prime CD4(+) helper and CD8(+) cytotoxic T-cell effector populations. |
| 669 | 19275918 | DC overexpressing ILT3 display lower phosphorylation levels of NF-kappaB and fail to stimulate the full program of Th proliferation and maturation eliciting instead the differentiation of CD8(+) T(S) and CD4(+) Treg. |
| 670 | 19539971 | We report that ERK2 phosphorylation, an event preceding and required for NF-kappaB activation, occurred rapidly after virus infection. |
| 671 | 19539971 | ERK2 and NF-kappaB remained inert when virus endocytosis was prevented, suggesting that virus-host cell interactions were insufficient for activating NF-kappaB. |
| 672 | 19539971 | We report that ERK2 phosphorylation, an event preceding and required for NF-kappaB activation, occurred rapidly after virus infection. |
| 673 | 19539971 | ERK2 and NF-kappaB remained inert when virus endocytosis was prevented, suggesting that virus-host cell interactions were insufficient for activating NF-kappaB. |
| 674 | 19540594 | Requirement of TLR4 and CD14 in dendritic cell activation by Hemagglutinin B from Porphyromonas gingivalis. |
| 675 | 19540594 | Using an endotoxin free rHagB preparation, our results show that stimulation of murine bone marrow-derived DC with rHagB leads to upregulation of the costimulatory molecules CD86 and CD40, activation of p38 and ERK MAP kinases, transcription factors NF-kappaB, CREB and IRF-3 and the production of IL-6, TNF-alpha, IL-12p40 and to a lesser extent IL-10 and IFN-beta. |
| 676 | 19540594 | This activation process was absolutely dependent on TLR4 and CD14. |
| 677 | 19540594 | While upregulation of CD86 was independent of the adaptor molecule MyD88, CD40 upregulation and optimal cytokine (IL-6, TNF-alpha, IL-12p40, IL-10 and IFN-beta) production required both MyD88 and TRIF molecules. |
| 678 | 19594424 | Additionally, US28 has been demonstrated to constitutively activate phospholipase C (PLC) and NF-kB signaling pathways. |
| 679 | 19596385 | Modified vaccinia virus Ankara can activate NF-kappaB transcription factors through a double-stranded RNA-activated protein kinase (PKR)-dependent pathway during the early phase of virus replication. |
| 680 | 19596385 | In human embryonic kidney (HEK 293T) cells, the MVA-induced depletion of IkappaBalpha required to activate NF-kappaB is inhibited by UV-inactivation of the virus, and begins before viral DNA replication. |
| 681 | 19596385 | In mouse embryonic fibroblasts (MEFs), MVA induction of IkappaBalpha depletion is dependent on the expression of mouse or human double-stranded RNA-activated protein kinase (PKR). |
| 682 | 19596385 | These results demonstrate that events during the early phase of MVA replication can induce PKR-mediated processes contributing both to the activation of NF-kappaB signaling, and to processes that may restrict viral replication. |
| 683 | 19596385 | Modified vaccinia virus Ankara can activate NF-kappaB transcription factors through a double-stranded RNA-activated protein kinase (PKR)-dependent pathway during the early phase of virus replication. |
| 684 | 19596385 | In human embryonic kidney (HEK 293T) cells, the MVA-induced depletion of IkappaBalpha required to activate NF-kappaB is inhibited by UV-inactivation of the virus, and begins before viral DNA replication. |
| 685 | 19596385 | In mouse embryonic fibroblasts (MEFs), MVA induction of IkappaBalpha depletion is dependent on the expression of mouse or human double-stranded RNA-activated protein kinase (PKR). |
| 686 | 19596385 | These results demonstrate that events during the early phase of MVA replication can induce PKR-mediated processes contributing both to the activation of NF-kappaB signaling, and to processes that may restrict viral replication. |
| 687 | 19596385 | Modified vaccinia virus Ankara can activate NF-kappaB transcription factors through a double-stranded RNA-activated protein kinase (PKR)-dependent pathway during the early phase of virus replication. |
| 688 | 19596385 | In human embryonic kidney (HEK 293T) cells, the MVA-induced depletion of IkappaBalpha required to activate NF-kappaB is inhibited by UV-inactivation of the virus, and begins before viral DNA replication. |
| 689 | 19596385 | In mouse embryonic fibroblasts (MEFs), MVA induction of IkappaBalpha depletion is dependent on the expression of mouse or human double-stranded RNA-activated protein kinase (PKR). |
| 690 | 19596385 | These results demonstrate that events during the early phase of MVA replication can induce PKR-mediated processes contributing both to the activation of NF-kappaB signaling, and to processes that may restrict viral replication. |
| 691 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 692 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 693 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 694 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 695 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 696 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 697 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 698 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 699 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 700 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 701 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 702 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 703 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 704 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 705 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 706 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 707 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 708 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 709 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 710 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 711 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 712 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 713 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 714 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 715 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 716 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 717 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 718 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 719 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 720 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 721 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 722 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 723 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 724 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 725 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 726 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 727 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 728 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 729 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 730 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 731 | 19793902 | Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway. |
| 732 | 19793902 | However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated. |
| 733 | 19793902 | In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner. |
| 734 | 19793902 | Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells. |
| 735 | 19793902 | Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid. |
| 736 | 19793902 | The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14. |
| 737 | 19793902 | Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. |
| 738 | 19793902 | These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway. |
| 739 | 19846517 | The enhanced IFN-inducing capacity of the C(ko) virus correlated with an enhanced activation of IFN regulatory factor 3 (IRF-3), NF-kappaB, and ATF-2 in C(ko)-infected compared to V(ko) or parental virus-infected cells. |
| 740 | 19846517 | Furthermore, protein kinase PKR and mitochondrial adapter IPS-1 were required for maximal C(ko)-mediated IFN-beta induction, which correlated with the PKR-mediated enhancement of mitogen-activated protein kinase and NF-kappaB activation. |
| 741 | 19846517 | Our results reveal multiple consequences of C protein expression and document an important function for PKR as an enhancer of IFN-beta induction during measles virus infection. |
| 742 | 19846517 | The enhanced IFN-inducing capacity of the C(ko) virus correlated with an enhanced activation of IFN regulatory factor 3 (IRF-3), NF-kappaB, and ATF-2 in C(ko)-infected compared to V(ko) or parental virus-infected cells. |
| 743 | 19846517 | Furthermore, protein kinase PKR and mitochondrial adapter IPS-1 were required for maximal C(ko)-mediated IFN-beta induction, which correlated with the PKR-mediated enhancement of mitogen-activated protein kinase and NF-kappaB activation. |
| 744 | 19846517 | Our results reveal multiple consequences of C protein expression and document an important function for PKR as an enhancer of IFN-beta induction during measles virus infection. |
| 745 | 19853910 | The effect of R1, R2 and R3 on the expression of the pro- and anti-inflammatory cytokines (TNF-alpha, IL-6, and IL-12) and the co-stimulatory molecules (CD40, CD80, CD86, and MHC class II) in MDDCs was examined. |
| 746 | 19853910 | The exposure of R1 caused a dose-dependent increase in the expression of TNF-alpha, IL-12, CD86 and CD40, while R2 and R3 did not up-regulate these cytokines and co-stimulatory molecules. |
| 747 | 19853910 | Furthermore, we found that R1 significantly increased the NF-kappaB expression in the nucleus (in a dose-dependent manner) and promoted the degradation of total IkappaBalpha levels, indicating that the NF-kappaB signaling pathway might involve in an R1-induced DC activation. |
| 748 | 19880213 | Activation of both cell types is associated with the induction of the MAP kinase pathway, the phosphorylation of STAT1, STAT5 and AKT and with transcription factor NF-kappaB activation in vitro and in vivo. |
| 749 | 20007537 | Moreover, only EFD BCG enhanced peroxisome proliferator-activated receptor gamma expression and blocked NF-kappaB activation, cyclooxygenase expression, and p38 MAPK phosphorylation. |
| 750 | 20039305 | Since natural lipid A from bacterial LPS depends on membrane-bound (mCD14) or soluble CD14 for its TLR4 ligand activity, we investigated the involvement of both forms of CD14 in the responses elicited by CRX-527. |
| 751 | 20039305 | First, we found that CRX-527 induces NF-kappaB and interferon regulatory factor-3 (IRF-3) activation in human embryonic kidney cells transfected with TLR4 and MD-2 genes alone, whereas the responses to LPS require either co-transfection of the gene encoding mCD14 or addition of soluble CD14. |
| 752 | 20039305 | We then observed that monocyte-derived DC, which are devoid of mCD14 respond to CRX-527 but not to LPS in serum-free medium. |
| 753 | 20039305 | Finally, we demonstrated that splenocytes from CD14-deficient mice produce cytokines in response to CRX-527 but not to LPS. |
| 754 | 20045502 | In the current study, we investigated the ability of our lipopeptides to activate nuclear factor-kappaB (NF-kappaB) in a toll-like receptor-2 (TLR2)-dependent manner as the possible mode of action and reported the structure-function requirements for novel TLR2 targeting lipopeptides based on LAAs. |
| 755 | 20176741 | Day 3 ROS(lo) DCs were highly responsive to TLR stimuli such as LPS and zymosan by rapid upregulation of CD80, CD86, and MHC class II, in contrast to the low response of day 6 ROS(hi) DCs. |
| 756 | 20176741 | ROS(hi) DCs could not initiate and sustain a significant level of NF-kappaB phosphorylation in response to LPS and zymosan, although demonstrating hyperactivation of p38 MAPK by LPS, in a fashion disparate to ROS(lo) DCs. |
| 757 | 20176745 | We further found that PE_PGRS protein-mediated activation of DCs involves participation of ERK1/2, p38 MAPK, and NF-kappaB signaling pathways. |
| 758 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 759 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 760 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 761 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 762 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 763 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 764 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 765 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 766 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 767 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 768 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 769 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 770 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 771 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 772 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 773 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 774 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 775 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 776 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 777 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 778 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 779 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 780 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 781 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 782 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 783 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 784 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 785 | 20200188 | The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). |
| 786 | 20200188 | TLR2/TLR4 expression was determined by real-time PCR, Western blotting, and an immunofluorescence assay. |
| 787 | 20200188 | In addition, cells were pretreated with different PD solutions and then incubated with Pam3CSK4 or lipopolysaccharide (LPS), and the degrees of MAPK and NF-kappaB activation were reflected by detecting the phosphorylation levels of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), p38, and p65, using a Western blot method. |
| 788 | 20200188 | TNF-alpha and IL-1beta mRNA expression was measured by real-time PCR. |
| 789 | 20200188 | Glucose-based peritoneal dialysis fluids suppressed the expression of TLR2 and TLR4 proteins in HPMCs. |
| 790 | 20200188 | Challenge of cells with either Pam3CSK4 or LPS resulted in impaired TNF-alpha and IL-1beta production. |
| 791 | 20200188 | Moreover, reduced TLR2 and TLR4 levels in glucose-based peritoneal dialysis solution-treated mesothelial cells were accompanied by reduced p42/44 (ERK1/2), JNK, p38 MAPK, and NF-kappaB p65 phosphorylation upon TLR ligand engagement. |
| 792 | 20200188 | No significant changes in MAPK and NF-kappaB signaling and TNF-alpha and IL-1beta mRNA expression were observed in icodextrin-based PD solution-treated mesothelial cells. |
| 793 | 20200188 | Glucose-based PD solution, but not icodextrin-based PD solution, downregulates expression of TLR2/TLR4 by human peritoneal mesothelial cells and triggers hyporesponsiveness to pathogen-associated molecular patterns. |
| 794 | 20386471 | Molecular analyses performed on immature bag-DCs showed them already engaged in a particular maturation process (early activation of nuclear factor kappa B and beta-catenin). |
| 795 | 20432202 | The cancer preventive or protective activities of the various immunomodulatory natural products lie in their effects on cellular defenses including detoxifying and antioxidant enzyme systems, and the induction of anti-inflammatory and antitumor or antimetastasis responses, often by targeting specific key transcription factors like nuclear factor kappa B (NF-kappaB), activator protein (AP-1), signal transducers and activators of transcription (STAT) and others. |
| 796 | 20444990 | Vaccinia virus (VACV) encodes multiple proteins to evade host innate immunity, including B14, a virulence factor that binds to the inhibitor of kappaB kinase beta (IKKbeta) and blocks nuclear factor kappaB (NF-kappaB) activation. |
| 797 | 20451253 | Production of monocyte chemoattractant protein-1 (MCP-1/CCL2), macrophage inflammatory protein-1 (MIP-1/CCL3) and regulated on activation, normal T cell expressed and secreted (RANTES/CCL5), were determined in cell culture supernatants by ELISA or cytokine cytometric bead array. |
| 798 | 20451253 | Pharmacological inhibitors of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), nuclear factor-kappaB (NF-kB) and phosphatidylinositol 3-kinase (PI3K), were used to investigate the role of signaling pathways. |
| 799 | 20451253 | TLR agonists induced significantly elevated MCP-1, RANTES, and MIP-1. |
| 800 | 20451253 | Production of RANTES and MIP-1 was particularly prominent after stimulation of DCs with TLR3 (Poly(I:C)), and TLR7/8 (R848) or TLR9 (CpG ODN) agonists, respectively. |
| 801 | 20451253 | A positive role was identified for NF-kB, PI3K and ERK, whereas JNK had a negative regulatory effect on chemokine production in DCs. |
| 802 | 20451253 | Positive and negative regulatory roles for the p38 MAPK pathway were observed. |
| 803 | 20451253 | Production of monocyte chemoattractant protein-1 (MCP-1/CCL2), macrophage inflammatory protein-1 (MIP-1/CCL3) and regulated on activation, normal T cell expressed and secreted (RANTES/CCL5), were determined in cell culture supernatants by ELISA or cytokine cytometric bead array. |
| 804 | 20451253 | Pharmacological inhibitors of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), nuclear factor-kappaB (NF-kB) and phosphatidylinositol 3-kinase (PI3K), were used to investigate the role of signaling pathways. |
| 805 | 20451253 | TLR agonists induced significantly elevated MCP-1, RANTES, and MIP-1. |
| 806 | 20451253 | Production of RANTES and MIP-1 was particularly prominent after stimulation of DCs with TLR3 (Poly(I:C)), and TLR7/8 (R848) or TLR9 (CpG ODN) agonists, respectively. |
| 807 | 20451253 | A positive role was identified for NF-kB, PI3K and ERK, whereas JNK had a negative regulatory effect on chemokine production in DCs. |
| 808 | 20451253 | Positive and negative regulatory roles for the p38 MAPK pathway were observed. |
| 809 | 20504922 | In this study, we demonstrated that the PRRSV nsp2 OTU domain antagonizes the type I interferon induction by interfering with the NF-kappaB signaling pathway. |
| 810 | 20504922 | Further analysis revealed that the nsp2 OTU domain possesses ubiquitin-deconjugating activity. |
| 811 | 20504922 | This domain has the ability to inhibit NF-kappaB activation by interfering with the polyubiquitination process of IkappaBalpha, which subsequently prevents IkappaBalpha degradation. |
| 812 | 20504922 | The OTU domain mutants were examined to determine whether mutations in the nsp2 OTU domain region altered virus ability to inhibit NF-kappaB activation. |
| 813 | 20504922 | In this study, we demonstrated that the PRRSV nsp2 OTU domain antagonizes the type I interferon induction by interfering with the NF-kappaB signaling pathway. |
| 814 | 20504922 | Further analysis revealed that the nsp2 OTU domain possesses ubiquitin-deconjugating activity. |
| 815 | 20504922 | This domain has the ability to inhibit NF-kappaB activation by interfering with the polyubiquitination process of IkappaBalpha, which subsequently prevents IkappaBalpha degradation. |
| 816 | 20504922 | The OTU domain mutants were examined to determine whether mutations in the nsp2 OTU domain region altered virus ability to inhibit NF-kappaB activation. |
| 817 | 20504922 | In this study, we demonstrated that the PRRSV nsp2 OTU domain antagonizes the type I interferon induction by interfering with the NF-kappaB signaling pathway. |
| 818 | 20504922 | Further analysis revealed that the nsp2 OTU domain possesses ubiquitin-deconjugating activity. |
| 819 | 20504922 | This domain has the ability to inhibit NF-kappaB activation by interfering with the polyubiquitination process of IkappaBalpha, which subsequently prevents IkappaBalpha degradation. |
| 820 | 20504922 | The OTU domain mutants were examined to determine whether mutations in the nsp2 OTU domain region altered virus ability to inhibit NF-kappaB activation. |
| 821 | 20558723 | SchuS4 infection also blocked signals required for macrophage cytokine production, including Akt phosphorylation, IkappaB alpha degradation, and NF-kappaB nuclear localization and activation. |
| 822 | 20558723 | Mutation of catalase (katG) sensitized F. tularensis to H(2)O(2) and enhanced PTEN oxidation, Akt phosphorylation, NF-kappaB activation, and inflammatory cytokine production. |
| 823 | 20558723 | SchuS4 infection also blocked signals required for macrophage cytokine production, including Akt phosphorylation, IkappaB alpha degradation, and NF-kappaB nuclear localization and activation. |
| 824 | 20558723 | Mutation of catalase (katG) sensitized F. tularensis to H(2)O(2) and enhanced PTEN oxidation, Akt phosphorylation, NF-kappaB activation, and inflammatory cytokine production. |
| 825 | 20610663 | Since Toll-like receptor 2 (TLR2), TLR4, and TLR9 activation have been involved in HIV-1 recrudescence, we sought to determine the role of these TLRs in HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis using BF24 monocytes/macrophages stably transfected with the HIV-1 promoter driving chloramphenicol acetyltransferase (CAT) expression and THP89GFP cells, a model of HIV-1 latency. |
| 826 | 20610663 | We demonstrated that TLR9 activation by F. nucleatum and TLR2 activation by both bacteria appear to be involved in HIV-1 reactivation; however, TLR4 activation had no effect. |
| 827 | 20610663 | Moreover, the autocrine activity of tumor necrosis factor alpha (TNF-alpha) but not interleukin-1beta (IL-1beta) produced in response to bacteria could impact viral reactivation. |
| 828 | 20610663 | The transcription factors NF-kappaB and Sp1 appear to be positively regulating HIV-1 reactivation induced by these oral pathogens. |
| 829 | 20610663 | These results suggest that oral Gram-negative bacteria (F. nucleatum and P. gingivalis) associated with oral and systemic chronic inflammatory disorders enhance HIV-1 reactivation in monocytes/macrophages through TLR2 and TLR9 activation in a mechanism that appears to be transcriptionally regulated. |
| 830 | 20625487 | Fifty six genes such as TNF, NFKB1, IL2, IL6, and MAPK8 were ranked among the top 25 by at least one of the centrality methods in one or both networks. |
| 831 | 21031251 | The innate immune response mainly represented by Toll-like receptors and Nod-like receptors that recognize their specific ligands, activate transcription factors as NF-kB, AP-1, CREB-1, inducing production of inflammatory cytokines such as IL -8, IL-12, IL-6, IL-1β, IL-18, TNF-α and IL-10. |
| 832 | 22083261 | NSs induces a shut-off of host transcription including interferon (IFN)-beta mRNA and promotes degradation of double-stranded RNA-dependent protein kinase (PKR) at the post-translational level. |
| 833 | 22083261 | IFN-beta is transcriptionally upregulated by interferon regulatory factor 3 (IRF-3), NF-kB and activator protein-1 (AP-1), and the binding of IFN-beta to IFN-alpha/beta receptor (IFNAR) stimulates the transcription of IFN-alpha genes or other interferon stimulated genes (ISGs), which induces host antiviral activities, whereas host transcription suppression including IFN-beta gene by NSs prevents the gene upregulations of those ISGs in response to viral replication although IRF-3, NF-kB and activator protein-1 (AP-1) can be activated by RVFV7. |
| 834 | 22986450 | Specific targets in this category included genes asso-ciated with the intrinsic and extrinsic apoptotic pathways (CFLAR, TNFAIP3, TNFRSF10D, SOD2, BCL2A1, BIRC4, PIM2, TNFSF10, TNFRSF10C, CASP2 and CASP8) and genes that act via the NFĸB pathway and other mechanisms to prolong cell viability (NFKB1, NFKB2 and RELA, IL1B, CAST, CDK2,GADD45B, BCL3, BIRC3, CDK2, IL1A, PBEF1, IL6, CXCL1, CCL4 and VEGF). |
| 835 | 22986450 | Moreover, we demonstrate that the X-linked inhibitor of apoptosis protein remained abundant in polymorphonuclear leukocytes over 48 h of LVS infection, whereas BAX mRNA and protein were progressively downregulated. |
| 836 | 23507086 | Molecular pathways upregulated by MA-CNTs included IL6, CD40, dendritic cell maturation, tumor necrosis factor-(TNF)-α/TNFR1-2, NFKB signaling and T helper 1 chemokine pathways (CXCR3 and CCR5 ligand pathways). |
| 837 | 23507086 | To confirm the results at protein level, the secretion of IL1β, TNFα, IL6 and IL10 by THP1 and primary monocytes was assessed by ELISA, corroborating gene-expression data. |
| 838 | 23845179 | IL4 and IFNalpha generation of dendritic cells reveals great migratory potential and NFkB and cJun expression in IL4DCs. |
| 839 | 23845179 | Dendritic cells (DCs) recently revealed as a potent tumor vaccine component, are commonly differentiated from monocytes by cultivation with IL-4 and GM-CSF. |
| 840 | 23845179 | The aim of this study was to compare the functionality and phenotypic characterization of monocyte-derived DC generated by IL-4 (IL4DC) and IFNalpha (IFNalphaDC) modified protocols. |
| 841 | 23845179 | We herein investigated the molecular mechanism underlying the parameters previously described, as the relative expression of NF-kB p65, c-fos and c-jun, transcription factors. |
| 842 | 23845179 | Our results demonstrated that IL4DC presented a stable phenotype, an increase in migratory capacity and NF-KB activation, in addition to lower levels of miR-146 a and miR-221. |
| 843 | 23845179 | IL4 and IFNalpha generation of dendritic cells reveals great migratory potential and NFkB and cJun expression in IL4DCs. |
| 844 | 23845179 | Dendritic cells (DCs) recently revealed as a potent tumor vaccine component, are commonly differentiated from monocytes by cultivation with IL-4 and GM-CSF. |
| 845 | 23845179 | The aim of this study was to compare the functionality and phenotypic characterization of monocyte-derived DC generated by IL-4 (IL4DC) and IFNalpha (IFNalphaDC) modified protocols. |
| 846 | 23845179 | We herein investigated the molecular mechanism underlying the parameters previously described, as the relative expression of NF-kB p65, c-fos and c-jun, transcription factors. |
| 847 | 23845179 | Our results demonstrated that IL4DC presented a stable phenotype, an increase in migratory capacity and NF-KB activation, in addition to lower levels of miR-146 a and miR-221. |
| 848 | 23845179 | IL4 and IFNalpha generation of dendritic cells reveals great migratory potential and NFkB and cJun expression in IL4DCs. |
| 849 | 23845179 | Dendritic cells (DCs) recently revealed as a potent tumor vaccine component, are commonly differentiated from monocytes by cultivation with IL-4 and GM-CSF. |
| 850 | 23845179 | The aim of this study was to compare the functionality and phenotypic characterization of monocyte-derived DC generated by IL-4 (IL4DC) and IFNalpha (IFNalphaDC) modified protocols. |
| 851 | 23845179 | We herein investigated the molecular mechanism underlying the parameters previously described, as the relative expression of NF-kB p65, c-fos and c-jun, transcription factors. |
| 852 | 23845179 | Our results demonstrated that IL4DC presented a stable phenotype, an increase in migratory capacity and NF-KB activation, in addition to lower levels of miR-146 a and miR-221. |
| 853 | 23901754 | Inhibition of toll-like receptor 2-mediated NF-kappaB activation in Vero cells with herpesvirus of turkeys. |
| 854 | 23901754 | The results demonstrate the significant characteristics of HVT in activating TLR2 signaling. chTLR1 plays a key role in TLR2 subfamily-mediated NF-kappaB inhibition after HVT infection. |
| 855 | 23901754 | Inhibition of toll-like receptor 2-mediated NF-kappaB activation in Vero cells with herpesvirus of turkeys. |
| 856 | 23901754 | The results demonstrate the significant characteristics of HVT in activating TLR2 signaling. chTLR1 plays a key role in TLR2 subfamily-mediated NF-kappaB inhibition after HVT infection. |
| 857 | 23968857 | NF-kB and STAT). |
| 858 | 24384074 | An in vitro model of antigen presentation showed that ligands for TLR-9, 7, 4 and 1/2 increased the ability of APCs to present antigen-85B of BCG to CD4 T cells, which correlated with an increase in MHC-II expression. |
| 859 | 24384074 | TLR-activation led to a down-regulation of MARCH1 ubiquitin ligase which prevents the degradation of MHC-II and decreased IL-10 also contributed to an increase in MHC-II. |
| 860 | 24384074 | TLR-activation induced up-regulation of MHC-II was inhibited by the blockade of IRAK, NF-kB, and MAPKs. |
| 861 | 24384074 | TLR-7 and TLR-9 ligands had the most effective adjuvant like effect on MHC-II of APCs which allowed BCG vaccine mediated activation of CD4 T cells. |
| 862 | 24799832 | The recognition of the importance of bone health and morbidity associated with skeletal related events has led to the introduction of the receptor activator of nuclear factor kappa-B-ligand inhibitor denosumab. |
| 863 | 25324841 | The 24-h network featured a small number of key hub and bottleneck gene nodes, including IKBKE, MYC, NFKB1, and EGR1 that differentiated the macrophage response to virulent and attenuated M. bovis strains, possibly via the modulation of host cell death mechanisms. |
| 864 | 25548469 | The MYD88-dependent pathway involves early-phase activation of nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (NF-κB1) and all the TLRs, except TLR3, have been shown to activate this pathway. |
| 865 | 25548469 | TLR3 and TLR4 act via MYD88-independent pathways with delayed activation of NF-κB signaling. |
| 866 | 25604387 | These protective effects might be ascribed to downregulation of Th17 cells and interleukin (IL)-17A production, upregulation of Treg and receptor activator of nuclear factor-kappa B ligand (RANKL)(+)CD4(+)T cells, and IL-10 and transforming growth factor-β1 production, and inhibition of lymphocyte proliferation. |
| 867 | 25668674 | Through intersection analysis of the microarray results, we found that the Toll-like receptor signaling pathway was significantly activated, and NF-kB, TRAF3 and IRF7 were activated as early as 12 h, and MyD88 was activated at 48 h post-stimulation. |
| 868 | 25668674 | Furthermore, the expression of the surface marker CD83 and the co-stimulatory molecules CD80 and CD86 was up-regulated as early as 24 h. |
| 869 | 26344618 | Co-Administration of Molecular Adjuvants Expressing NF-Kappa B Subunit p65/RelA or Type-1 Transactivator T-bet Enhance Antigen Specific DNA Vaccine-Induced Immunity. |