Tumor necrosis factor alpha inhibits type I collagen synthesis through repressive CCAAT/enhancer-binding proteins - Wikidata - awgldk - TriplyDB

Tumor necrosis factor alpha inhibits type I collagen synthesis through repressive CCAAT/enhancer-binding proteins

Tumor necrosis factor alpha inhibits type I collagen synthesis through repressive CCAAT/enhancer-binding proteins

http://www.wikidata.org/entity/Q24554328

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Classification of human B-ZIP proteins based on dimerization properties Occlusion regulates epidermal cytokine production and inhibits scar formation Prdm5 regulates collagen gene transcription by association with RNA polymerase II in developing bone The RFX family interacts at the collagen (COL1A2) start site and represses transcription Transcriptional Co-activators CREB-binding protein/p300 increase chondrocyte Cd-rap gene expression by multiple mechanisms including sequestration of the repressor CCAAT/enhancer-binding protein Timcodar (VX-853) Is a Non-FKBP12 Binding Macrolide Derivative That Inhibits PPARγ and Suppresses Adipogenesis Arylhydrocarbon receptor activation in NCI-H441 cells and C57BL/6 mice: possible mechanisms for lung dysfunction Viral induction of central nervous system innate immune responses.Effects of CD14 macrophages and proinflammatory cytokines on chondrogenesis in osteoarthritic synovium-derived stem cells.Molecular characterization and expressional affirmation of the beta proteasome subunit cluster in rock bream immune defense.Transcriptional regulation of adipocyte differentiation: a central role for CCAAT/enhancer-binding protein (C/EBP) β.CCAAT/enhancer binding protein β-deficiency enhances type 1 diabetic bone phenotype by increasing marrow adiposity and bone resorption Transcriptional activation of histone H4 by C/EBPβ during the mitotic clonal expansion of 3T3-L1 adipocyte differentiation Dominant-negative C/EBP disrupts mitotic clonal expansion and differentiation of 3T3-L1 preadipocytes.Myocardin-related transcription factor-A complexes activate type I collagen expression in lung fibroblasts.Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats Idiopathic pulmonary fibrosis: emerging concepts on pharmacotherapy.Emerging drugs for idiopathic pulmonary fibrosis.The inflammation-induced down-regulation of plasma Fetuin-A (alpha2HS-Glycoprotein) in liver results from the loss of interaction between long C/EBP isoforms at two neighbouring binding sites Idiopathic pulmonary fibrosis : new concepts in pathogenesis and implications for drug therapy Temporal retinal transcriptome and systems biology analysis identifies key pathways and hub genes in Staphylococcus aureus endophthalmitis Emerging insights into Transforming growth factor beta Smad signal in hepatic fibrogenesis.C/EBP maintains chromatin accessibility in liver and facilitates glucocorticoid receptor recruitment to steroid response elements TNF-alpha suppresses prolyl-4-hydroxylase alpha1 expression via the ASK1-JNK-NonO pathway.Oxidative and nitrosative stress and fibrogenic response.The Dysregulation of Polyamine Metabolism in Colorectal Cancer Is Associated with Overexpression of c-Myc and C/EBPβ rather than Enterotoxigenic Bacteroides fragilis Infection 5'UTR of the neurogenic bHLH Nex1/MATH-2/NeuroD6 gene is regulated by two distinct promoters through CRE and C/EBP binding sites Neuregulin-1 attenuates mortality associated with experimental cerebral malaria.Cellular/extracellular matrix cross-talk in scar evolution and control.Host cell cytokines induced by Chlamydia pneumoniae decrease the expression of interstitial collagens and fibronectin in fibroblasts.Extracellular matrix synthesis in vascular disease: hypertension, and atherosclerosis.CCAAT/enhancer-binding proteins beta and delta mediate the repression of gene transcription of cartilage-derived retinoic acid-sensitive protein induced by interleukin-1 beta.Y-box-binding protein YB-1 mediates transcriptional repression of human alpha 2(I) collagen gene expression by interferon-gamma.Characterization of the c-Myb-responsive region and regulation of the human type I collagen alpha 2 chain gene by c-Myb.Advances in the treatment of idiopathic pulmonary fibrosis.Development of a high throughput luciferase reporter gene system for screening activators and repressors of human collagen Iα2 gene expression.Role of basic region leucine zipper transcription factors cyclic AMP response element binding protein (CREB), CREB2, activating transcription factor 2 and CAAT/enhancer binding protein alpha in cyclic AMP response element-mediated transcription.Erythroid gene suppression by NF-kappa B.Egr-1 mediates transcriptional repression of COL2A1 promoter activity by interleukin-1beta.Characterization of an evolutionarily conserved far-upstream enhancer in the human alpha 2(I) collagen (COL1A2) gene.

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Tumor necrosis factor alpha inhibits type I collagen synthesis through repressive CCAAT/enhancer-binding proteins

http://www.wikidata.org/entity/Q24554328

description

2000 nî lūn-bûn

@nan

2000 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2000 թվականի փետրվարին հրատարակված գիտական հոդված

@hy

2000年の論文

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2000年論文

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2000年論文

@zh-hant

2000年論文

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2000年論文

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2000年論文

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2000年论文

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Molecular and Cellular Biology

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P2860

Modulation of life and death by the TNF receptor superfamily

In situ detection of sequence-specific DNA binding activity specified by a recombinant bacteriophage

A dominant-negative inhibitor of CREB reveals that it is a general mediator of stimulus-dependent transcription of c-fos

C/EBPalpha regulates generation of C/EBPbeta isoforms through activation of specific proteolytic cleavage

Tumor necrosis factor-alpha and interferon-gamma suppress the activation of human type I collagen gene expression by transforming growth factor-beta 1. Evidence for two distinct mechanisms of inhibition at the transcriptional and posttranscriptional

Induction of the transcription factor IRF-1 and interferon-beta mRNAs by cytokines and activators of second-messenger pathways

Life without white fat: a transgenic mouse

Tumor necrosis factor-induced reversal of adipocytic phenotype of 3T3-L1 cells is preceded by a loss of nuclear CCAAT/enhancer binding protein (C/EBP).

C/ATF, a member of the activating transcription factor family of DNA-binding proteins, dimerizes with CAAT/enhancer-binding proteins and directs their binding to cAMP response elements

Tyrosine dephosphorylation of nuclear proteins mimics transforming growth factor beta 1 stimulation of alpha 2(I) collagen gene expression.

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