Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells. - Wikidata - awgldk - TriplyDB

Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells.

Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells.

http://www.wikidata.org/entity/Q53565021

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Redox warfare between airway epithelial cells and Pseudomonas: dual oxidase versus pyocyanin SIRT1: A Novel Target for the Treatment of Muscular Dystrophies Reciprocal regulation of TGF-β and reactive oxygen species: A perverse cycle for fibrosis Detection of superoxide anion and hydrogen peroxide production by cellular NADPH oxidases Hepatitis C Virus (HCV) Proteins Induce NADPH Oxidase 4 Expression in a Transforming Growth Factor -Dependent Manner: a New Contributor to HCV-Induced Oxidative Stress Oxidative stress and glutathione in TGF-beta-mediated fibrogenesis Upregulation of Nox4 in the aging vasculature and its association with smooth muscle cell polyploidy Airway smooth muscle relaxation is impaired in mice lacking the p47phox subunit of NAD(P)H oxidase Nox4-generated superoxide drives angiotensin II-induced neural stem cell proliferation.Bromodomain and extraterminal proteins suppress NF-E2-related factor 2-mediated antioxidant gene expression.Wild-type and mutant p53 differentially regulate NADPH oxidase 4 in TGF-β-mediated migration of human lung and breast epithelial cells ROS signaling by NOX4 drives fibroblast-to-myofibroblast differentiation in the diseased prostatic stroma Role of Nox4 and Nox2 in hyperoxia-induced reactive oxygen species generation and migration of human lung endothelial cells.A differential role for endocytosis in receptor-mediated activation of Nox1.The Role of NOX4 and TRX2 in Angiogenesis and Their Potential Cross-Talk.Oxidative modification of nuclear mitogen-activated protein kinase phosphatase 1 is involved in transforming growth factor beta1-induced expression of plasminogen activator inhibitor 1 in fibroblasts.Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype Oxidative stress and hepatic Nox proteins in chronic hepatitis C and hepatocellular carcinoma.Motility, survival, and proliferation.The NADPH oxidases NOX4 and DUOX2 regulate cell cycle entry via a p53-dependent pathway.PPAR{gamma} regulates hypoxia-induced Nox4 expression in human pulmonary artery smooth muscle cells through NF-{kappa}B.The Nox4 inhibitor GKT137831 attenuates hypoxia-induced pulmonary vascular cell proliferation NOX4/NADPH oxidase expression is increased in pulmonary fibroblasts from patients with idiopathic pulmonary fibrosis and mediates TGFbeta1-induced fibroblast differentiation into myofibroblasts.TGF-β regulates Nox4, MnSOD and catalase expression, and IL-6 release in airway smooth muscle cells.Store-operated Ca2+ entry is involved in transforming growth factor-β1 facilitated proliferation of rat airway smooth muscle cells.Redox regulation of cardiomyocyte cell cycling via an ERK1/2 and c-Myc-dependent activation of cyclin D2 transcription Nox4 regulates Nrf2 and glutathione redox in cardiomyocytes in vivo.Nox4: a hydrogen peroxide-generating oxygen sensor.Galangin attenuates airway remodelling by inhibiting TGF-β1-mediated ROS generation and MAPK/Akt phosphorylation in asthma Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets NOX4-Dependent Hydrogen Peroxide Overproduction in Human Atrial Fibrillation and HL-1 Atrial Cells: Relationship to Hypertension.How do cytokines trigger genomic instability?The NOX toolbox: validating the role of NADPH oxidases in physiology and disease.Transforming growth factor-β and nuclear factor E2–related factor 2 regulate antioxidant responses in airway smooth muscle cells: role in asthma.NADPH oxidase 4 is required for interleukin-1β-mediated activation of protein kinase Cδ and downstream activation of c-jun N-terminal kinase signaling in smooth muscle.NADPH oxidases in lung biology and pathology: host defense enzymes, and more.Regulation of smooth muscle by inducible nitric oxide synthase and NADPH oxidase in vascular proliferative diseases Airway smooth muscle in the pathophysiology and treatment of asthma.Prolonged fasting activates Nrf2 in post-weaned elephant seals.Airway smooth muscle growth in asthma: proliferation, hypertrophy, and migration.

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P2860

Nox4 mediates TGF-beta1-induced retinoblastoma protein phosphorylation, proliferation, and hypertrophy in human airway smooth muscle cells.

http://www.wikidata.org/entity/Q53565021

description

2007 nî lūn-bûn

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name

Nox4 mediates TGF-beta1-induce ...... an airway smooth muscle cells.

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Nox4 mediates TGF-beta1-induce ...... an airway smooth muscle cells.

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Nox4 mediates TGF-beta1-induce ...... an airway smooth muscle cells.

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Nox4 mediates TGF-beta1-induce ...... an airway smooth muscle cells.

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Nox4 mediates TGF-beta1-induce ...... an airway smooth muscle cells.

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Nox4 mediates TGF-beta1-induce ...... an airway smooth muscle cells.

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American Journal of Physiology - Lung Cellular and Molecular Physiology

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Nox4 mediates TGF-beta1-induce ...... an airway smooth muscle cells.

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Anne Sturrock

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John R Hoidal

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Karl Sanders

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Kimberly Norman

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Kimberly Wilson

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Pasquale Chitano

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Thomas M Murphy

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Thomas P Huecksteadt

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Thomas P Kennedy

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P2860

HBP1 repression of the p47phox gene: cell cycle regulation via the NADPH oxidase

Smad-dependent and Smad-independent pathways in TGF-beta family signalling

Pocket proteins and cell cycle control

Functional analysis of Nox4 reveals unique characteristics compared to other NADPH oxidases

Angiotensin II-induced ERK1/ERK2 activation and protein synthesis are redox-dependent in glomerular mesangial cells

Reversible oxidation and inactivation of protein tyrosine phosphatases in vivo

How cells read TGF-beta signals

Regulation of translation initiation by FRAP/mTOR

TGF-beta promotes proliferation of cultured SMC via both PDGF-AA-dependent and PDGF-AA-independent mechanisms.

Changes in biophysical and biochemical properties of single bronchial smooth muscle cells from asthmatic subjects.

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phosphorylation