Interdependence of HIF-1α and TGF-β/Smad3 signaling in normoxic and hypoxic renal epithelial cell collagen expression. - Wikidata - awgldk - TriplyDB

Interdependence of HIF-1α and TGF-β/Smad3 signaling in normoxic and hypoxic renal epithelial cell collagen expression.

Interdependence of HIF-1α and TGF-β/Smad3 signaling in normoxic and hypoxic renal epithelial cell collagen expression.

http://www.wikidata.org/entity/Q34784162

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Sequential pathogenesis of metastatic VHL mutant clear cell renal cell carcinoma: putting it together with a translational perspective Tubulointerstitial injury and the progression of chronic kidney disease Fibroblasts and myofibroblasts in wound healing Hypoxia and Integrin-Mediated Epithelial Restitution during Mucosal Inflammation Reactive oxygen species and fibrosis: further evidence of a significant liaison Hypoxia, HIF, and Associated Signaling Networks in Chronic Kidney Disease.Signalling pathways involved in hypoxia-induced renal fibrosis.Tissue injury and hypoxia promote malignant progression of prostate cancer by inducing CXCL13 expression in tumor myofibroblasts.Transforming growth factor-β induced Warburg-like metabolic reprogramming may underpin the development of peritoneal endometriosis.Losartan alleviates renal fibrosis by down-regulating HIF-1α and up-regulating MMP-9/TIMP-1 in rats with 5/6 nephrectomy.HDAC6 deacetylase activity is required for hypoxia-induced invadopodia formation and cell invasion.TGFβ-induced deptor suppression recruits mTORC1 and not mTORC2 to enhance collagen I (α2) gene expression.Inhibition of survivin reduces HIF-1α, TGF-β1 and TFE3 in salivary adenoid cystic carcinoma.Urinary hypoxia-inducible factor-1alpha levels are associated with histologic chronicity changes and renal function in patients with lupus nephritis.Cross regulation between hypoxia-inducible transcription factor-1α (HIF-1α) and transforming growth factor (TGF)-ß1 mediates nickel oxide nanoparticles (NiONPs)-induced pulmonary fibrosis Hypoxia-inducible factor prolyl-hydroxylase-2 mediates transforming growth factor beta 1-induced epithelial-mesenchymal transition in renal tubular cells.Remnant nephron physiology and the progression of chronic kidney disease.Hypoxia-inducible factor-2α and TGF-β signaling interact to promote normoxic glomerular fibrogenesis.TGF-β/Smad3 activates mammalian target of rapamycin complex-1 to promote collagen production by increasing HIF-1α expression.Serine-204 in the linker region of Smad3 mediates the collagen-I response to TGF-β in a cell phenotype-specific manner.Mechanotransduction drives post ischemic revascularization through K(ATP) channel closure and production of reactive oxygen species.Cell differentiation versus cell death: extracellular glucose is a key determinant of cell fate following oxidative stress exposure.Regulation of wound healing and fibrosis by hypoxia and hypoxia-inducible factor-1.The role of hypoxia and Morg1 in renal injury.ID2 mediates the transforming growth factor-β1-induced Warburg-like effect seen in the peritoneum of women with endometriosis.Hypoxia in tissue repair and fibrosis.The role of endoglin in post-ischemic revascularization.The Tubulointerstitial Pathophysiology of Progressive Kidney Disease.Vitamin D and its receptor regulate lipopolysaccharide-induced transforming growth factor-β, angiotensinogen expression and podocytes apoptosis through the nuclear factor-κB pathway Hypoxia induces calpain activity and degrades SMAD2 to attenuate TGFβ signaling in macrophages.Hypoxia-inducible factor-1α promotes glomerulosclerosis and regulates COL1A2 expression through interactions with Smad3.Regulation of Na,K-ATPase β1-subunit in TGF-β2-mediated epithelial-to-mesenchymal transition in human retinal pigmented epithelial cells.Rapamycin inhibits transforming growth factor β-induced peritoneal angiogenesis by blocking the secondary hypoxic response.Profibrotic up-regulation of glucose transporter 1 by TGF-β involves activation of MEK and mammalian target of rapamycin complex 2 pathways.Hyperglycemia of tumor microenvironment modulates stage-dependent tumor progression and multidrug resistance: implication of cell survival regulatory molecules and altered glucose transport.Glutaminolysis is required for TGF-β1-induced myofibroblast differentiation and activation.PDGF receptor-β uses Akt/mTORC1 signaling node to promote high glucose-induced renal proximal tubular cell collagen I (α2) expression.Renal hypoxia in kidney disease: Cause or consequence?Siah2-deficient mice show impaired skin wound repair.Advances in Molecular Mechanisms and Treatment of Radiation-Induced Pulmonary Fibrosis

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Interdependence of HIF-1α and TGF-β/Smad3 signaling in normoxic and hypoxic renal epithelial cell collagen expression.

http://www.wikidata.org/entity/Q34784162

description

2011 nî lūn-bûn

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2011 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2011 թվականի հունվարին հրատարակված գիտական հոդված

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2011年の論文

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Interdependence of HIF-1α and ...... lial cell collagen expression.

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Interdependence of HIF-1α and ...... lial cell collagen expression.

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AJPRENAL.00335.2010

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American Journal of Physiology - Renal Physiology

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Interdependence of HIF-1α and ...... lial cell collagen expression.

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Constance E Runyan

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H William Schnaper

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Paul T Schumacker

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Rajit K Basu

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Susan Hubchak

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Tomoko Hayashida

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P2860

The Smad pathway

Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition

Cellular response to hypoxia involves signaling via Smad proteins

Transforming growth factor beta-induced phosphorylation of Smad3 is required for growth inhibition and transcriptional induction in epithelial cells

Sp1 and Smad proteins cooperate to mediate transforming growth factor-beta 1-induced alpha 2(I) collagen expression in human glomerular mesangial cells

Regulation of mammalian O2 homeostasis by hypoxia-inducible factor 1

Human Smad3 and Smad4 are sequence-specific transcription activators

Hypoxia-inducible factors in the kidney

Induction of the plasminogen activator inhibitor-1 gene expression by mild hypoxia via a hypoxia response element binding the hypoxia-inducible factor-1 in rat hepatocytes

Reactive oxygen species generated at mitochondrial complex III stabilize hypoxia-inducible factor-1alpha during hypoxia: a mechanism of O2 sensing

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F898-905

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10.1152/AJPRENAL.00335.2010

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4

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300

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49731475

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21209004

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