Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression. - Wikidata - awgldk - TriplyDB

Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression.

Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression.

http://www.wikidata.org/entity/Q33443692

about

The potential utilizations of hydrogen as a promising therapeutic strategy against ocular diseases NF-κB, JNK, and TLR Signaling Pathways in Hepatocarcinogenesis Computer-aided quantification of retinal neovascularization.Perturbation of mouse retinal vascular morphogenesis by anthrax lethal toxin.Cucurbitacin-I (JSI-124) activates the JNK/c-Jun signaling pathway independent of apoptosis and cell cycle arrest in B leukemic cells.Retinopathy of prematurity promising newer modalities of treatment.JNK inhibition reduces apoptosis and neovascularization in a murine model of age-related macular degeneration.TNF-α decreases VEGF secretion in highly polarized RPE cells but increases it in non-polarized RPE cells related to crosstalk between JNK and NF-κB pathways.AMD-associated genes encoding stress-activated MAPK pathway constituents are identified by interval-based enrichment analysis JNK-1 deficiency limits macrophage-mediated antigen-induced arthritis.Activation of cytosolic phospholipase A2 downstream of the Src-phospholipase D1 (PLD1)-protein kinase C γ (PKCγ) signaling axis is required for hypoxia-induced pathological retinal angiogenesis Consequences and utility of the zinc-dependent metalloprotease activity of anthrax lethal toxin.Oxygen-dependent cleavage of the p75 neurotrophin receptor triggers stabilization of HIF-1α.Erythropoietin receptor antibody inhibits oxidative stress induced retinal neovascularization in mice.Endoplasmic reticulum stress and inflammation: mechanisms and implications in diabetic retinopathy.Prevention of VEGF-induced growth and tube formation in human retinal endothelial cells by aldose reductase inhibition c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases.SPAG9 controls the cell motility, invasion and angiogenesis of human osteosarcoma cells.Suppression of ischemia in arterial occlusive disease by JNK-promoted native collateral artery development.Sustained inhibition of neovascularization in vldlr-/- mice following intravitreal injection of cerium oxide nanoparticles and the role of the ASK1-P38/JNK-NF-κB pathway.RhoB regulates the function of macrophages in the hypoxia-induced inflammatory response.HIF-1α siRNA reduces retinal neovascularization in a mouse model of retinopathy of prematurity.Activation of endoplasmic reticulum stress by hyperglycemia is essential for Müller cell-derived inflammatory cytokine production in diabetes.ERK5 Contributes to VEGF Alteration in Diabetic Retinopathy.JNK2 up-regulates hypoxia-inducible factors and contributes to hypoxia-induced erythropoiesis and pulmonary hypertension.Hydrogen saline treatment attenuates hyperoxia-induced retinopathy by inhibition of oxidative stress and reduction of VEGF expression.Increased expression of c-Fos, c-Jun and c-Jun N-terminal kinase associated with neuronal cell death in retinas of diabetic patients.

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P2860

Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression.

http://www.wikidata.org/entity/Q33443692

description

2009 nî lūn-bûn

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2009 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2009 թվականի մայիսին հրատարակված գիտական հոդված

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2009年の論文

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Genetic and pharmacological in ...... rference with VEGF expression.

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Genetic and pharmacological in ...... rference with VEGF expression.

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Gabriel G Haddad

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James D Lindsey

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Jordi Rius

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Karen X Duong-Polk

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Monica Guma

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P2860

Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1

Pegaptanib and ranibizumab for neovascular age-related macular degeneration: a systematic review

A novel bHLH-PAS factor with close sequence similarity to hypoxia-inducible factor 1alpha regulates the VEGF expression and is potentially involved in lung and vascular development

Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation

Reactive oxygen species promote TNFalpha-induced death and sustained JNK activation by inhibiting MAP kinase phosphatases

c-Jun can recruit JNK to phosphorylate dimerization partners via specific docking interactions

Inhibition of c-Jun N-terminal kinase 1, but not c-Jun N-terminal kinase 2, suppresses apoptosis induced by ischemia/reoxygenation in rat cardiac myocytes

T2-TrpRS inhibits preretinal neovascularization and enhances physiological vascular regrowth in OIR as assessed by a new method of quantification

Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene

Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele

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