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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 | 35295738 | The 36 core targets in the PPI network were clustered in the phosphatidylinositol 3 kinase-RAC serine/threonine-protein kinase (PI3K-AKT) and nuclear factor kappa-B (NF-κB) signaling pathways. |
| 2 | 34626587 | FOXM1-activated SIRT4 inhibits NF-κB signaling and NLRP3 inflammasome to alleviate kidney injury and podocyte pyroptosis in diabetic nephropathy. |
| 3 | 34626587 | FOXM1 overexpression improved kidney function and reduced pathological changes in mice, and it increased the expression of the podocyte marker Nephrin in kidney tissues. |
| 4 | 34626587 | In vitro, FOXM1 increased viability and reduced pyroptosis of the HG-treated MPC5 cells, and it elevated the expression of the podocyte marker Nephrin whereas reduced the expression of pyroptosis-related NLRP3 inflammasome and cleaved caspase 1. |
| 5 | 34626587 | FOXM1 bound to the promoter of sirtuin 4 (SIRT4) to induce transcriptional activation. |
| 6 | 34626587 | Downregulation of SIRT4 blocked the protective roles of FOXM1 both in vivo and in vitro. |
| 7 | 34626587 | Phosphorylation of nuclear factor-kappa B (NF-κB) in HG-treated cells was suppressed by FOXM1 but restored after SIRT4 inhibition. |
| 8 | 34626587 | In conclusion, this study suggested that FOXM1 transcriptionally activates SIRT4 and inhibits NF-κB signaling and the NLRP3 inflammasome to alleviate kidney injury and podocyte pyroptosis in DN. |
| 9 | 33263178 | The 24-h urinary albumin was determined each week, renal pathological changes were observed, and expression of ANGPTL2 and nuclear factor-kappa B (NF-κB) in rat renal tissue was assessed by immunohistochemistry. |
| 10 | 33263178 | The mRNA levels of ANGPTL2 and monocyte chemotactic protein 1 (MCP-1) were assessed by real-time polymerase chain reaction. |
| 11 | 33263178 | In podocytes cultured in elevated glucose, ANGPTL2 and phosphorylated IκB-α were overexpressed at the protein level, and ANGPTL2 and MCP-1 were highly expressed at the mRNA level. |
| 12 | 33263178 | Irbesartan down-regulated ANGPTL2 and phosphorylated IκB-αexpression at the protein level and inhibited ANGPTL2 and MCP-1 expression at the mRNA level. |
| 13 | 32993539 | A case of minimal change disease after the administration of anti receptor activator of nuclear factor kappa B ligand (RANKL) monoclonal antibody: a case report. |
| 14 | 32664235 | Tacrolimus Prevents TWEAK-Induced PLA2R Expression in Cultured Human Podocytes. |
| 15 | 32664235 | Tacrolimus Prevents TWEAK-Induced PLA2R Expression in Cultured Human Podocytes. |
| 16 | 32664235 | Primary membranous nephropathy is usually caused by antibodies against the podocyte antigen membrane M-type phospholipase A2 receptor (PLA2R). |
| 17 | 32664235 | Primary membranous nephropathy is usually caused by antibodies against the podocyte antigen membrane M-type phospholipase A2 receptor (PLA2R). |
| 18 | 32664235 | We have now identified key TNF receptor superfamily members in podocytes and explored the regulation of PLA2R expression and the impact of tacrolimus. |
| 19 | 32664235 | We have now identified key TNF receptor superfamily members in podocytes and explored the regulation of PLA2R expression and the impact of tacrolimus. |
| 20 | 32664235 | Data mining of single cell transcriptomics and glomerular transcriptomics data identified TNFRSF12a/Fn14 as the highest expressed TNF receptor superfamily gene in human membranous nephropathy, and this was confirmed by immunohistochemistry that also identified NFκB activation in membranous nephropathy podocytes. |
| 21 | 32664235 | Data mining of single cell transcriptomics and glomerular transcriptomics data identified TNFRSF12a/Fn14 as the highest expressed TNF receptor superfamily gene in human membranous nephropathy, and this was confirmed by immunohistochemistry that also identified NFκB activation in membranous nephropathy podocytes. |
| 22 | 32664235 | Furthermore, in cultured human podocytes, TWEAK increased the expression of PLA2R as well as the expression of other genes recently identified by GWAS as linked to membranous nephropathy: NFKB1 and IRF4. |
| 23 | 32664235 | Furthermore, in cultured human podocytes, TWEAK increased the expression of PLA2R as well as the expression of other genes recently identified by GWAS as linked to membranous nephropathy: NFKB1 and IRF4. |
| 24 | 32664235 | Interestingly, IRF4 encodes the FK506-binding protein 52 (FKBP52), a protein associated with tacrolimus. |
| 25 | 32664235 | Interestingly, IRF4 encodes the FK506-binding protein 52 (FKBP52), a protein associated with tacrolimus. |
| 26 | 32664235 | Tacrolimus prevented the increased expression of PLA2R, NFKB1 and IRF4 induced by TWEAK in cultured podocytes. |
| 27 | 32664235 | Tacrolimus prevented the increased expression of PLA2R, NFKB1 and IRF4 induced by TWEAK in cultured podocytes. |
| 28 | 31727625 | Using luciferase reporter assays, we did not observe activation of the NOTCH4 promoter with the HIV protein Nef in podocytes. |
| 29 | 31727625 | Further, we observed upregulated expression of a gamma secretase complex protein, presenilin 1, but not Notch4, in podocytes infected with an HIV-1 expression construct. |
| 30 | 31727625 | Consistent with the diminished inflammation, kidneys from Notch4d1/Tg26+ mice also showed a significant decrease in expression of the inflammatory cytokine transcripts Il-6 and Ccl2, as well as the master inflammatory transcription factor NF-κB (Nfkb1 transcripts and p65 protein). |
| 31 | 31399972 | Aldosterone acts on renal vessels, renal cells (glomerular mesangial cells, podocytes, vascular smooth muscle cells, tubular epithelial cells, and interstitial fibroblasts), and infiltrating inflammatory cells, inducing reactive oxygen species (ROS) production, upregulated epithelial growth factor receptor (EGFR), and type 1 angiotensin (AT1) receptor expressions, and activating nuclear factor kappa B (NF-κB), activator protein-1 (AP-1), and EGFR to further promote cell proliferation, apoptosis, and proliferation. |
| 32 | 31399972 | Phenotypic transformation of epithelial cells stimulates the expression of transforming growth factor-β (TGF-β), connective tissue growth factor (CTGF), osteopontin (OPN), and plasminogen activator inhibitor-1 (PAI-1), eventually leading to renal fibrosis. |
| 33 | 31281825 | This study is aimed at exploring the mechanism by which the -254C>G single nucleotide polymorphism (SNP) on the transient receptor potential cation channel 6 (TRPC6) gene promoter could increase its activation in steroid-resistant nephrotic syndrome children of China. |
| 34 | 31281825 | We further predicted and verified that this variation was mediated by the nuclear factor kappa B (NF-κB) subunit RELA, and TNF-α significantly enhanced the transcription activity of TRPC6 with the -254G allele. |
| 35 | 30805933 | A20 overexpression exerts protective effects on podocyte injury in lupus nephritis by downregulating UCH-L1. |
| 36 | 30805933 | The study aims to explore the effect of A20 on LN in relation to the nuclear factor-kappa B (NF-κB) signaling pathway. |
| 37 | 30805933 | Next, A20, UCH-L1, and NF-κB expression in LN patients and MRL/lpr mice was determined. |
| 38 | 30805933 | A20 was downregulated, whereas UCH-L1 was upregulated in LN. |
| 39 | 30805933 | Overexpressed A20 declined NF-κB, UCH-L1 expression, and the extent of p65 phosphorylation. |
| 40 | 30805933 | A20 overexpression or UCH-L1 inhibition increased expression of synaptoporin and nephrin but decreased desmin expression and ubiquitin accumulation level in podocytes. |
| 41 | 30805933 | Moreover, A20 overexpression or UCH-L1 inhibition increased the podocyte number but decreased protein level of cleaved caspase-3, podocyte lesion improvement, decreased foot process width, glomerulus basement membrane, and foot process fusion rate. |
| 42 | 30805933 | In addition, urine protein, blood urea nitrogen, serum creatinine, and ds-DNA antibody levels decreased with elevated A20 or depleted UCH-L1. |
| 43 | 30805933 | Collectively, it could be concluded that A20 protects against podocyte injury in LN via UCH-L1 by inactivating the NF-κB signaling pathway. |
| 44 | 30716432 | Poricoic acid A enhances melatonin inhibition of AKI-to-CKD transition by regulating Gas6/AxlNFκB/Nrf2 axis. |
| 45 | 30716432 | Our results further showed that treatment with melatonin and PAA ameliorated renal fibrosis and podocyte injury by attenuating oxidative stress and inflammation via regulation of nuclear factor-kappa B (NF-κB) and nuclear factor-erythroid-2-related factor 2 (Nrf2) pathways in IRI rats. |
| 46 | 30716432 | Melatonin and PAA protected against AKI-to-CKD transition by regulating growth arrest-specific 6 (Gas6)/AxlNFκB/Nrf2 signaling cascade. |
| 47 | 30716432 | Melatonin and PAA initiallyupregulated Gas6/Axl signaling to reduce oxidative stress and inflammation in AKI and subsequently downregulated Gas6/Axl signaling to attenuate renal fibrosis and progression to CKD. |
| 48 | 30716432 | Poricoic acid A enhances melatonin-mediated inhibition of AKI-to-CKD transition by the regulating Gas6/AxlNFκB/Nrf2 signaling cascade. |
| 49 | 29218112 | Consistently, Triptolide also prevented TGF-β-induced signaling activation of MAPK p38, NFkB (p65) and calcineurin/NFATC3, which are known to be downstream mediators of podocyte injury. |
| 50 | 29207635 | SOCS2 overexpression alleviates diabetic nephropathy in rats by inhibiting the TLR4/NF-κB pathway. |
| 51 | 29207635 | Western blot was carried out to determine the expressions of SOCS2, Toll-like receptors 4 (TLR4) and nuclear factor kappa B (NF-κB) pathway-related proteins in DN patients, streptozotocin (STZ)-induced DN rats and high glucose (HG)-stimulated podocytes. |
| 52 | 29207635 | The effects of SOCS2 overexpression on renal injury, the inflammatory cytokines production, renal pathological changes, apoptosis and the TLR4/NF-κB pathway in DN rats or HG-stimulated podocytes were investigated. |
| 53 | 29207635 | TLR4 antagonist TAK-242 and NF-κB inhibitor PDTC were used to confirm the functional mechanism of SOCS2 overexpression in HG-stimulated podocytes. |
| 54 | 29207635 | SOCS2 was down-regulated, while TLR4 and NF-κB were up-regulated in renal tissues of DN patients and DN rats. |
| 55 | 29207635 | Ad-SOCS2 infection alleviated STZ-induced renal injury and pathological changes and inhibited STZ-induced IL-6, IL-1β and MCP-1 generation and activation of the TLR4/NF-κB pathway in DN rats. |
| 56 | 29207635 | SOCS2 overexpression attenuated apoptosis, suppressed the inflammatory cytokines expression, and inactivated the TLR4/NF-κB pathway in HG-stimulated podocytes. |
| 57 | 29207635 | Suppression of the TLR4/NF-κB pathway enhanced the inhibitory effect of SOCS2 overexpression on apoptosis and inflammatory cytokines expressions in HG-stimulated podocytes. |
| 58 | 29207635 | SOCS2 overexpression alleviated the development of DN by inhibiting the TLR4/NF-κB pathway, contributing to developing new therapeutic strategies against DN. |
| 59 | 29179438 | Upon stimulation with lipopolysaccharide (LPS), a prototypical pathogen-associated molecular pattern, podocytes demonstrated de novo expression of a variety of NFkB-dependent immune molecules that are pivotal for immune response, including major histocompatibility complex (MHC) class II, costimulatory molecule CD80, lysosomal protease cathepsin L as well as CC chemokine ligand 2 and 5, ultimately resulting in podocyte dysfunction, characterized by cellular shrinkage, a spindle-like or asterlike cell shape and impairment of actin cytoskeleton integrity. |
| 60 | 28318634 | The expression of DNA methyltransferase 1 (Dnmt1), nuclear factor Sp1, and nuclear factor kappa B (NFκB)-p65 markedly increased in podocytes in vivo and in vitro under the diabetic state. |
| 61 | 28318634 | Further studies found that increased Sp1 and NFκB-p65 interacted in the nucleus of podocytes incubated with high glucose, and Sp1 bound to the Dnmt1 promoter region. |
| 62 | 28318634 | The involvement of the Sp1/NFκB-p65 complex in Dnmt1 regulation was confirmed by the observation that Sp1 knockdown using mithramycin A or siRNA decreased Dnmt1 protein levels. |
| 63 | 28318634 | The luciferase reporter assay further indicated that Dnmt1 was a direct target of Sp1. |
| 64 | 28211114 | The old rats exhibited a dysregulation of the expression of proteins related to oxidative stress and inflammation in the kidneys, and MLB administration significantly reduced the protein expression of major subunits of nicotinamide adenine dinucleotide phosphate oxidase (Nox4 and p22phox ), phospho-p38, nuclear factor-kappa B p65, cyclooxygenase-2, and inducible nitric oxide synthase. |
| 65 | 28211114 | In addition, MLB-treated old rats showed lower levels of senescence-related proteins such as p16, ADP-ribosylation factor 6, p53, and p21 through effects on the mitogen-activated protein kinase pathway. |
| 66 | 28115850 | Gold-quercetin nanoparticles prevent metabolic endotoxemia-induced kidney injury by regulating TLR4/NF-κB signaling and Nrf2 pathway in high fat diet fed mice. |
| 67 | 28115850 | Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) and oxidative stress-related Nrf2/Keap1 were regarded as the key target points involved in metabolic inflammation and kidney injury. |
| 68 | 28115850 | However, the molecular mechanism of interaction between TLR4/NF-κB and Nrf2 activation in high-fat diet-induced renal injury is not absolutely understood. |
| 69 | 28115850 | For this study, C57BL/6 mice fed fat-rich fodder were used as the metabolic syndrome model to evaluate the protective effects of GQ on kidney injury and to determine whether TLR4/NF-κB and Nrf2 pathways were associated with the process. |
| 70 | 28115850 | TLR4/NF-κB and Nrf2 pathways were upregulated with high-fat diet intake in mice, resulting in reduction of superoxide dismutase activity and increase in superoxide radical, H2O2, malondialdehyde, XO, XDH, and XO/XDH ratio. |
| 71 | 28115850 | Also, it may prevent kidney injury by inhibition of TLR4/NF-κB and oxidative stress, further increasing superoxide dismutase activity. |
| 72 | 28005239 | In cultured podocytes, CSZ suppressed LPS-induced activation of nuclear factor-kappa B (NF-κB) and phosphorylation of p44/42 mitogen-activated protein kinase (MAPK). |
| 73 | 27273997 | In MCD mouse model and human kidney tissues, the expressions of podocyte slit membrane protein-nephrin and podocin, skeleton protein-synaptopodin are decreased, and the expression of synaptopodin is correlated with the response to hormone therapy. |
| 74 | 27273997 | In addition, newest studies focused on another two potocyte associated proteins, CD80 and Angiopoietin-like-4. |
| 75 | 27273997 | Angiopoietin-like-4 can be expressed in normal potocytes, but over-expression of angiopoietin-like-4 may injure the GBM charge barrier and induce the foot process fusion, leading to MCD. |
| 76 | 27273997 | However, further studies on the factors inducing CD80 and Angiopoietin-like-4 expression, and the interaction between glomerular basement membrane and the two proteins are needed. |
| 77 | 27273997 | Based on the mechanism of MCD, NF-kappa B inhibitors and sialylation therapy would be a novel non-immune therapy for MCD. |
| 78 | 26934958 | Since TLR9 activates p38 MAPK and NFkB that are known to mediate podocyte apoptosis, we hypothesized that TLR9 induces podocyte apoptosis in glomerular diseases. |
| 79 | 26934958 | Prevention of TLR9 upregulation by siRNA significantly attenuated NFκB p65 or p38 activity and apoptosis, demonstrating that TLR9 mediates podocyte apoptosis. |
| 80 | 26934958 | We next showed that endogenous mitochondrial DNA (mtDNA), whose CpG motifs are also unmethylated, is the ligand for TLR9, because PAN induced mtDNA accumulation in endolysosomes where TLR9 is localized, overexpression of endolysosomal DNase 2 attenuated PAN-induced p38 or p65 activity and podocyte apoptosis, and DNase 2 silencing was sufficient to activate p38 or p65 and induce apoptosis. |
| 81 | 26550927 | CML treatment induced both NF-kB and Zeb2 promoter activity and suppressed E-cadherin promoter activity. |
| 82 | 26347890 | Tripterygium Glycosides Tablet Ameliorates Renal Tubulointerstitial Fibrosis via the Toll-Like Receptor 4/Nuclear Factor Kappa B Signaling Pathway in High-Fat Diet Fed and Streptozotocin-Induced Diabetic Rats. |
| 83 | 26347890 | Further studies showed that TGT administration markedly reduced expression of TLR4, NF-κB, IL-1β, and MCP-1 in TGT-treated diabetic rats. |
| 84 | 26206887 | At clinically relevant concentrations, lyso-Gb3 activates podocyte Notch1 signaling, resulting in increased active Notch1 and HES1, a canonical Notch transcriptional target. |
| 85 | 26206887 | A γ-secretase inhibitor or specific Notch1 small interfering RNA (siRNA) inhibited HES1 upregulation in response to lyso-Gb3. |
| 86 | 26206887 | Notch1 siRNA or γ-secretase inhibition also prevented the lyso-Gb3-induced upregulation of Notch1, Notch ligand Jagged1 and chemokine (MCP1, RANTES) expression. |
| 87 | 26206887 | Notch siRNA prevented the activation of nuclear factor kappa B (NFκB), and NFκB activation contributed to Notch1-mediated inflammatory responses as the NFκB inhibitor, parthenolide, prevented lyso-Gb3-induced chemokine upregulation. |
| 88 | 26206887 | Supporting the clinical relevance of cell culture findings, active Notch1, Jagged1 and HES1 were observed in Fabry kidney biopsies. |
| 89 | 25821833 | PACAP was effective in the downregulation of proinflammatory cytokines, such as monocyte chemoattractant protein-1 (MCP-1) and interleukin-6, which had been induced by the activation of toll-like receptor (TLR) with lipopolysaccharide. |
| 90 | 25821833 | PACAP also had downregulated the expression of MCP-1 through the protein kinase A signaling pathway; this led to the attenuation of the activation of extracellular signal-regulated kinase and nuclear factor-kappa B signaling. |
| 91 | 25171769 | Biochemical, clinical and experimental procedures included measurement of total urinary protein, renal biopsy and gene expression analysis of the receptor activator of NF-kappaB (RANK). |
| 92 | 24392227 | Constitutional Nephrin Deficiency in Conditionally Immortalized Human Podocytes Induced Epithelial-Mesenchymal Transition, Supported by β-Catenin/NF-kappa B Activation: A Consequence of Cell Junction Impairment? |
| 93 | 24392227 | In fact, a model of human podocyte with engineered nephrin deficiency constitutionally expressed high levels of α-SMA, vimentin, fibronectin, and other hallmarks of EMT. |
| 94 | 24392227 | The most intriguing was the activation of β-catenin pathway, which plays a critical role in podocyte ontogenesis as well as in the nephrin expression and EMT regulation. |
| 95 | 24339827 | TWEAK/Fn14 and Non-Canonical NF-kappaB Signaling in Kidney Disease. |
| 96 | 24339827 | In particular TWEAK/Fn14 targeting may preserve renal function and decrease cell death, inflammation, proteinuria, and fibrosis in mouse animal models. |
| 97 | 24339827 | Activation of the non-canonical NF-κB pathway is a critical difference between TWEAK and TNF. |
| 98 | 23296190 | In addition to these receptors, Toll-like receptor 3 (TLR3) and retinoic acid-inducible gene 1 (RIG-I)-like helicases (RLHs), podocytes express the collateral proteins required to support intracellular signaling. |
| 99 | 23296190 | The transcription factor interferon regulatory factor 3 (IRF3) and nuclear factor kappa B (NF-ĸB) are phosphorylated and translocate to the nucleus, and dsRNA increases synthesis of proteins driven by IRF3 (P54, P56 and P60) or NF-ĸB (interleukin 8 and A20). |
| 100 | 23296190 | Furthermore, dsRNA suppresses podocyte cell migration, alters the expression of a panel of podocyte essential proteins (nephrin, podocin and CD2-associated protein or CD2AP) and changes transepithelial albumin flux. |
| 101 | 21704028 | The study determines the effect of genistein on inflammatory status and expression of nuclear factor-kappa B (NF-κB p65), transforming growth factor-β1 (TGF-β1) and receptor for advanced glycation end products (RAGE) in kidney of fructose-fed rats. |
| 102 | 21704028 | The expression of NF-κB P(65), TGF-β1 and RAGE, histochemical localization of α-smooth muscle actin (α-SMA), levels of tumour necrosis factor-α (TNF-α) and interleukin-6(IL-6) and ultrastructural analysis were performed at the end of the experimental period. |
| 103 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 104 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 105 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 106 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 107 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 108 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 109 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 110 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 111 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 112 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 113 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 114 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 115 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 116 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 117 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 118 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 119 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 120 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 121 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 122 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 123 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 124 | 19918242 | Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF. |
| 125 | 19918242 | Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF. |
| 126 | 19918242 | Glomerular function, GLUT1, signaling, albumin excretion, and structural and ultrastructural changes were assessed. |
| 127 | 19918242 | Glomerular function, GLUT1, signaling, albumin excretion, and structural and ultrastructural changes were assessed. |
| 128 | 19918242 | These changes were associated with the activation of glomerular PKCbeta1 and NF-kappaB p50 which contribute to ECM accumulation. |
| 129 | 19918242 | These changes were associated with the activation of glomerular PKCbeta1 and NF-kappaB p50 which contribute to ECM accumulation. |
| 130 | 19918242 | The FvbROP Os/+ mice exhibited an early increase in glomerular GLUT1 leading to increased glomerular glucose uptake PKCbeta1, and NF-kappaB activation, with excess ECM accumulation. |
| 131 | 19918242 | The FvbROP Os/+ mice exhibited an early increase in glomerular GLUT1 leading to increased glomerular glucose uptake PKCbeta1, and NF-kappaB activation, with excess ECM accumulation. |
| 132 | 19546355 | TRPC6 up-regulation in Ang II-induced podocyte apoptosis might result from ERK activation and NF-kappaB translocation. |
| 133 | 19546355 | TRPC6 up-regulation in Ang II-induced podocyte apoptosis might result from ERK activation and NF-kappaB translocation. |
| 134 | 19546355 | TRPC6 up-regulation in Ang II-induced podocyte apoptosis might result from ERK activation and NF-kappaB translocation. |
| 135 | 19546355 | TRPC6 up-regulation in Ang II-induced podocyte apoptosis might result from ERK activation and NF-kappaB translocation. |
| 136 | 19546355 | Transient receptor potential cation channel 6 (TRPC6) is a calcium channel located in podocyte membrane. |
| 137 | 19546355 | Transient receptor potential cation channel 6 (TRPC6) is a calcium channel located in podocyte membrane. |
| 138 | 19546355 | Transient receptor potential cation channel 6 (TRPC6) is a calcium channel located in podocyte membrane. |
| 139 | 19546355 | Transient receptor potential cation channel 6 (TRPC6) is a calcium channel located in podocyte membrane. |
| 140 | 19546355 | The present study evaluated the alteration of TRPC6 expression and the Ca(2+) influx involved in Ang II-induced podocyte apoptosis. |
| 141 | 19546355 | The present study evaluated the alteration of TRPC6 expression and the Ca(2+) influx involved in Ang II-induced podocyte apoptosis. |
| 142 | 19546355 | The present study evaluated the alteration of TRPC6 expression and the Ca(2+) influx involved in Ang II-induced podocyte apoptosis. |
| 143 | 19546355 | The present study evaluated the alteration of TRPC6 expression and the Ca(2+) influx involved in Ang II-induced podocyte apoptosis. |
| 144 | 19546355 | The possible pathways related to TRPC6 in Ang II-induced podocyte apoptosis were also investigated. |
| 145 | 19546355 | The possible pathways related to TRPC6 in Ang II-induced podocyte apoptosis were also investigated. |
| 146 | 19546355 | The possible pathways related to TRPC6 in Ang II-induced podocyte apoptosis were also investigated. |
| 147 | 19546355 | The possible pathways related to TRPC6 in Ang II-induced podocyte apoptosis were also investigated. |
| 148 | 19546355 | The protein level of TRPC6 was increased markedly in response to Ang II stimulation, and the intracellular Ca(2+) concentration was elevated. |
| 149 | 19546355 | The protein level of TRPC6 was increased markedly in response to Ang II stimulation, and the intracellular Ca(2+) concentration was elevated. |
| 150 | 19546355 | The protein level of TRPC6 was increased markedly in response to Ang II stimulation, and the intracellular Ca(2+) concentration was elevated. |
| 151 | 19546355 | The protein level of TRPC6 was increased markedly in response to Ang II stimulation, and the intracellular Ca(2+) concentration was elevated. |
| 152 | 19546355 | By transfection with TRPC6 siRNA, Ang II-induced podocyte apoptosis and the transient Ca(2+) influx were inhibited. |
| 153 | 19546355 | By transfection with TRPC6 siRNA, Ang II-induced podocyte apoptosis and the transient Ca(2+) influx were inhibited. |
| 154 | 19546355 | By transfection with TRPC6 siRNA, Ang II-induced podocyte apoptosis and the transient Ca(2+) influx were inhibited. |
| 155 | 19546355 | By transfection with TRPC6 siRNA, Ang II-induced podocyte apoptosis and the transient Ca(2+) influx were inhibited. |
| 156 | 19546355 | Treated with extracellular signal-regulated kinase (ERK) pathway specific inhibitor U0126 or nuclear factor-kappaB (NF-kappaB) pathway specific inhibitor ammonium pyrrolidinedithiocarbamate (PDTC) and Ang II, respectively in podocytes, not only was the TRPC6 up-regulation reduced, but the podocyte apoptosis was also decreased. |
| 157 | 19546355 | Treated with extracellular signal-regulated kinase (ERK) pathway specific inhibitor U0126 or nuclear factor-kappaB (NF-kappaB) pathway specific inhibitor ammonium pyrrolidinedithiocarbamate (PDTC) and Ang II, respectively in podocytes, not only was the TRPC6 up-regulation reduced, but the podocyte apoptosis was also decreased. |
| 158 | 19546355 | Treated with extracellular signal-regulated kinase (ERK) pathway specific inhibitor U0126 or nuclear factor-kappaB (NF-kappaB) pathway specific inhibitor ammonium pyrrolidinedithiocarbamate (PDTC) and Ang II, respectively in podocytes, not only was the TRPC6 up-regulation reduced, but the podocyte apoptosis was also decreased. |
| 159 | 19546355 | Treated with extracellular signal-regulated kinase (ERK) pathway specific inhibitor U0126 or nuclear factor-kappaB (NF-kappaB) pathway specific inhibitor ammonium pyrrolidinedithiocarbamate (PDTC) and Ang II, respectively in podocytes, not only was the TRPC6 up-regulation reduced, but the podocyte apoptosis was also decreased. |
| 160 | 19546355 | Moreover, the translocation of NF-kappaB in nucleus resulted from Ang II was reduced by treatment with U0126. |
| 161 | 19546355 | Moreover, the translocation of NF-kappaB in nucleus resulted from Ang II was reduced by treatment with U0126. |
| 162 | 19546355 | Moreover, the translocation of NF-kappaB in nucleus resulted from Ang II was reduced by treatment with U0126. |
| 163 | 19546355 | Moreover, the translocation of NF-kappaB in nucleus resulted from Ang II was reduced by treatment with U0126. |
| 164 | 19546355 | The activation of ERK pathway and subsequent translocation of NF-kappaB was possibly necessary for the up-regulation TRPC6 induced by Ang II. |
| 165 | 19546355 | The activation of ERK pathway and subsequent translocation of NF-kappaB was possibly necessary for the up-regulation TRPC6 induced by Ang II. |
| 166 | 19546355 | The activation of ERK pathway and subsequent translocation of NF-kappaB was possibly necessary for the up-regulation TRPC6 induced by Ang II. |
| 167 | 19546355 | The activation of ERK pathway and subsequent translocation of NF-kappaB was possibly necessary for the up-regulation TRPC6 induced by Ang II. |
| 168 | 19507273 | The expressions of nephrin, tumor necrosis factor-alpha (TNF-alpha), NF-kappaB p65 and 3-nitrotyrosine (3-NT) protein were determined by immunoinfluorescence or Western blot analysis in the kidneys. |
| 169 | 19507273 | The expressions of nephrin, tumor necrosis factor-alpha (TNF-alpha), NF-kappaB p65 and 3-nitrotyrosine (3-NT) protein were determined by immunoinfluorescence or Western blot analysis in the kidneys. |
| 170 | 19507273 | The expressions of TNF-alpha, NF-kappaB p65 and 3-NT protein were significantly increased in the kidneys of diabetic rats, which were all significantly inhibited by TGP treatment. |
| 171 | 19507273 | The expressions of TNF-alpha, NF-kappaB p65 and 3-NT protein were significantly increased in the kidneys of diabetic rats, which were all significantly inhibited by TGP treatment. |
| 172 | 19497968 | Nephrin deficiency activates NF-kappaB and promotes glomerular injury. |
| 173 | 19497968 | Nephrin deficiency activates NF-kappaB and promotes glomerular injury. |
| 174 | 19497968 | Nephrin deficiency activates NF-kappaB and promotes glomerular injury. |
| 175 | 19497968 | Nephrin deficiency activates NF-kappaB and promotes glomerular injury. |
| 176 | 19497968 | Absence of the podocyte protein nephrin resulted in NF-kappaB activation, suggesting that nephrin negatively regulates the NF-kappaB pathway. |
| 177 | 19497968 | Absence of the podocyte protein nephrin resulted in NF-kappaB activation, suggesting that nephrin negatively regulates the NF-kappaB pathway. |
| 178 | 19497968 | Absence of the podocyte protein nephrin resulted in NF-kappaB activation, suggesting that nephrin negatively regulates the NF-kappaB pathway. |
| 179 | 19497968 | Absence of the podocyte protein nephrin resulted in NF-kappaB activation, suggesting that nephrin negatively regulates the NF-kappaB pathway. |
| 180 | 19497968 | Signal transduction assays supported a functional relationship between nephrin and NF-kappaB and suggested the involvement of atypical protein kinase C (aPKCzeta/lambda/iota) as an intermediary. |
| 181 | 19497968 | Signal transduction assays supported a functional relationship between nephrin and NF-kappaB and suggested the involvement of atypical protein kinase C (aPKCzeta/lambda/iota) as an intermediary. |
| 182 | 19497968 | Signal transduction assays supported a functional relationship between nephrin and NF-kappaB and suggested the involvement of atypical protein kinase C (aPKCzeta/lambda/iota) as an intermediary. |
| 183 | 19497968 | Signal transduction assays supported a functional relationship between nephrin and NF-kappaB and suggested the involvement of atypical protein kinase C (aPKCzeta/lambda/iota) as an intermediary. |
| 184 | 19497968 | In summary, nephrin may normally limit NF-kappaB activity in the podocyte, suggesting a mechanism by which it might discourage the evolution of glomerular disease. |
| 185 | 19497968 | In summary, nephrin may normally limit NF-kappaB activity in the podocyte, suggesting a mechanism by which it might discourage the evolution of glomerular disease. |
| 186 | 19497968 | In summary, nephrin may normally limit NF-kappaB activity in the podocyte, suggesting a mechanism by which it might discourage the evolution of glomerular disease. |
| 187 | 19497968 | In summary, nephrin may normally limit NF-kappaB activity in the podocyte, suggesting a mechanism by which it might discourage the evolution of glomerular disease. |
| 188 | 19273289 | The hallmark of NF-kappaB activation is the nuclear translocation of dimeric Rel protein transcription factors, which regulate hundreds of kappaB-dependent genes that are involved in inflammation, immunity, apoptosis, cell proliferation and differentiation. |
| 189 | 19273289 | The hallmark of NF-kappaB activation is the nuclear translocation of dimeric Rel protein transcription factors, which regulate hundreds of kappaB-dependent genes that are involved in inflammation, immunity, apoptosis, cell proliferation and differentiation. |
| 190 | 19273289 | The hallmark of NF-kappaB activation is the nuclear translocation of dimeric Rel protein transcription factors, which regulate hundreds of kappaB-dependent genes that are involved in inflammation, immunity, apoptosis, cell proliferation and differentiation. |
| 191 | 19273289 | In addition, cell-surface receptors (TNFR, Toll-like and angiotensin II, type 1 receptors), inhibitory kappaB kinases (IKK proteins), I kappaB proteins and factors regulating the post-translational modification of the Rel proteins (acetylation, phosphorylation), are other intracellular components that regulate NF-kappaB activation. |
| 192 | 19273289 | In addition, cell-surface receptors (TNFR, Toll-like and angiotensin II, type 1 receptors), inhibitory kappaB kinases (IKK proteins), I kappaB proteins and factors regulating the post-translational modification of the Rel proteins (acetylation, phosphorylation), are other intracellular components that regulate NF-kappaB activation. |
| 193 | 19273289 | In addition, cell-surface receptors (TNFR, Toll-like and angiotensin II, type 1 receptors), inhibitory kappaB kinases (IKK proteins), I kappaB proteins and factors regulating the post-translational modification of the Rel proteins (acetylation, phosphorylation), are other intracellular components that regulate NF-kappaB activation. |
| 194 | 19273289 | Over the last decade, in vitro studies, animal models and human studies have provided evidence that upregulation of the canonical (RelA/p50) NF- kappaB isoform (in tubular epithelial cells, podocytes, mesangial cells, macrophages) has a pathogenic role in mediating chronic inflammation in chronic kidney disease (CKD). |
| 195 | 19273289 | Over the last decade, in vitro studies, animal models and human studies have provided evidence that upregulation of the canonical (RelA/p50) NF- kappaB isoform (in tubular epithelial cells, podocytes, mesangial cells, macrophages) has a pathogenic role in mediating chronic inflammation in chronic kidney disease (CKD). |
| 196 | 19273289 | Over the last decade, in vitro studies, animal models and human studies have provided evidence that upregulation of the canonical (RelA/p50) NF- kappaB isoform (in tubular epithelial cells, podocytes, mesangial cells, macrophages) has a pathogenic role in mediating chronic inflammation in chronic kidney disease (CKD). |
| 197 | 19193728 | Our previous studies demonstrated that 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] plays a renoprotective role by suppressing the RAS, with renin and angiotensinogen (AGT) as the main targets. |
| 198 | 19193728 | Our previous studies demonstrated that 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] plays a renoprotective role by suppressing the RAS, with renin and angiotensinogen (AGT) as the main targets. |
| 199 | 19193728 | Our previous studies demonstrated that 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] plays a renoprotective role by suppressing the RAS, with renin and angiotensinogen (AGT) as the main targets. |
| 200 | 19193728 | Our previous studies demonstrated that 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] plays a renoprotective role by suppressing the RAS, with renin and angiotensinogen (AGT) as the main targets. |
| 201 | 19193728 | The mechanism whereby 1,25(OH)(2)D(3) transcriptionally suppresses renin gene expression has been elucidated; however, how vitamin D regulates AGT remains unknown. |
| 202 | 19193728 | The mechanism whereby 1,25(OH)(2)D(3) transcriptionally suppresses renin gene expression has been elucidated; however, how vitamin D regulates AGT remains unknown. |
| 203 | 19193728 | The mechanism whereby 1,25(OH)(2)D(3) transcriptionally suppresses renin gene expression has been elucidated; however, how vitamin D regulates AGT remains unknown. |
| 204 | 19193728 | The mechanism whereby 1,25(OH)(2)D(3) transcriptionally suppresses renin gene expression has been elucidated; however, how vitamin D regulates AGT remains unknown. |
| 205 | 19193728 | In mesangial cells, the stimulation was inhibited by 1,25(OH)(2)D(3) (20 nM) or NF-kappaB inhibitor BAY 11-7082, suggesting the involvement of NF- kappaB in HG-induced AGT expression and the interaction between 1,25(OH)(2)D(3) and NF-kappaB in the regulation. |
| 206 | 19193728 | In mesangial cells, the stimulation was inhibited by 1,25(OH)(2)D(3) (20 nM) or NF-kappaB inhibitor BAY 11-7082, suggesting the involvement of NF- kappaB in HG-induced AGT expression and the interaction between 1,25(OH)(2)D(3) and NF-kappaB in the regulation. |
| 207 | 19193728 | In mesangial cells, the stimulation was inhibited by 1,25(OH)(2)D(3) (20 nM) or NF-kappaB inhibitor BAY 11-7082, suggesting the involvement of NF- kappaB in HG-induced AGT expression and the interaction between 1,25(OH)(2)D(3) and NF-kappaB in the regulation. |
| 208 | 19193728 | In mesangial cells, the stimulation was inhibited by 1,25(OH)(2)D(3) (20 nM) or NF-kappaB inhibitor BAY 11-7082, suggesting the involvement of NF- kappaB in HG-induced AGT expression and the interaction between 1,25(OH)(2)D(3) and NF-kappaB in the regulation. |
| 209 | 19193728 | EMSA and ChIP assays demonstrated increased p65/p50 binding to a NF-kappaB binding site at -1734 in the AGT gene promoter upon high glucose stimulation, and the binding was disrupted by 1,25(OH)(2)D(3) treatment. |
| 210 | 19193728 | EMSA and ChIP assays demonstrated increased p65/p50 binding to a NF-kappaB binding site at -1734 in the AGT gene promoter upon high glucose stimulation, and the binding was disrupted by 1,25(OH)(2)D(3) treatment. |
| 211 | 19193728 | EMSA and ChIP assays demonstrated increased p65/p50 binding to a NF-kappaB binding site at -1734 in the AGT gene promoter upon high glucose stimulation, and the binding was disrupted by 1,25(OH)(2)D(3) treatment. |
| 212 | 19193728 | EMSA and ChIP assays demonstrated increased p65/p50 binding to a NF-kappaB binding site at -1734 in the AGT gene promoter upon high glucose stimulation, and the binding was disrupted by 1,25(OH)(2)D(3) treatment. |
| 213 | 19193728 | Overexpression of p65/p50 overcame 1,25(OH)(2)D(3) suppression, and mutation of this NF-kappaB binding site blunted 1,25(OH)(2)D(3) suppression of the promoter activity. |
| 214 | 19193728 | Overexpression of p65/p50 overcame 1,25(OH)(2)D(3) suppression, and mutation of this NF-kappaB binding site blunted 1,25(OH)(2)D(3) suppression of the promoter activity. |
| 215 | 19193728 | Overexpression of p65/p50 overcame 1,25(OH)(2)D(3) suppression, and mutation of this NF-kappaB binding site blunted 1,25(OH)(2)D(3) suppression of the promoter activity. |
| 216 | 19193728 | Overexpression of p65/p50 overcame 1,25(OH)(2)D(3) suppression, and mutation of this NF-kappaB binding site blunted 1,25(OH)(2)D(3) suppression of the promoter activity. |
| 217 | 19193728 | In mice lacking the vitamin D receptor, AGT mRNA expression in the kidney was markedly increased compared with wild-type mice, and AGT induction in diabetic mice was suppressed by treatment with a vitamin D analog. |
| 218 | 19193728 | In mice lacking the vitamin D receptor, AGT mRNA expression in the kidney was markedly increased compared with wild-type mice, and AGT induction in diabetic mice was suppressed by treatment with a vitamin D analog. |
| 219 | 19193728 | In mice lacking the vitamin D receptor, AGT mRNA expression in the kidney was markedly increased compared with wild-type mice, and AGT induction in diabetic mice was suppressed by treatment with a vitamin D analog. |
| 220 | 19193728 | In mice lacking the vitamin D receptor, AGT mRNA expression in the kidney was markedly increased compared with wild-type mice, and AGT induction in diabetic mice was suppressed by treatment with a vitamin D analog. |
| 221 | 19193728 | These data indicate that 1,25(OH)(2)D(3) suppresses hyperglycemia-induced AGT expression by blocking NF-kappaB-mediated pathway. |
| 222 | 19193728 | These data indicate that 1,25(OH)(2)D(3) suppresses hyperglycemia-induced AGT expression by blocking NF-kappaB-mediated pathway. |
| 223 | 19193728 | These data indicate that 1,25(OH)(2)D(3) suppresses hyperglycemia-induced AGT expression by blocking NF-kappaB-mediated pathway. |
| 224 | 19193728 | These data indicate that 1,25(OH)(2)D(3) suppresses hyperglycemia-induced AGT expression by blocking NF-kappaB-mediated pathway. |
| 225 | 18443355 | Treatment of podocytes with recombinant Opn activated the NF-kappaB pathway, increased expression of urokinase plasminogen activator and matrix metalloproteinases 2 and 9, and increased podocyte motility. |
| 226 | 17466922 | In this review, the role of Wilms tumor 1 (WT1), LIM homeobox transcription factor 1, beta (Lmx1b), pod1, pax-2, kreisler, nuclear factor-kappa B (NF-kappaB), smad7, and zinc fingers and homeoboxes (ZHX) proteins in the development of podocyte disease is outlined. |
| 227 | 17148661 | Stx-2 enhanced ET-1 mRNA and protein expression via activation of nuclear factor kappaB (NF-kappaB) and activator protein-1 (Ap-1) to the extent that transfection with the dominant-negative mutant of IkappaB-kinase 2 or with Ap-1 decoy oligodeoxynucleotides reduced ET-1 mRNA levels. |
| 228 | 17148661 | Stx-2 enhanced ET-1 mRNA and protein expression via activation of nuclear factor kappaB (NF-kappaB) and activator protein-1 (Ap-1) to the extent that transfection with the dominant-negative mutant of IkappaB-kinase 2 or with Ap-1 decoy oligodeoxynucleotides reduced ET-1 mRNA levels. |
| 229 | 17148661 | We propose a role for p38 and p42/44 mitogen-activated protein kinases (MAPKs) in mediating NF-kappaB-dependent gene transcription induced by Stx-2, based on data that Stx-2 phosphorylated p38 and p42/44 MAPKs and that MAPK inhibitors reduced transcription of NF-kappaB promoter/luciferase reporter gene construct induced by Stx-2. |
| 230 | 17148661 | We propose a role for p38 and p42/44 mitogen-activated protein kinases (MAPKs) in mediating NF-kappaB-dependent gene transcription induced by Stx-2, based on data that Stx-2 phosphorylated p38 and p42/44 MAPKs and that MAPK inhibitors reduced transcription of NF-kappaB promoter/luciferase reporter gene construct induced by Stx-2. |
| 231 | 17148661 | Stx-2 caused F-actin redistribution and intercellular gaps via production of ET-1 acting on ETA receptor, because cytoskeleton changes were prevented by ETA receptor blockade. |
| 232 | 17148661 | Stx-2 caused F-actin redistribution and intercellular gaps via production of ET-1 acting on ETA receptor, because cytoskeleton changes were prevented by ETA receptor blockade. |
| 233 | 17148661 | Exogenous ET-1 induced cytoskeleton rearrangement and intercellular gaps via phosphatidylinositol-3 kinase and Rho-kinase pathway and increased protein permeability across the podocyte monolayer. |
| 234 | 17148661 | Exogenous ET-1 induced cytoskeleton rearrangement and intercellular gaps via phosphatidylinositol-3 kinase and Rho-kinase pathway and increased protein permeability across the podocyte monolayer. |
| 235 | 16452496 | Immunofluorescence studies of podocyte-associated proteins nephrin and podocin revealed diminished and discontinuous staining patterns in rats with PAN nephrosis, indicating severe podocyte injury. |
| 236 | 16452496 | Fluvastatin also mitigated tubulointerstitial damage in PAN nephrosis, with the repression of PAN-induced NF-kappaB and activator protein-1 activation in the kidneys. |
| 237 | 16205945 | The expression of NF-kappaB subunits p65 and p50, and the NF-kappaB regulated proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) as well as CD68 and synaptopodin was examined by Southwestern histochemistry (SWH) or immunohistochemistry. |
| 238 | 16205945 | The expression of NF-kappaB subunits p65 and p50, and the NF-kappaB regulated proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) as well as CD68 and synaptopodin was examined by Southwestern histochemistry (SWH) or immunohistochemistry. |
| 239 | 16205945 | The expression of NF-kappaB subunits p65 and p50, and the NF-kappaB regulated proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) as well as CD68 and synaptopodin was examined by Southwestern histochemistry (SWH) or immunohistochemistry. |
| 240 | 16205945 | The expression of NF-kappaB subunits p65 and p50, and the NF-kappaB regulated proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) as well as CD68 and synaptopodin was examined by Southwestern histochemistry (SWH) or immunohistochemistry. |
| 241 | 16205945 | The expression of NF-kappaB subunits p65 and p50, and the NF-kappaB regulated proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) as well as CD68 and synaptopodin was examined by Southwestern histochemistry (SWH) or immunohistochemistry. |
| 242 | 16205945 | In contrast to non-proliferative glomerulopathy and normal controls, NF-kappaB activation (both p65 and p50) was enhanced in glomerular endothelial, mesangial cells or infiltrating cells in class IV LN, along with upregulation of TNF-alpha, IL-1beta, IL-6 and ICAM-1 expression. |
| 243 | 16205945 | In contrast to non-proliferative glomerulopathy and normal controls, NF-kappaB activation (both p65 and p50) was enhanced in glomerular endothelial, mesangial cells or infiltrating cells in class IV LN, along with upregulation of TNF-alpha, IL-1beta, IL-6 and ICAM-1 expression. |
| 244 | 16205945 | In contrast to non-proliferative glomerulopathy and normal controls, NF-kappaB activation (both p65 and p50) was enhanced in glomerular endothelial, mesangial cells or infiltrating cells in class IV LN, along with upregulation of TNF-alpha, IL-1beta, IL-6 and ICAM-1 expression. |
| 245 | 16205945 | In contrast to non-proliferative glomerulopathy and normal controls, NF-kappaB activation (both p65 and p50) was enhanced in glomerular endothelial, mesangial cells or infiltrating cells in class IV LN, along with upregulation of TNF-alpha, IL-1beta, IL-6 and ICAM-1 expression. |
| 246 | 16205945 | In contrast to non-proliferative glomerulopathy and normal controls, NF-kappaB activation (both p65 and p50) was enhanced in glomerular endothelial, mesangial cells or infiltrating cells in class IV LN, along with upregulation of TNF-alpha, IL-1beta, IL-6 and ICAM-1 expression. |
| 247 | 16205945 | Glomerular endothelial and mesangial activation of NF-kappaB and mesangial ICAM-1 expression correlated with disease activity and the level of glomerular macrophage infiltration. |
| 248 | 16205945 | Glomerular endothelial and mesangial activation of NF-kappaB and mesangial ICAM-1 expression correlated with disease activity and the level of glomerular macrophage infiltration. |
| 249 | 16205945 | Glomerular endothelial and mesangial activation of NF-kappaB and mesangial ICAM-1 expression correlated with disease activity and the level of glomerular macrophage infiltration. |
| 250 | 16205945 | Glomerular endothelial and mesangial activation of NF-kappaB and mesangial ICAM-1 expression correlated with disease activity and the level of glomerular macrophage infiltration. |
| 251 | 16205945 | Glomerular endothelial and mesangial activation of NF-kappaB and mesangial ICAM-1 expression correlated with disease activity and the level of glomerular macrophage infiltration. |
| 252 | 16205945 | Podocyte NF-kappaB overactivation (predominantly p65) paralleled podocyte expression of TNF-alpha and IL-1beta in patients with LN and non-proliferative glomerulopathy. |
| 253 | 16205945 | Podocyte NF-kappaB overactivation (predominantly p65) paralleled podocyte expression of TNF-alpha and IL-1beta in patients with LN and non-proliferative glomerulopathy. |
| 254 | 16205945 | Podocyte NF-kappaB overactivation (predominantly p65) paralleled podocyte expression of TNF-alpha and IL-1beta in patients with LN and non-proliferative glomerulopathy. |
| 255 | 16205945 | Podocyte NF-kappaB overactivation (predominantly p65) paralleled podocyte expression of TNF-alpha and IL-1beta in patients with LN and non-proliferative glomerulopathy. |
| 256 | 16205945 | Podocyte NF-kappaB overactivation (predominantly p65) paralleled podocyte expression of TNF-alpha and IL-1beta in patients with LN and non-proliferative glomerulopathy. |
| 257 | 16205945 | Podocyte staining scores of NF-kappaB and p65 were positively correlated with the severity of proteinuria in LN and non-proliferative glomerulopathy. |
| 258 | 16205945 | Podocyte staining scores of NF-kappaB and p65 were positively correlated with the severity of proteinuria in LN and non-proliferative glomerulopathy. |
| 259 | 16205945 | Podocyte staining scores of NF-kappaB and p65 were positively correlated with the severity of proteinuria in LN and non-proliferative glomerulopathy. |
| 260 | 16205945 | Podocyte staining scores of NF-kappaB and p65 were positively correlated with the severity of proteinuria in LN and non-proliferative glomerulopathy. |
| 261 | 16205945 | Podocyte staining scores of NF-kappaB and p65 were positively correlated with the severity of proteinuria in LN and non-proliferative glomerulopathy. |
| 262 | 16204413 | Although podocytes produce p50, p52, RelA, RelB, and c-Rel, electrophoretic mobility shift assays and immunocytochemistry showed a predominant nuclear accumulation of p50/RelA-containing NF-kappaB dimers in HIV-1-expressing podocytes compared with normal. |
| 263 | 16204413 | Although podocytes produce p50, p52, RelA, RelB, and c-Rel, electrophoretic mobility shift assays and immunocytochemistry showed a predominant nuclear accumulation of p50/RelA-containing NF-kappaB dimers in HIV-1-expressing podocytes compared with normal. |
| 264 | 16204413 | The mechanism of NF-kappaB activation involved increased phosphorylation of IkappaBalpha, resulting in an enhanced turnover of the IkappaBalpha protein. |
| 265 | 16204413 | The mechanism of NF-kappaB activation involved increased phosphorylation of IkappaBalpha, resulting in an enhanced turnover of the IkappaBalpha protein. |
| 266 | 15975999 | Whether the epithelial apoptosis in HIVAN is mediated by NF-kappaB-activated Fas ligand expression was investigated here. |
| 267 | 15975999 | Whether the epithelial apoptosis in HIVAN is mediated by NF-kappaB-activated Fas ligand expression was investigated here. |
| 268 | 15975999 | Whether the epithelial apoptosis in HIVAN is mediated by NF-kappaB-activated Fas ligand expression was investigated here. |
| 269 | 15975999 | Whether the epithelial apoptosis in HIVAN is mediated by NF-kappaB-activated Fas ligand expression was investigated here. |
| 270 | 15975999 | Podocyte cell lines that were derived from HIV-1 transgenic mice showed a similar upregulation of Fas receptor expression and de novo expression of Fas ligand by semiquantitative reverse transcription-PCR and Western blotting. |
| 271 | 15975999 | Podocyte cell lines that were derived from HIV-1 transgenic mice showed a similar upregulation of Fas receptor expression and de novo expression of Fas ligand by semiquantitative reverse transcription-PCR and Western blotting. |
| 272 | 15975999 | Podocyte cell lines that were derived from HIV-1 transgenic mice showed a similar upregulation of Fas receptor expression and de novo expression of Fas ligand by semiquantitative reverse transcription-PCR and Western blotting. |
| 273 | 15975999 | Podocyte cell lines that were derived from HIV-1 transgenic mice showed a similar upregulation of Fas receptor expression and de novo expression of Fas ligand by semiquantitative reverse transcription-PCR and Western blotting. |
| 274 | 15975999 | In cultured podocytes, cross-linking of the Fas receptor to mimic ligand binding induced caspase 8 activity and apoptosis in both normal and HIVAN podocytes. |
| 275 | 15975999 | In cultured podocytes, cross-linking of the Fas receptor to mimic ligand binding induced caspase 8 activity and apoptosis in both normal and HIVAN podocytes. |
| 276 | 15975999 | In cultured podocytes, cross-linking of the Fas receptor to mimic ligand binding induced caspase 8 activity and apoptosis in both normal and HIVAN podocytes. |
| 277 | 15975999 | In cultured podocytes, cross-linking of the Fas receptor to mimic ligand binding induced caspase 8 activity and apoptosis in both normal and HIVAN podocytes. |
| 278 | 15975999 | Because constitutive NF-kappaB activity has been demonstrated in HIVAN epithelia, evidence for transcriptional control of the Fas ligand expression by NF-kappaB was sought. |
| 279 | 15975999 | Because constitutive NF-kappaB activity has been demonstrated in HIVAN epithelia, evidence for transcriptional control of the Fas ligand expression by NF-kappaB was sought. |
| 280 | 15975999 | Because constitutive NF-kappaB activity has been demonstrated in HIVAN epithelia, evidence for transcriptional control of the Fas ligand expression by NF-kappaB was sought. |
| 281 | 15975999 | Because constitutive NF-kappaB activity has been demonstrated in HIVAN epithelia, evidence for transcriptional control of the Fas ligand expression by NF-kappaB was sought. |
| 282 | 15975999 | With the use of cultured podocytes, expression of a Fas ligand promoter reporter plasmid was higher in HIVAN podocytes, indicating increased transcriptional activity. |
| 283 | 15975999 | With the use of cultured podocytes, expression of a Fas ligand promoter reporter plasmid was higher in HIVAN podocytes, indicating increased transcriptional activity. |
| 284 | 15975999 | With the use of cultured podocytes, expression of a Fas ligand promoter reporter plasmid was higher in HIVAN podocytes, indicating increased transcriptional activity. |
| 285 | 15975999 | With the use of cultured podocytes, expression of a Fas ligand promoter reporter plasmid was higher in HIVAN podocytes, indicating increased transcriptional activity. |
| 286 | 15975999 | In addition, chromatin immunoprecipitation assays were performed to demonstrate that p65-containing (RelA) complexes bound the Fas ligand promoter and that suppression of activated NF-kappaB with a peptide inhibitor could reduce the expression of Fas ligand mRNA in HIVAN podocytes. |
| 287 | 15975999 | In addition, chromatin immunoprecipitation assays were performed to demonstrate that p65-containing (RelA) complexes bound the Fas ligand promoter and that suppression of activated NF-kappaB with a peptide inhibitor could reduce the expression of Fas ligand mRNA in HIVAN podocytes. |
| 288 | 15975999 | In addition, chromatin immunoprecipitation assays were performed to demonstrate that p65-containing (RelA) complexes bound the Fas ligand promoter and that suppression of activated NF-kappaB with a peptide inhibitor could reduce the expression of Fas ligand mRNA in HIVAN podocytes. |
| 289 | 15975999 | In addition, chromatin immunoprecipitation assays were performed to demonstrate that p65-containing (RelA) complexes bound the Fas ligand promoter and that suppression of activated NF-kappaB with a peptide inhibitor could reduce the expression of Fas ligand mRNA in HIVAN podocytes. |
| 290 | 15975999 | These results suggest that NF-kappaB may regulate Fas-mediated apoptosis in HIVAN by controlling the expression of Fas ligand in renal epithelium. |
| 291 | 15975999 | These results suggest that NF-kappaB may regulate Fas-mediated apoptosis in HIVAN by controlling the expression of Fas ligand in renal epithelium. |
| 292 | 15975999 | These results suggest that NF-kappaB may regulate Fas-mediated apoptosis in HIVAN by controlling the expression of Fas ligand in renal epithelium. |
| 293 | 15975999 | These results suggest that NF-kappaB may regulate Fas-mediated apoptosis in HIVAN by controlling the expression of Fas ligand in renal epithelium. |
| 294 | 15855633 | Both Y27632, which inhibits Rho kinase-dependent stress fiber formation, and jasplakinolide, an F-actin stabilizer, decreased NF-kappaB and Ap-1 activity and reduced ET-1 expression. |
| 295 | 15855633 | Both Y27632, which inhibits Rho kinase-dependent stress fiber formation, and jasplakinolide, an F-actin stabilizer, decreased NF-kappaB and Ap-1 activity and reduced ET-1 expression. |
| 296 | 15855633 | Both Y27632, which inhibits Rho kinase-dependent stress fiber formation, and jasplakinolide, an F-actin stabilizer, decreased NF-kappaB and Ap-1 activity and reduced ET-1 expression. |
| 297 | 15855633 | This suggested a role for the cytoskeleton, through activated Rho, in the regulation of the ET-1 peptide. |
| 298 | 15855633 | This suggested a role for the cytoskeleton, through activated Rho, in the regulation of the ET-1 peptide. |
| 299 | 15855633 | This suggested a role for the cytoskeleton, through activated Rho, in the regulation of the ET-1 peptide. |
| 300 | 15855633 | Focal adhesion kinase (FAK), an integrin-associated nonreceptor tyrosine kinase, was phosphorylated by albumin treatment via Rho kinase-triggered actin reorganization. |
| 301 | 15855633 | Focal adhesion kinase (FAK), an integrin-associated nonreceptor tyrosine kinase, was phosphorylated by albumin treatment via Rho kinase-triggered actin reorganization. |
| 302 | 15855633 | Focal adhesion kinase (FAK), an integrin-associated nonreceptor tyrosine kinase, was phosphorylated by albumin treatment via Rho kinase-triggered actin reorganization. |
| 303 | 15855633 | FAK activation led to NF-kappaB- and Ap-1-dependent ET-1 expression. |
| 304 | 15855633 | FAK activation led to NF-kappaB- and Ap-1-dependent ET-1 expression. |
| 305 | 15855633 | FAK activation led to NF-kappaB- and Ap-1-dependent ET-1 expression. |
| 306 | 15855633 | These data suggest that reorganization of the actin cytoskeletal network in response to protein load is implicated in modulation of the ET-1 gene via Rho kinase-dependent FAK activation of NF-kappaB and Ap-1 in differentiated podocytes. |
| 307 | 15855633 | These data suggest that reorganization of the actin cytoskeletal network in response to protein load is implicated in modulation of the ET-1 gene via Rho kinase-dependent FAK activation of NF-kappaB and Ap-1 in differentiated podocytes. |
| 308 | 15855633 | These data suggest that reorganization of the actin cytoskeletal network in response to protein load is implicated in modulation of the ET-1 gene via Rho kinase-dependent FAK activation of NF-kappaB and Ap-1 in differentiated podocytes. |
| 309 | 15606719 | A variety of growth factors and cytokines are then induced through complex signal transduction pathways involving protein kinase C, mitogen-activated protein kinases, and the transcription factor NF-kappaB. |
| 310 | 15606719 | Activation of the renin-angiotensin system by high glucose, mechanical stress, and proteinuria with an increase in local formation of angiotensin II (ANG II) causes many of the pathophysiological changes associated with diabetic nephropathy. |
| 311 | 12732207 | In this study we show that exposure of human embryonic kidney epithelial A293 cells to the proinflammatory cytokine interleukin-1beta (IL-1beta) causes a dose-dependent upregulation of nephrin mRNA level. |
| 312 | 12732207 | Furthermore, nephrin protein is also elevated by IL-1beta treatment. |
| 313 | 12732207 | Tumor necrosis factor-alpha (TNFalpha) exerted a comparable effect on nephrin mRNA and protein expression. |
| 314 | 12732207 | The IL-1beta-induced upregulation of nephrin expression occurs independently of nitric oxide (NO) generation, since the NO-synthase inhibitor N(G)-monomethyl-L-arginine does not block the IL-1beta effect. |
| 315 | 12732207 | Mechanistically, we found that the IL-1beta-induced response does not involve protein kinase C, protein kinase A, the classical mitogen-activated protein kinase (MAPK), the stress-activated p38-MAPK, or the NF-kappaB cascade, since selective inhibitors of these pathways were unable to alter the IL-1beta response. |
| 316 | 12732207 | Moreover, neither unselective cyclooxygenase (COX) inhibitors, like indomethacin, nor COX-2-selective inhibitors, like flosulide and NS 398, nor the anti-inflammatory glucocorticoid dexamethasone were able to alter IL-1beta-induced nephrin expression. |
| 317 | 12732207 | The only inhibitor that was able to block IL-1beta- and TNFalpha-induced nephrin upregulation was rottlerin, which has been suggested to act as a selective PKCdelta inhibitor. |
| 318 | 12732207 | In summary, these data show for the first time that inflammatory cytokines like IL-1beta or TNFalpha can upregulate nephrin expression and this mechanistically involves a rottlerin-sensitive protein kinase. |
| 319 | 12397035 | Smad6 and Smad7 are inhibitory SMADs with putative functional roles at the intersection of major intracellular signaling networks, including TGF-beta, receptor tyrosine kinase (RTK), JAK/STAT, and NF-kappaB pathways. |
| 320 | 12397035 | This study reports differential functional roles and regulation of Smad6 and Smad7 in TGF-beta signaling in renal cells, in murine models of renal disease and in human glomerular diseases. |
| 321 | 12397035 | Smad7 is upregulated in podocytes in all examined glomerular diseases (focal segmental glomerulosclerosis [FSGS], minimal-change disease [MCD], membranous nephropathy [MNP], lupus nephritis [LN], and diabetic nephropathy [DN]) with a statistically significant upregulation in "classical" podocyte-diseases such as FSGS and MCD. |
| 322 | 12397035 | TGF-beta induces Smad7 synthesis in cultured podocytes and Smad6 synthesis in cultured mesangial cells. |
| 323 | 12397035 | Although Smad7 expression inhibited both Smad2- and Smad3-mediated TGF-beta signaling in podocytes, it inhibited only Smad3 but not Smad2 signaling in mesangial cells. |
| 324 | 12397035 | In contrast, Smad6 had no effect on TGF-beta/Smad signaling in podocytes and enhanced Smad3 signaling in mesangial cells. |
| 325 | 12397035 | These data suggest that Smad7 is activated in injured podocytes in vitro and in human glomerular disease and participates in negative control of TGF-beta/Smad signaling in addition to its pro-apoptotic activity, whereas Smad6 has no role in TGF-beta response and injury in podocytes. |
| 326 | 12397035 | These data indicate an important role for Smad6 and Smad7 in glomerular cells in vivo that could be important for the cell homeostasis in physiologic and pathologic conditions. |
| 327 | 11752025 | Reactive oxygen species alter gene expression in podocytes: induction of granulocyte macrophage-colony-stimulating factor. |
| 328 | 11752025 | One differentially expressed clone was identified as the proinflammatory cytokine granulocyte macrophage-colony-stimulating factor (GM-CSF). |
| 329 | 11752025 | GM-CSF release by podocytes was also stimulated by lipopolysaccharide (LPS), interleukin-1 (IL-1), and phorbolester (PMA). |
| 330 | 11752025 | Dimethyl-thio-urea significantly inhibited the LPS-, IL-1-, and PMA-induced GM-CSF production. |
| 331 | 11752025 | Activation of the transcription factor nuclear factor-kappaB (NF-kappaB) but not activator protein-1 was involved in the upregulation of ROS-induced GM-CSF production. |
| 332 | 11752025 | ROS also partially mediate the effects of PMA and IL-1 on podocyte GM-CSF production. |
| 333 | 11560950 | Apoptosis in podocytes induced by TGF-beta and Smad7. |
| 334 | 11560950 | TGF-beta1 and Smad7 each induce apoptosis in podocytes, and their coexpression has an additive effect. |
| 335 | 11560950 | Activation of p38 MAP kinase and caspase-3 is required for TGF-beta-mediated apoptosis, but not for apoptosis induced by Smad7. |
| 336 | 11560950 | Unlike TGF-beta, Smad7 inhibits nuclear translocation and transcriptional activity of the cell survival factor NF-kappaB. |