Sublytic C5b-9 triggers glomerular mesangial cell apoptosis via XAF1 gene activation mediated by p300-dependent IRF-1 acetylation.
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The Origin and Activities of IgA1-Containing Immune Complexes in IgA NephropathyCurrent Understanding of the Role of Complement in IgA NephropathyC5a Induces the Synthesis of IL-6 and TNF-α in Rat Glomerular Mesangial Cells through MAPK Signaling Pathways.Tumor suppression in mice lacking GABARAP, an Atg8/LC3 family member implicated in autophagy, is associated with alterations in cytokine secretion and cell death.Thy-1 interaction with Fas in lipid rafts regulates fibroblast apoptosis and lung injury resolution.Asymmetric dimethylarginine (ADMA) treatment induces apoptosis in cultured rat mesangial cells via endoplasmic reticulum stress activation.PCAF-mediated Akt1 acetylation enhances the proliferation of human glioblastoma cells.Lipotoxicity-Induced PRMT1 Exacerbates Mesangial Cell Apoptosis via Endoplasmic Reticulum Stress.IL-17A promotes the proliferation of human nasopharyngeal carcinoma cells through p300-mediated Akt1 acetylation.Up-Regulation of Interferon Regulatory Factor 3 Involves in Neuronal Apoptosis After Intracerebral Hemorrhage in Adult Rats.Upregulation of Interferon Regulatory Factor 6 Promotes Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats.Sublytic C5b-9 Induces Glomerular Mesangial Cell Apoptosis through the Cascade Pathway of MEKK2-p38 MAPK-IRF-1-TRADD-Caspase 8 in Rat Thy-1 Nephritis.Sublytic C5b-9 triggers glomerular mesangial cell apoptosis in rat Thy-1 nephritis via Gadd45 activation mediated by Egr-1 and p300-dependent ATF3 acetylation.Activation of the complement system in an osteosarcoma cell line promotes angiogenesis through enhanced production of growth factors.The Emerging Role of Pathogenesis of IgA Nephropathy
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Sublytic C5b-9 triggers glomerular mesangial cell apoptosis via XAF1 gene activation mediated by p300-dependent IRF-1 acetylation.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 17 April 2014
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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Sublytic C5b-9 triggers glomer ...... 0-dependent IRF-1 acetylation.
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Sublytic C5b-9 triggers glomer ...... 0-dependent IRF-1 acetylation.
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label
Sublytic C5b-9 triggers glomer ...... 0-dependent IRF-1 acetylation.
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Sublytic C5b-9 triggers glomer ...... 0-dependent IRF-1 acetylation.
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prefLabel
Sublytic C5b-9 triggers glomer ...... 0-dependent IRF-1 acetylation.
@en
Sublytic C5b-9 triggers glomer ...... 0-dependent IRF-1 acetylation.
@nl
P2093
P2860
P356
P1476
Sublytic C5b-9 triggers glomer ...... 0-dependent IRF-1 acetylation.
@en
P2093
P2860
P356
10.1038/CDDIS.2014.153
P577
2014-04-17T00:00:00Z