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Gene Information
Gene symbol: CASP3
Gene name: caspase 3, apoptosis-related cysteine peptidase
HGNC ID: 1504
Synonyms: CPP32, CPP32B, Yama, apopain
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 10689134 | Both CD4+ and CD8+ T cell subsets from aged subjects demonstrated increased sensitivity to TNFR-mediated and Fas-mediated apoptosis that was associated with overexpression of death receptors and adapter molecules associated with death signaling. |
| 2 | 10689134 | An increased expression and activity of both initiator (caspase 8) and effector (caspase 3) caspases was observed in lymphocytes from aged subjects as compared to young individuals. |
| 3 | 10689134 | Furthermore, an increased expression of Bax and decreased expression of Bcl-2 (both at the protein and mRNA level) was found in lymphocytes from aged subjects. |
| 4 | 12040466 | Attenuated murine caspase 2 and a chimera of murine caspase 2 prodomain and human caspase 3 strongly enhanced humoral and cell-mediated immune response to hemagglutinin when they were co-administered with an immunogen DNA. |
| 5 | 12040466 | ELISPOT assays showed that CD4 T cells were preferentially activated, while CD8 T cell response remained at marginal level. |
| 6 | 12055253 | Mycobacterium tuberculosis promotes apoptosis in human neutrophils by activating caspase-3 and altering expression of Bax/Bcl-xL via an oxygen-dependent pathway. |
| 7 | 12055253 | The Mtb-induced apoptosis was associated with a speedy and transient increase in expression of Bax protein, a proapoptotic member of the Bcl-2 family, and a more prominent reduction in expression of the antiapoptotic protein Bcl-x(L). |
| 8 | 12055253 | Pretreatment with an inhibitor of NADPH oxidase distinctly suppressed the Mtb-stimulated activation of caspase-3 and alteration of Bax/Bcl-x(L) expression in neutrophils. |
| 9 | 12055253 | These results indicate that infection with Mtb causes ROS-dependent alteration of Bax/Bcl-x(L) expression and activation of caspase-3, and thereby induces apoptosis in human neutrophils. |
| 10 | 12055253 | Mycobacterium tuberculosis promotes apoptosis in human neutrophils by activating caspase-3 and altering expression of Bax/Bcl-xL via an oxygen-dependent pathway. |
| 11 | 12055253 | The Mtb-induced apoptosis was associated with a speedy and transient increase in expression of Bax protein, a proapoptotic member of the Bcl-2 family, and a more prominent reduction in expression of the antiapoptotic protein Bcl-x(L). |
| 12 | 12055253 | Pretreatment with an inhibitor of NADPH oxidase distinctly suppressed the Mtb-stimulated activation of caspase-3 and alteration of Bax/Bcl-x(L) expression in neutrophils. |
| 13 | 12055253 | These results indicate that infection with Mtb causes ROS-dependent alteration of Bax/Bcl-x(L) expression and activation of caspase-3, and thereby induces apoptosis in human neutrophils. |
| 14 | 12055253 | Mycobacterium tuberculosis promotes apoptosis in human neutrophils by activating caspase-3 and altering expression of Bax/Bcl-xL via an oxygen-dependent pathway. |
| 15 | 12055253 | The Mtb-induced apoptosis was associated with a speedy and transient increase in expression of Bax protein, a proapoptotic member of the Bcl-2 family, and a more prominent reduction in expression of the antiapoptotic protein Bcl-x(L). |
| 16 | 12055253 | Pretreatment with an inhibitor of NADPH oxidase distinctly suppressed the Mtb-stimulated activation of caspase-3 and alteration of Bax/Bcl-x(L) expression in neutrophils. |
| 17 | 12055253 | These results indicate that infection with Mtb causes ROS-dependent alteration of Bax/Bcl-x(L) expression and activation of caspase-3, and thereby induces apoptosis in human neutrophils. |
| 18 | 12140745 | Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8. |
| 19 | 12140745 | In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression. |
| 20 | 12140745 | Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3. |
| 21 | 12140745 | Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8. |
| 22 | 12140745 | In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression. |
| 23 | 12140745 | Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3. |
| 24 | 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. |
| 25 | 12717553 | In this study we examined the dynamic of PBL Fas and FasL expression, the first-step dead caspase-8, -2, -9 and effector caspase-3, -7 and -10 activity in freshly isolated PBL lysates, and anti-CD3-induced PBL mitogenic response and apoptosis in patients with Puumala virus (PUUV) associated hemorrhagic fever with the renal syndrome (HFRS). |
| 26 | 12717553 | Data reported summarize the initial demonstration of increased Fas/FasL and activation of the initializing (caspase-2, -8 and -9) and the effector caspase-3, -7 and -10 in PBML during acute and convalescent phases of the hantavirus infection. |
| 27 | 12717553 | In this study we examined the dynamic of PBL Fas and FasL expression, the first-step dead caspase-8, -2, -9 and effector caspase-3, -7 and -10 activity in freshly isolated PBL lysates, and anti-CD3-induced PBL mitogenic response and apoptosis in patients with Puumala virus (PUUV) associated hemorrhagic fever with the renal syndrome (HFRS). |
| 28 | 12717553 | Data reported summarize the initial demonstration of increased Fas/FasL and activation of the initializing (caspase-2, -8 and -9) and the effector caspase-3, -7 and -10 in PBML during acute and convalescent phases of the hantavirus infection. |
| 29 | 12810656 | Specific tumoricidal activity of a secreted proapoptotic protein consisting of HER2 antibody and constitutively active caspase-3. |
| 30 | 12810656 | In this study, a novel approach to antitumor therapy was devised by generating a chimeric tumor-targeted killer protein, referred to as immunocasp-3, that comprises a single-chain anti-erbB2/HER2 antibody with a NH(2)-terminal signal sequence, a Pseudomonas exotoxin A translocation domain, and a constitutively active caspase-3 molecule. |
| 31 | 12810656 | Specific tumoricidal activity of a secreted proapoptotic protein consisting of HER2 antibody and constitutively active caspase-3. |
| 32 | 12810656 | In this study, a novel approach to antitumor therapy was devised by generating a chimeric tumor-targeted killer protein, referred to as immunocasp-3, that comprises a single-chain anti-erbB2/HER2 antibody with a NH(2)-terminal signal sequence, a Pseudomonas exotoxin A translocation domain, and a constitutively active caspase-3 molecule. |
| 33 | 12874344 | Moreover, activation of caspase 9 and the executioner caspase 3 was also observed in the LVS-infected J774A.1 macrophages. |
| 34 | 12874344 | The activated caspase 3 degraded poly(ADP-ribose) polymerase (PARP). |
| 35 | 12874344 | The internucleosomal fragmentation and PARP degradation resulting from activation of this apoptotic pathway was prevented by the caspase 3 inhibitor Z-DEVD-fmk. |
| 36 | 12874344 | No involvement of caspase 1, caspase 8, Bcl-2, or Bid was observed. |
| 37 | 12874344 | Moreover, activation of caspase 9 and the executioner caspase 3 was also observed in the LVS-infected J774A.1 macrophages. |
| 38 | 12874344 | The activated caspase 3 degraded poly(ADP-ribose) polymerase (PARP). |
| 39 | 12874344 | The internucleosomal fragmentation and PARP degradation resulting from activation of this apoptotic pathway was prevented by the caspase 3 inhibitor Z-DEVD-fmk. |
| 40 | 12874344 | No involvement of caspase 1, caspase 8, Bcl-2, or Bid was observed. |
| 41 | 12874344 | Moreover, activation of caspase 9 and the executioner caspase 3 was also observed in the LVS-infected J774A.1 macrophages. |
| 42 | 12874344 | The activated caspase 3 degraded poly(ADP-ribose) polymerase (PARP). |
| 43 | 12874344 | The internucleosomal fragmentation and PARP degradation resulting from activation of this apoptotic pathway was prevented by the caspase 3 inhibitor Z-DEVD-fmk. |
| 44 | 12874344 | No involvement of caspase 1, caspase 8, Bcl-2, or Bid was observed. |
| 45 | 14654940 | It induced cleavage of eukaryotic translation initiation factor 4G, leading to cell death through a mechanism involving activation of caspase-9, caspase-3 and poly(ADP-ribose)polymerase. |
| 46 | 14976038 | In the current study, we tested whether higher numbers of hematopoietic stem cells correlate with the speed of immune reconstitution in a congenic transplantation model (C57BL/Ka, CD45.1, Thy1.1-->C57BL/6, CD45.2, Thy1.2) using purified hematopoietic stem cells (c-Kit(+)Thy1.1(low)Lin(-/low)Sca-1(+)). |
| 47 | 14976038 | Phenotypic analyses in peripheral blood and spleen demonstrated that higher numbers of infused stem cells are associated with more rapid regeneration of T cells (CD4(+), CD8(+), naive CD4(+), naive CD8(+)) and B cells at early time points. |
| 48 | 15153784 | We have shown that DNA encoding the anti-apoptotic protein Bcl-xL enhances E7-specific CD8+ T-cell responses and DNA encoding pro-apoptotic protein caspase-3 suppresses E7-specific CD8+ T-cell responses when co-administered intradermally via gene gun with DNA encoding human papillomavirus type 16 (HPV-16) E7 linked to the sorting signal of the lysosome-associated membrane protein type 1 (LAMP-1). |
| 49 | 15153784 | We vaccinated C57BL/6 mice with pVITRO-SEL-Bcl-xL, pVITRO-SEL-mtBcl-xL, pVITRO-SEL, or pVITRO-SEL-caspase-3 intradermally via gene gun and intramuscularly via injection. |
| 50 | 15153784 | We demonstrated that vaccination with pVITRO achieved similar results to a co-administration strategy: that Bcl-xL enhanced the E7-specific CTL response and caspase-3 suppressed the E7-specific CTL response. |
| 51 | 15153784 | Thus, intradermal vaccination with a pVITRO vector combining an anti-apoptotic strategy (Bcl-xL) and an intracellular targeting strategy (SEL) further enhances the E7-specific CD8+ T-cell response and guarantees co-expression of both encoded molecules in transfected cells. |
| 52 | 15153784 | We have shown that DNA encoding the anti-apoptotic protein Bcl-xL enhances E7-specific CD8+ T-cell responses and DNA encoding pro-apoptotic protein caspase-3 suppresses E7-specific CD8+ T-cell responses when co-administered intradermally via gene gun with DNA encoding human papillomavirus type 16 (HPV-16) E7 linked to the sorting signal of the lysosome-associated membrane protein type 1 (LAMP-1). |
| 53 | 15153784 | We vaccinated C57BL/6 mice with pVITRO-SEL-Bcl-xL, pVITRO-SEL-mtBcl-xL, pVITRO-SEL, or pVITRO-SEL-caspase-3 intradermally via gene gun and intramuscularly via injection. |
| 54 | 15153784 | We demonstrated that vaccination with pVITRO achieved similar results to a co-administration strategy: that Bcl-xL enhanced the E7-specific CTL response and caspase-3 suppressed the E7-specific CTL response. |
| 55 | 15153784 | Thus, intradermal vaccination with a pVITRO vector combining an anti-apoptotic strategy (Bcl-xL) and an intracellular targeting strategy (SEL) further enhances the E7-specific CD8+ T-cell response and guarantees co-expression of both encoded molecules in transfected cells. |
| 56 | 15153784 | We have shown that DNA encoding the anti-apoptotic protein Bcl-xL enhances E7-specific CD8+ T-cell responses and DNA encoding pro-apoptotic protein caspase-3 suppresses E7-specific CD8+ T-cell responses when co-administered intradermally via gene gun with DNA encoding human papillomavirus type 16 (HPV-16) E7 linked to the sorting signal of the lysosome-associated membrane protein type 1 (LAMP-1). |
| 57 | 15153784 | We vaccinated C57BL/6 mice with pVITRO-SEL-Bcl-xL, pVITRO-SEL-mtBcl-xL, pVITRO-SEL, or pVITRO-SEL-caspase-3 intradermally via gene gun and intramuscularly via injection. |
| 58 | 15153784 | We demonstrated that vaccination with pVITRO achieved similar results to a co-administration strategy: that Bcl-xL enhanced the E7-specific CTL response and caspase-3 suppressed the E7-specific CTL response. |
| 59 | 15153784 | Thus, intradermal vaccination with a pVITRO vector combining an anti-apoptotic strategy (Bcl-xL) and an intracellular targeting strategy (SEL) further enhances the E7-specific CD8+ T-cell response and guarantees co-expression of both encoded molecules in transfected cells. |
| 60 | 15193412 | Immunization for the treatment of cancer requires an adjuvant, a source of tumor-associated antigen(s), for example apoptotic cancer cells, and a way to overcome the escape of tumor cells from the immune system, for example the up-regulation of Fas ligand (FasL) on the surface of cancer cells. |
| 61 | 15193412 | The results show that phosphodiester 5'G3AG23' and 5'G3TG23' oligonucleotides have a direct activity on a number of different cancer cells by inducing apoptosis (release of cytochrome C, activation of caspase-3, cleavage of poly [ADP-ribose] polymerase, degradation of nuclear mitotic apparatus protein and translocation of phophatidylserine at the cell surface). |
| 62 | 15585842 | To test whether tumor-reactive CD8(+) T cells specifically home to tumor, we assessed the trafficking of gp100-specific pmel-1 cells to large, vascularized tumors that express or do not express the target Ag. |
| 63 | 15585842 | Activation of tumor-specific CD8(+) pmel-1 T cells with IL-2 and vaccination with an altered peptide ligand caused regression of gp100-positive tumors (B16), but not gp100-negative tumors (methylcholanthrene 205), implanted on opposing flanks of the same mouse. |
| 64 | 15585842 | Most importantly, evidence for T cell function, as measured by production of IFN-gamma, release of perforin, and activation of caspase-3 in target cells, was confined to Ag-expressing tumor. |
| 65 | 15869795 | Cytochrome c was shown to leak from the mitochondria, followed by caspase 9 cleavage within 8 h of treatment. |
| 66 | 15869795 | In addition, poly(ADP-ribose) polymerase (PARP) was cleaved to form a 85 kDa fragment following maximal caspase 3 activation at 24 h. |
| 67 | 16907958 | We also found that CDV-Ond infection induced activation of caspase-3 and caspase-8. |
| 68 | 16907958 | In contrast, the expressions of Bcl-2 and Bax, regulators for intrinsic apoptotic signaling through the mitochondria, did not change. |
| 69 | 16907958 | These results suggest that CDV-Ond induced apoptosis by activating caspase-3, possibly through caspase-8 signaling rather than through p53/Bax-mediated, mitochondrial signaling in the infected cells. |
| 70 | 16907958 | We also found that CDV-Ond infection induced activation of caspase-3 and caspase-8. |
| 71 | 16907958 | In contrast, the expressions of Bcl-2 and Bax, regulators for intrinsic apoptotic signaling through the mitochondria, did not change. |
| 72 | 16907958 | These results suggest that CDV-Ond induced apoptosis by activating caspase-3, possibly through caspase-8 signaling rather than through p53/Bax-mediated, mitochondrial signaling in the infected cells. |
| 73 | 17188256 | Induction of primary anti-HIV CD4 and CD8 T cell responses by dendritic cells transduced with self-inactivating lentiviral vectors. |
| 74 | 17188256 | In this study, we demonstrate that a minimal self-inactivating (SIN) lentiviral vector (LV) that does not encode any human immunodeficiency virus (HIV) genes is able to induce HIV-specific CD4 and CD8 T cell responses after transduction of dendritic cells (DCs). |
| 75 | 17188256 | The LV-DC-primed T cells displayed HIV-specific lytic degranulation, as illustrated by acquisition of CD107a/b expression on the cell surface and up-regulation of active caspase 3. |
| 76 | 17188256 | These results demonstrate that DCs transduced with the minimal SIN-LV can efficiently induce HIV-specific CD4 and CD8 T cell responses. |
| 77 | 17202676 | Furthermore, the activated lymphocytes (CD8+) were capable of infiltrating into the tumor site, and much more apoptotic cells along with activation of caspase-3 were observed in the tumors from vaccinated-mice. |
| 78 | 17202676 | Also, high expression levels of human IFN-gamma, TNF-alpha, granzyme B and perforin were detected in the tumors from vaccinated-mice. |
| 79 | 17545626 | Furthermore, the tumors displayed significant morphologic changes and increased apoptosis, as shown by up-regulation of gene expression of the proapoptotic markers Fas, caspase-8, and caspase-3. |
| 80 | 17545626 | The residual tumor masses seen in the HC-Vacc/ACT-treated mice were infiltrated with CD4+ and CD8+ lymphocytes and showed elevated IFNgamma expression. |
| 81 | 17545626 | Moreover, splenic enlargement observed in HC-Vacc/ACT-treated mice reflected the increased functionality of T cells, as also indicated by increased expression of markers for CTL activation, differentiation, and proliferation (Cd28, Icosl, Tnfrsf13, and Tnfsf14). |
| 82 | 17570527 | HlyA oligomer-treated murine B-1a cells up-regulated TLR2 and involved the signaling molecules MyD88, TRAF6 and NF-kappaB. |
| 83 | 17570527 | Apoptosis was detected in majority of the monomer-treated cells that involved caspase-9 and caspase-3. |
| 84 | 17686866 | We evaluated the role of the three major UPR pathways, namely, inositol-requiring enzyme 1-dependent splicing of X box binding protein 1 (XBP1) mRNA, activation of activating transcription factor 6 (ATF6), and protein kinase R-like endoplasmic reticulum (ER) kinase-dependent eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation, in WNV-infected cells. |
| 85 | 17686866 | We further observed a transient phosphorylation of eIF2alpha and induction of the proapoptotic cyclic AMP response element-binding transcription factor homologous protein (CHOP). |
| 86 | 17686866 | WNV-infected cells exhibited a number of apoptotic phenotypes, such as (i) induction of growth arrest and DNA damage-inducible gene 34, (ii) activation of caspase-3, and (iii) cleavage of poly(ADP-ribose) polymerase. |
| 87 | 17698513 | Thimerosal-induced apoptosis in human SCM1 gastric cancer cells: activation of p38 MAP kinase and caspase-3 pathways without involvement of [Ca2+]i elevation. |
| 88 | 17698513 | Although immunoblotting data revealed that thimerosal could activate the phosphorylation of extracellular signal-regulated kinase, c-Jun NH2-terminal protein kinase, and p38 mitogen-activated protein kinase (p38 MAPK), only SB203580 (a p38 MAPK inhibitor) partially prevented cells from apoptosis. |
| 89 | 17698513 | The results suggest that in SCM1 cells, thimerosal caused Ca2+-independent apoptosis via phosphorylating p38 MAPK resulting in caspase-3 activation. |
| 90 | 17698513 | Thimerosal-induced apoptosis in human SCM1 gastric cancer cells: activation of p38 MAP kinase and caspase-3 pathways without involvement of [Ca2+]i elevation. |
| 91 | 17698513 | Although immunoblotting data revealed that thimerosal could activate the phosphorylation of extracellular signal-regulated kinase, c-Jun NH2-terminal protein kinase, and p38 mitogen-activated protein kinase (p38 MAPK), only SB203580 (a p38 MAPK inhibitor) partially prevented cells from apoptosis. |
| 92 | 17698513 | The results suggest that in SCM1 cells, thimerosal caused Ca2+-independent apoptosis via phosphorylating p38 MAPK resulting in caspase-3 activation. |
| 93 | 18242797 | Finally, in order to study the envelope glycoprotein effects on pathogenesis, we have used an in vitro model of co-culture of envelope-expressing cells as effectors and CD4+ T cells as targets. |
| 94 | 18242797 | The apoptotic pathway initiated by this interaction involves caspase-3-dependent mitochondrial depolarization and reactive oxygen species production, which depends on the phenotype of the envelope glycoprotein associated with the virus. |
| 95 | 18280621 | In an attempt to increase cross-presentation through apoptosis, the DNA-encoding caspase-2 prodomain followed by wild-type or catalytically inactive mutated caspase-3 was inserted into a plasmid encoding the 32 kDa mycolyl transferase (Ag85A) from Mycobacterium tuberculosis. |
| 96 | 18280621 | Vaccination with pro-apoptotic plasmids triggered more Ag85A specific IFN-gamma producing spleen cells, and more efficient IL-2 and IFN-gamma producing memory cells in spleen and lungs after M. tuberculosis challenge. |
| 97 | 18280621 | Compared to DNA-encoding secreted Ag85A, vaccination with DNA co-expressing wild-type caspase increased protection after infection with M. tuberculosis, while vaccination with plasmid co-expressing mutated caspase was not protective, possibly due to the stimulation of IL-6, IL-10 and IL-17A production. |
| 98 | 18516300 | The results show that during early onset of a T. brucei infection, spleen remodeling results in the rapid loss of the IgM(+) marginal zone (IgM(+)MZ) B cell population characterized as B220(+)IgM(High)IgD(Int) CD21(High)CD23(Low)CD1d(+)CD138(-). |
| 99 | 18516300 | Elevated caspase-3 mRNA levels coincided with decreased mRNA levels of the anti-apoptotic Bcl-2 protein and BAFF receptor (BAFF-R), indicating the onset of apoptosis. |
| 100 | 18579692 | We evaluated the adhesion of H. pylori by in situ immunofluorescence; epithelial barrier function by measurement of transepithelial resistance; apoptosis by measurement of caspase 3 activation; cell membrane leakage by measurement of lactate dehydrogenase release; and inflammation by measurement of interleukin-8 (IL-8), IL-10, prostaglandin E(2) (PGE(2)), and leukotriene B(4) (LTB(4)) release. |
| 101 | 19234198 | Fas ligand is required for the development of respiratory syncytial virus vaccine-enhanced disease. |
| 102 | 19234198 | Fas ligand (FasL) is a major immune effector molecule that can contribute to the clearance of respiratory viruses. |
| 103 | 19234198 | Furthermore, we show that CD4 T cells isolated after RSV challenge of vacvG-immunized gld mice exhibit enhanced expression of Annexin V and caspase 3/7 indicating that FasL is important for either the survival or the expansion of virus-specific secondary effector CD4 T cells. |
| 104 | 19234198 | Taken together, these data identify a previously undefined role for FasL in the accumulation of secondary effector CD4 T cells and the development of RSV vaccine-enhanced disease. |
| 105 | 20930069 | IL-6 in human cytomegalovirus secretome promotes angiogenesis and survival of endothelial cells through the stimulation of survivin. |
| 106 | 20930069 | Several cytokines were significantly induced in the HCMV secretomes including interleukin-6 (IL-6), granulocyte macrophage colony-stimulating factor, and IL-8/CXCL8. |
| 107 | 20930069 | In these cells, IL-6 prevented apoptosis by blocking caspase-3 and -7 activation through the induction of survivin. |
| 108 | 20930069 | Neutralization of IL-6 receptor on ECs abolished the ability of HCMV secretome to increase survivin expression and activated effector caspases. |
| 109 | 21225508 | They included: ischaemic degeneration of neurons and "dark" neurons in the prefrontal and temporal cortex, the hippocampus and the cerebellum, pathological changes of the blood vessels in the temporal cortex, diminished synaptophysin reaction in the hippocampus, atrophy of astroglia in the hippocampus and cerebellum, and positive caspase-3 reaction in Bergmann astroglia. |
| 110 | 21288491 | Since the activity of large yellow croaker caspase-9 (Lyccasp9) in the spleen and kidney also increased when the fish was stimulated with the poly(I:C) or bacterial vaccine [1], we therefore proposed that the intrinsic apoptotic pathway, which is initiated by caspase-9 and executed by caspase-3, was activated during the immune response induced by poly(I:C) or bacterial vaccine in large yellow croaker. |
| 111 | 21505013 | Active and inactive SLE individuals had more CD38 molecules/CD8+ T cells and more CD4+ T, CD8+ T and B cells in apoptosis (as assessed by caspase-3 expression) than the control group. |
| 112 | 21505013 | Patients with active SLE had a diminished CD28 expression on both CD4+ T and on CD8+ T cells and a higher CD86 expression on B cells than the control group. |
| 113 | 21525352 | NSCs were induced to differentiate in culture dishes coated with poly-l-lysine and mouse laminin in the presence of fibroblast growth factor 2 (FGF-2), nerve growth factor (NGF), brain-derived neurotropic factor (BDNF), dibutyryl cyclic AMP, and retinoic acid. |
| 114 | 21525352 | VZV induced apoptosis in fibroblasts, as shown by activation of caspase 3 and by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining, but not in neurons. |
| 115 | 22159511 | In a previous study, we constructed a recombinant caspase-3 expression vector under the 2'-5'-oligoadenylate synthetase gene (OAS) promoter (pGL3-OAS-re-caspase-3) and demonstrated that it is an effective gene therapy for HCV core-positive liver cells in vitro. |
| 116 | 22159511 | Tumor-bearing mice were treated with an intratumoral injection of pGL3-OAS-re-caspase-3. |
| 117 | 22159511 | The subcutaneous hepatoma in vivo mouse models stably expressing HCV core protein and co-expressing HCV core protein and pGL3-OAS-re-caspase-3 were established. |
| 118 | 22159511 | Double-label immunofluorescence staining showed that the percentage of co-expression of both HCV core and caspase-3 was 76 ± 6% in the group treated with pGL3-OAS-re-caspase-3. |
| 119 | 22159511 | There was a significant increase in the number of apoptotic cells in the group treated with the pGL3-OAS-re-caspase-3 system by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and transmission electron microscopy. |
| 120 | 22159511 | The results suggest that the pGL3-OAS-re-caspase-3 construct can effectively induce apoptosis in HCV core-positive hepatocytes in vivo. |
| 121 | 22159511 | The results presented strongly suggest that the transfer of pGL3-OAS-re-caspase-3 is an effective and promising gene therapy strategy for HCV infection. |
| 122 | 22159511 | In a previous study, we constructed a recombinant caspase-3 expression vector under the 2'-5'-oligoadenylate synthetase gene (OAS) promoter (pGL3-OAS-re-caspase-3) and demonstrated that it is an effective gene therapy for HCV core-positive liver cells in vitro. |
| 123 | 22159511 | Tumor-bearing mice were treated with an intratumoral injection of pGL3-OAS-re-caspase-3. |
| 124 | 22159511 | The subcutaneous hepatoma in vivo mouse models stably expressing HCV core protein and co-expressing HCV core protein and pGL3-OAS-re-caspase-3 were established. |
| 125 | 22159511 | Double-label immunofluorescence staining showed that the percentage of co-expression of both HCV core and caspase-3 was 76 ± 6% in the group treated with pGL3-OAS-re-caspase-3. |
| 126 | 22159511 | There was a significant increase in the number of apoptotic cells in the group treated with the pGL3-OAS-re-caspase-3 system by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and transmission electron microscopy. |
| 127 | 22159511 | The results suggest that the pGL3-OAS-re-caspase-3 construct can effectively induce apoptosis in HCV core-positive hepatocytes in vivo. |
| 128 | 22159511 | The results presented strongly suggest that the transfer of pGL3-OAS-re-caspase-3 is an effective and promising gene therapy strategy for HCV infection. |
| 129 | 22159511 | In a previous study, we constructed a recombinant caspase-3 expression vector under the 2'-5'-oligoadenylate synthetase gene (OAS) promoter (pGL3-OAS-re-caspase-3) and demonstrated that it is an effective gene therapy for HCV core-positive liver cells in vitro. |
| 130 | 22159511 | Tumor-bearing mice were treated with an intratumoral injection of pGL3-OAS-re-caspase-3. |
| 131 | 22159511 | The subcutaneous hepatoma in vivo mouse models stably expressing HCV core protein and co-expressing HCV core protein and pGL3-OAS-re-caspase-3 were established. |
| 132 | 22159511 | Double-label immunofluorescence staining showed that the percentage of co-expression of both HCV core and caspase-3 was 76 ± 6% in the group treated with pGL3-OAS-re-caspase-3. |
| 133 | 22159511 | There was a significant increase in the number of apoptotic cells in the group treated with the pGL3-OAS-re-caspase-3 system by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and transmission electron microscopy. |
| 134 | 22159511 | The results suggest that the pGL3-OAS-re-caspase-3 construct can effectively induce apoptosis in HCV core-positive hepatocytes in vivo. |
| 135 | 22159511 | The results presented strongly suggest that the transfer of pGL3-OAS-re-caspase-3 is an effective and promising gene therapy strategy for HCV infection. |
| 136 | 22159511 | In a previous study, we constructed a recombinant caspase-3 expression vector under the 2'-5'-oligoadenylate synthetase gene (OAS) promoter (pGL3-OAS-re-caspase-3) and demonstrated that it is an effective gene therapy for HCV core-positive liver cells in vitro. |
| 137 | 22159511 | Tumor-bearing mice were treated with an intratumoral injection of pGL3-OAS-re-caspase-3. |
| 138 | 22159511 | The subcutaneous hepatoma in vivo mouse models stably expressing HCV core protein and co-expressing HCV core protein and pGL3-OAS-re-caspase-3 were established. |
| 139 | 22159511 | Double-label immunofluorescence staining showed that the percentage of co-expression of both HCV core and caspase-3 was 76 ± 6% in the group treated with pGL3-OAS-re-caspase-3. |
| 140 | 22159511 | There was a significant increase in the number of apoptotic cells in the group treated with the pGL3-OAS-re-caspase-3 system by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and transmission electron microscopy. |
| 141 | 22159511 | The results suggest that the pGL3-OAS-re-caspase-3 construct can effectively induce apoptosis in HCV core-positive hepatocytes in vivo. |
| 142 | 22159511 | The results presented strongly suggest that the transfer of pGL3-OAS-re-caspase-3 is an effective and promising gene therapy strategy for HCV infection. |
| 143 | 22159511 | In a previous study, we constructed a recombinant caspase-3 expression vector under the 2'-5'-oligoadenylate synthetase gene (OAS) promoter (pGL3-OAS-re-caspase-3) and demonstrated that it is an effective gene therapy for HCV core-positive liver cells in vitro. |
| 144 | 22159511 | Tumor-bearing mice were treated with an intratumoral injection of pGL3-OAS-re-caspase-3. |
| 145 | 22159511 | The subcutaneous hepatoma in vivo mouse models stably expressing HCV core protein and co-expressing HCV core protein and pGL3-OAS-re-caspase-3 were established. |
| 146 | 22159511 | Double-label immunofluorescence staining showed that the percentage of co-expression of both HCV core and caspase-3 was 76 ± 6% in the group treated with pGL3-OAS-re-caspase-3. |
| 147 | 22159511 | There was a significant increase in the number of apoptotic cells in the group treated with the pGL3-OAS-re-caspase-3 system by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and transmission electron microscopy. |
| 148 | 22159511 | The results suggest that the pGL3-OAS-re-caspase-3 construct can effectively induce apoptosis in HCV core-positive hepatocytes in vivo. |
| 149 | 22159511 | The results presented strongly suggest that the transfer of pGL3-OAS-re-caspase-3 is an effective and promising gene therapy strategy for HCV infection. |
| 150 | 22159511 | In a previous study, we constructed a recombinant caspase-3 expression vector under the 2'-5'-oligoadenylate synthetase gene (OAS) promoter (pGL3-OAS-re-caspase-3) and demonstrated that it is an effective gene therapy for HCV core-positive liver cells in vitro. |
| 151 | 22159511 | Tumor-bearing mice were treated with an intratumoral injection of pGL3-OAS-re-caspase-3. |
| 152 | 22159511 | The subcutaneous hepatoma in vivo mouse models stably expressing HCV core protein and co-expressing HCV core protein and pGL3-OAS-re-caspase-3 were established. |
| 153 | 22159511 | Double-label immunofluorescence staining showed that the percentage of co-expression of both HCV core and caspase-3 was 76 ± 6% in the group treated with pGL3-OAS-re-caspase-3. |
| 154 | 22159511 | There was a significant increase in the number of apoptotic cells in the group treated with the pGL3-OAS-re-caspase-3 system by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and transmission electron microscopy. |
| 155 | 22159511 | The results suggest that the pGL3-OAS-re-caspase-3 construct can effectively induce apoptosis in HCV core-positive hepatocytes in vivo. |
| 156 | 22159511 | The results presented strongly suggest that the transfer of pGL3-OAS-re-caspase-3 is an effective and promising gene therapy strategy for HCV infection. |
| 157 | 22159511 | In a previous study, we constructed a recombinant caspase-3 expression vector under the 2'-5'-oligoadenylate synthetase gene (OAS) promoter (pGL3-OAS-re-caspase-3) and demonstrated that it is an effective gene therapy for HCV core-positive liver cells in vitro. |
| 158 | 22159511 | Tumor-bearing mice were treated with an intratumoral injection of pGL3-OAS-re-caspase-3. |
| 159 | 22159511 | The subcutaneous hepatoma in vivo mouse models stably expressing HCV core protein and co-expressing HCV core protein and pGL3-OAS-re-caspase-3 were established. |
| 160 | 22159511 | Double-label immunofluorescence staining showed that the percentage of co-expression of both HCV core and caspase-3 was 76 ± 6% in the group treated with pGL3-OAS-re-caspase-3. |
| 161 | 22159511 | There was a significant increase in the number of apoptotic cells in the group treated with the pGL3-OAS-re-caspase-3 system by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and transmission electron microscopy. |
| 162 | 22159511 | The results suggest that the pGL3-OAS-re-caspase-3 construct can effectively induce apoptosis in HCV core-positive hepatocytes in vivo. |
| 163 | 22159511 | The results presented strongly suggest that the transfer of pGL3-OAS-re-caspase-3 is an effective and promising gene therapy strategy for HCV infection. |
| 164 | 22249285 | We report that hepatitis B vaccine exposure resulted in significant upregulation of the key genes encoding caspase 7, caspase 9, Inhibitor caspase-activated DNase (ICAD), Rho-associated coiled-coil containing protein kinase 1 (ROCK-1), and Apoptotic protease activating factor 1 (Apaf-1). |
| 165 | 22249285 | Upregulation of cleaved caspase 3,7 were detected by western blot in addition to Apaf-1 and caspase 9 expressions argues that cell death takes place via the intrinsic apoptotic pathway in which release of cytochrome c from the mitochondria triggers the assembly of a caspase activation complex. |
| 166 | 22295090 | The induced anti-tumor activity was well correlated with FAS expression, caspase-3 activation, and cancer cell apoptosis. |
| 167 | 22361584 | We observed that the knockdown of essential autophagy-related genes (ATG3, ATG5, ATG7 and BECN1) abolishes the pre-apoptotic secretion of ATP by several human and murine cancer cell lines undergoing ICD. |
| 168 | 22361584 | Cancer cell lines stably depleted of ATG5 or ATG7 normally generate tumors in vivo, and such autophagy-deficient neoplasms, upon systemic treatment with ICD inducers, exhibit the same levels of apoptosis (as monitored by nuclear shrinkage and caspase-3 activation) and necrosis (as determined by following the kinetics of HMGB1 release) as their autophagy-proficient counterparts. |
| 169 | 22419388 | Induction of proapoptotic antibodies to triple-negative breast cancer by vaccination with TRAIL death receptor DR5 DNA. |
| 170 | 22419388 | TNF-related apoptosis-inducing ligand receptor 2 [TRAIL-R2 or death receptor 5 (DR5)] is expressed at elevated levels in a broad range of solid tumors to mediate apoptotic signals from TRAIL or agonist antibodies. |
| 171 | 22419388 | Apoptotic cell death induced by anti-DR5 antibody was shown by the cleavage of PARP and caspase-3. |
| 172 | 22473996 | We here demonstrate that M. bovis BCG triggers Toll-like receptor 2 (TLR2)-dependent microRNA-155 (miR-155) expression, which involves signaling cross talk among phosphatidylinositol 3-kinase (PI3K), protein kinase Cδ (PKCδ), and mitogen-activated protein kinases (MAPKs) and recruitment of NF-κB and c-ETS to miR-155 promoter. |
| 173 | 22473996 | Genetic and signaling perturbations presented the evidence that miR-155 regulates PKA signaling by directly targeting a negative regulator of PKA, protein kinase inhibitor alpha (PKI-α). |
| 174 | 22473996 | The miR-155-triggered activation of caspase-3, BAK1, and cytochrome c translocation involved signaling integration of MAPKs and epigenetic or posttranslational modification of histones or CREB. |
| 175 | 23028860 | Previously we have screened out Insulin-like Growth Factor Binding Protein 7 (IGFBP7) as a differentially expressed gene in post-implantation uterus versus pre-implantation uterus by suppressive subtractive hybridation. |
| 176 | 23028860 | After specific inhibition of IGFBP7, the T helper type 1 (Th1) cytokine IFNγ, was significantly elevated (p<0.05) and the Th2 cytokines IL-4 and IL-10, were reduced in uteri (p<0.05). |
| 177 | 23028860 | The expression of decidualization marker IGFBP1 and angiogenesis regulator VEGF were declined in uteri (p<0.05). |
| 178 | 23028860 | The expression of apoptosis-associated proteins, caspase3 and Bcl-2, were also declined (p<0.05). |
| 179 | 23294316 | Although anthocyanins induced apoptosis in some leukaemia cell lines, the level of caspase-3, caspase-8 and caspase-9 was significantly lower compared with imatinib and 6-MP. |
| 180 | 23353645 | Modulation of the NADPH oxidase activity by either the antibodies, the receptor agonist acetylcholine or the antagonist of the α7-type nicotinic acetylcholine receptors α-bungarotoxin was vital in inhibiting both amyloid-β induced ROS production, caspase 3 cleavage as well as cell death. |
| 181 | 23449791 | To address this, we performed cross-sectional and longitudinal analysis of proapoptotic (cleaved caspase-3) and antiapoptotic (Bcl-2) markers of cytomegalovirus (CMV) and HIV-specific CD8 T cells in a cohort of HIV-infected subjects with various degrees of viral control on and off ART. |
| 182 | 23529623 | Importance of PdpC, IglC, IglI, and IglG for modulation of a host cell death pathway induced by Francisella tularensis. |
| 183 | 23529623 | To better understand the prerequisites of this cell death, macrophages were infected with the F. tularensis live vaccine strain (LVS), and the effects were compared to those resulting from infections with deletion mutants lacking expression of either of the pdpC, iglC, iglG, or iglI genes, which encode components of the Francisella pathogenicity island (FPI), a type VI secretion system. |
| 184 | 23529623 | Within 12 h, a majority of the J774 cells infected with the LVS strain showed production of mitochondrial superoxide and, after 24 h, marked signs of mitochondrial damage, caspase-9 and caspase-3 activation, phosphatidylserine expression, nucleosome formation, and membrane leakage. |
| 185 | 23536633 | This was associated with higher rates of apoptosis in precursor cells and increased expression of cleaved caspase-3 and BCL-xL and downregulation of cyclin B1. |
| 186 | 23536633 | Further, blockade of fatty-acid synthesis decreased DC expression of MHC class II, ICAM-1, B7-1, and B7-2 but increased their production of selected proinflammatory cytokines including IL-12 and MCP-1. |
| 187 | 23536633 | Accordingly, inhibition of fatty-acid synthesis enhanced DC capacity to activate allogeneic as well as Ag-restricted CD4(+) and CD8(+) T cells and induce CTL responses. |
| 188 | 23536633 | We found that inhibition of fatty-acid synthesis resulted in elevated expression of numerous markers of ER stress in humans and mice and was associated with increased MAPK and Akt signaling. |
| 189 | 23949283 | Improved cytotoxic T-lymphocyte immune responses to a tumor antigen by vaccines co-expressing the SLAM-associated adaptor EAT-2. |
| 190 | 23949283 | Also, an increase in MC-38 tumor cell apoptosis (as measured by hematoxylin and eosin staining, active caspase-3 and granzyme B levels within the tumors) was observed. |
| 191 | 23964513 | Here we investigated an effect of affinity purified antibodies to synthetic fragment 95-123 of the prion protein on beta-amyloid induced cell death, Ca(2+)-signal, reactive oxygen species production and caspase 3 activation. |
| 192 | 23964513 | However, the antibodies significantly reduced Abeta induced reactive oxygen species production in astrocytes and decreased caspase 3 activation in neurons and astrocytes. |
| 193 | 23964513 | Here we investigated an effect of affinity purified antibodies to synthetic fragment 95-123 of the prion protein on beta-amyloid induced cell death, Ca(2+)-signal, reactive oxygen species production and caspase 3 activation. |
| 194 | 23964513 | However, the antibodies significantly reduced Abeta induced reactive oxygen species production in astrocytes and decreased caspase 3 activation in neurons and astrocytes. |
| 195 | 24350060 | Previously we demonstrated that live attenuated cattle vaccine strain Brucella abortus RB51 induces caspase-2-mediated and caspase-1-independent PCD of infected macrophages. |
| 196 | 24350060 | We also discovered that rough attenuated B. suis strain VTRS1 induces a caspase-2-mediated and caspase-1-independent proinflammatory cell death in infected macrophages, which was tentatively coined "caspase-2-mediated pyroptosis". |
| 197 | 24350060 | Caspase-2 regulated mitochondrial cytochrome c release and TNFα production, both of which are known to activate caspase-3 and caspase-8, respectively. |
| 198 | 24350060 | In addition to TNFα, RB51-induced caspase-1 and IL-1β production was also driven by caspase-2-mediated mitochondrial dysfunction. |
| 199 | 24350060 | Our data suggest that caspase-2 acts as an initiator caspase that mediates a novel RB51-induced hybrid cell death that simulates but differs from typical non-proinflammatory apoptosis and caspase-1-mediated proinflammatory pyroptosis. |
| 200 | 24350060 | Caspase-2 also regulated caspase-3 and -8 activation, as well as cell death in macrophages treated with each of the three reagents. |
| 201 | 24350060 | Previously we demonstrated that live attenuated cattle vaccine strain Brucella abortus RB51 induces caspase-2-mediated and caspase-1-independent PCD of infected macrophages. |
| 202 | 24350060 | We also discovered that rough attenuated B. suis strain VTRS1 induces a caspase-2-mediated and caspase-1-independent proinflammatory cell death in infected macrophages, which was tentatively coined "caspase-2-mediated pyroptosis". |
| 203 | 24350060 | Caspase-2 regulated mitochondrial cytochrome c release and TNFα production, both of which are known to activate caspase-3 and caspase-8, respectively. |
| 204 | 24350060 | In addition to TNFα, RB51-induced caspase-1 and IL-1β production was also driven by caspase-2-mediated mitochondrial dysfunction. |
| 205 | 24350060 | Our data suggest that caspase-2 acts as an initiator caspase that mediates a novel RB51-induced hybrid cell death that simulates but differs from typical non-proinflammatory apoptosis and caspase-1-mediated proinflammatory pyroptosis. |
| 206 | 24350060 | Caspase-2 also regulated caspase-3 and -8 activation, as well as cell death in macrophages treated with each of the three reagents. |
| 207 | 24690681 | We report that ex-vivo exposure of quiescent or TCR-activated primary human T cells to thimerosal induced a dose-dependent apoptotic cell death associated with depolarization of mitochondrial membrane, generation of reactive oxygen species, cytochrome c release from the mitochondria and caspase-3 activation. |
| 208 | 24690681 | Moreover, exposure to non-toxic concentrations of thimerosal induced cell cycle arrest in G0/G1 phase of TCR-activated T cells, and inhibition of the release of proinflammatory cytokines such as IFN gamma, IL-1 beta, TNF alpha, IL-2, as well as the chemokine MCP1. |
| 209 | 24732116 | A novel berbamine derivative inhibits cell viability and induces apoptosis in cancer stem-like cells of human glioblastoma, via up-regulation of miRNA-4284 and JNK/AP-1 signaling. |
| 210 | 24732116 | Induction of apoptosis in these CSCs is dependent upon activation of caspase-3 and cleavage of poly (ADP-ribose) polymerase (PARP). |
| 211 | 24732116 | BBMD3 also increased phosphorylation of the c-Jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK), resulting in an increase expression of phosphorylated c-Jun and total c-Fos; the major components of transcriptional factor AP-1. |
| 212 | 24732116 | The JNK-c-Jun/AP-1 signaling pathway plays an important role in the induction of apoptosis in response to UV irradiation and some drug treatments. |
| 213 | 24738081 | LQ strikingly reduced cell viability, enhanced apoptotic rate, induced lactate dehydrogenase over-release, and increased intracellular reactive oxygen species (ROS) level and caspase 3 activity in both PLC/PRL/5 and HepG2 cells. |
| 214 | 24738081 | LQ treatment resulted in a reduction of the expressions of B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma-extra large (Bcl-xL), and an increase of the phosphorylation of c-Jun N-terminal kinases (JNK) and P38. |
| 215 | 24738081 | LQ-mediated cell viability reduction, mitochondrial dysfunction, apoptosis related protein abnormal expressions, and JNK and P38 activation were partially abolished by N-Acetyl-L-cysteine (a ROS inhibitor) pretreatment. |
| 216 | 24738081 | This antitumor activity was further confirmed in PLC/PRL/5-xenografted mice model. |
| 217 | 24794706 | Loss of Lkb1 and Pten leads to lung squamous cell carcinoma with elevated PD-L1 expression. |
| 218 | 24794706 | We demonstrate that biallelic inactivation of Lkb1 and Pten in the mouse lung leads to SCC that recapitulates the histology, gene expression, and microenvironment found in human disease. |
| 219 | 24794706 | Lkb1;Pten null (LP) tumors expressed the squamous markers KRT5, p63 and SOX2, and transcriptionally resembled the basal subtype of human SCC. |
| 220 | 24794706 | SCA1(+)NGFR(+) fractions were enriched for tumor-propagating cells (TPCs) that could serially transplant the disease in orthotopic assays. |
| 221 | 25201410 | CRM197 is a naturally nontoxic diphtheria toxin mutant that binds and inhibits heparin-binding epidermal growth factor-like growth factor. |
| 222 | 25201410 | Activation of cleaved caspase-3, 8, and 9, activity of matrix metalloproteinase-2/9 (MMP-2/9), and expression of phosphorylated Akt (p-Akt) were also checked. |
| 223 | 25201410 | The activation of cleaved caspase-3, 8, 9 was promoted, activity of MMP-2 and MMP-9 and expression of p-Akt were inhibited significantly by the treatment of CRM197 and shRNA-VCAM-1 alone or in combination, indicating that the combination of CRM197 with shRNA-VCAM-1 additively inhibited the malignant behavior of human glioblastoma cells via activating caspase-3, 8, 9 as well as inhibiting MMP-2, MMP-9, and Akt pathway. |
| 224 | 25201410 | CRM197 is a naturally nontoxic diphtheria toxin mutant that binds and inhibits heparin-binding epidermal growth factor-like growth factor. |
| 225 | 25201410 | Activation of cleaved caspase-3, 8, and 9, activity of matrix metalloproteinase-2/9 (MMP-2/9), and expression of phosphorylated Akt (p-Akt) were also checked. |
| 226 | 25201410 | The activation of cleaved caspase-3, 8, 9 was promoted, activity of MMP-2 and MMP-9 and expression of p-Akt were inhibited significantly by the treatment of CRM197 and shRNA-VCAM-1 alone or in combination, indicating that the combination of CRM197 with shRNA-VCAM-1 additively inhibited the malignant behavior of human glioblastoma cells via activating caspase-3, 8, 9 as well as inhibiting MMP-2, MMP-9, and Akt pathway. |
| 227 | 25368912 | Further studies showed that apoptosis was associated with increases in caspase 3 and cleaved Poly (ADP-ribose) polymerase, and activation of the p53 signaling pathway. |
| 228 | 25482339 | For protein-based vaccines, the main biological barrier to overcome is the default MHC class-II-pathway, with activation of CD4 T cells rather than CD8 T cells. |
| 229 | 25482339 | The latter requires antigens to access the cytosol and MHC class I antigen presentation. |
| 230 | 25482339 | This "photochemical internalisation" resulted in activation, proliferation, and IFN-γ production of cytotoxic CD8 T cells, which suppressed tumour growth by infiltrating CD8 T cells and caspase-3-dependent apoptosis. |
| 231 | 25482339 | The process was independent of MHC class II, MyD88, and TLR4 signalling, but dependent on trypsin- and caspase-like proteasome activity and partly also on chloroquine. |
| 232 | 25546504 | We have successfully isolated the stem cell antigen (Sca)-1(+) CD45(-) CD31(-) cells which were proposed to be LR-MSCs by magnetic-activated cell sorting (MACS). |
| 233 | 25550785 | Overexpression of GRIM-19, a mitochondrial respiratory chain complex I protein, suppresses hepatocellular carcinoma growth. |
| 234 | 25550785 | AKT1, pAKT1, cyclinD1, CDK4, PCNA, Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3, and cytochrome C were detected by Western blot and immunofluorescence. |
| 235 | 25550785 | We also found that AKT1 expression and phosphorylation were regulated by the expression of GRIM-19. |
| 236 | 25550785 | Collectively, our study demonstrated that GRIM-19 overexpression suppressed HCC growth and downregulated AKT1 expression, suggesting that GRIM-19 might play a crucial role in hepatocarcinogenesis through negatively regulating the PI3K/AKT signaling pathway. |
| 237 | 25633898 | Finally, we discovered the over-expression of GRP78, ATF4, ATF6, PERK, eIF2α, CHOP, and cytochrome c (Cyt-c) but not IRE1, xbp-1, and caspase-3 in B.suis.S2 (HK)-attacked and B.suis.S2-infected cells, suggesting that the molecular mechanism of ER stress sensor activation by B.suis.S2 is basically concomitant with that by B.suis.S2 (HK) and that ER stress, especially the PERK pathway, plays an important role in the process of B.suis.S2 infecting EEC, which may, in part, explain the role of the uterus in the pathogenesis of B.suis.S2. |
| 238 | 25793397 | Although the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway is one of the targets of NS1, the MFPTr virus suppressed the phosphorylation of Akt when compared with the wild-type (WT) virus. |
| 239 | 25793397 | It was suggested that this might lead to the subsequent inhibition of the cleavage of PARP-1 and caspase-3, which is important for the progression of apoptosis. |
| 240 | 26101550 | The mechanism of action is shown to be related to the buildup of abasic sites that cause PARP activation and PARP cleavage, and the activation of caspase-3 and caspase-7, which is consistent with cell death by apoptosis. |
| 241 | 26132569 | Treatment of the human SW480 cancer cells with Echinacoside resulted in marked apoptosis and cell cycle arrest, together with a significant increase in active caspase 3 and cleaved PARP, and upregulation of the G1/S-CDK blocker CDKN1B (p21). |
| 242 | 26225923 | Interleukin-24 (IL-24), a member of the IL-10 cytokine gene family, causes growth suppression and apoptosis in various solid tumor cells. |
| 243 | 26225923 | In addition, IL-24 expression could significantly induce apoptosis of the THP-1 cells. |
| 244 | 26225923 | Ad.RGD-IL-24 had a potent effect on the up-regulation of the expression of GRP78/Bip, GADD34 and Bax, down-regulation of the expression of Bcl-2 and Mcl-1, and induced the activation of Caspase-3, which may be responsible for its apoptosis-inducing effect on THP-1 cells. |
| 245 | 26303768 | Human CD8(+) T lymphocytes infiltrated the tumor sites, and high levels of human IFN-γ, TNF-α, and caspase-3 were also detected in the tumors from G22-I50-vaccinated and -treated mice. |
| 246 | 26367324 | Interleukin-24 inhibits influenza A virus replication in vitro through induction of toll-like receptor 3 dependent apoptosis. |
| 247 | 26367324 | Recently, we have shown that interleukin-24 (IL-24) sensitizes tumor cells to toll-like receptor 3 (TLR3) mediated apoptosis. |
| 248 | 26367324 | As influenza A virus stimulates the TLR3 receptor, we hypothesized that IL-24 might also exert an anti-viral effect. |
| 249 | 26367324 | The anti-viral effect of IL-24 correlated with caspase-3 activation and could be blocked by a pan-caspase inhibitor and by small interfering RNA (siRNA) directed towards TLR3. |
| 250 | 26367324 | Surprisingly, caspase-3 activation in influenza A virus/IL-24-stimulated cells correlated with the down-regulation of the B-cell lymphoma 2 (Bcl-2) family member myeloid cell leukemia 1 (Mcl-1). |
| 251 | 26367324 | We conclude that IL-24 exerts an anti-viral role selectively purging virally infected cells by leading to a down-regulation of Mcl-1. |
| 252 | 26367324 | Interleukin-24 inhibits influenza A virus replication in vitro through induction of toll-like receptor 3 dependent apoptosis. |
| 253 | 26367324 | Recently, we have shown that interleukin-24 (IL-24) sensitizes tumor cells to toll-like receptor 3 (TLR3) mediated apoptosis. |
| 254 | 26367324 | As influenza A virus stimulates the TLR3 receptor, we hypothesized that IL-24 might also exert an anti-viral effect. |
| 255 | 26367324 | The anti-viral effect of IL-24 correlated with caspase-3 activation and could be blocked by a pan-caspase inhibitor and by small interfering RNA (siRNA) directed towards TLR3. |
| 256 | 26367324 | Surprisingly, caspase-3 activation in influenza A virus/IL-24-stimulated cells correlated with the down-regulation of the B-cell lymphoma 2 (Bcl-2) family member myeloid cell leukemia 1 (Mcl-1). |
| 257 | 26367324 | We conclude that IL-24 exerts an anti-viral role selectively purging virally infected cells by leading to a down-regulation of Mcl-1. |