The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy. - Wikidata - awgldk - TriplyDB

The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy.

The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy.

http://www.wikidata.org/entity/Q34793636

about

A RING to rule them all? Insights into the Map3k1 PHD motif provide a new mechanistic understanding into the diverse roles of Map3k1 Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.MAP3K1 function is essential for cytoarchitecture of the mouse organ of Corti and survival of auditory hair cells.Myocyte-restricted focal adhesion kinase deletion attenuates pressure overload-induced hypertrophy Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction.The AP-1 transcription factor c-Jun prevents stress-imposed maladaptive remodeling of the heart.Inhibition of endogenous thioredoxin in the heart increases oxidative stress and cardiac hypertrophy.The role of MEKK1 in hypertrophic cardiomyopathy.Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives Ablation of phospholamban and sarcolipin results in cardiac hypertrophy and decreased cardiac contractility c-Jun N-terminal kinase (JNK-1) confers protection against brief but not extended ischemia during acute myocardial infarction.Peroxisome proliferator-activated receptor (PPAR) gene profiling uncovers insulin-like growth factor-1 as a PPARalpha target gene in cardioprotection.MAP3Ks as central regulators of cell fate during development.Telomere attrition and Chk2 activation in human heart failure Activation of Mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophy.Phosphoinositide 3-kinase(p110alpha) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy.Steroidal Saponin Diosgenin from Dioscorea bulbifera Protects Cardiac Cells from Hypoxia-reoxygenation Injury Through Modulation of Pro-survival and Pro-death Molecules Differences between pathological and physiological cardiac hypertrophy: novel therapeutic strategies to treat heart failure.Novel methods for measuring cardiac autophagy in vivo.Mitogen-activated protein kinases in heart development and diseases Stretch-induced regulation of angiotensinogen gene expression in cardiac myocytes and fibroblasts: opposing roles of JNK1/2 and p38alpha MAP kinases The rationale for cardiomyocyte resuscitation in myocardial salvage.Elucidation of thioredoxin target protein networks in mouse.Crocetin protects against cardiac hypertrophy by blocking MEK-ERK1/2 signalling pathway.Cdc42 is an antihypertrophic molecular switch in the mouse heart.Adenylyl cyclase type 5 protein expression during cardiac development and stress.Genetic inhibition of calcineurin induces diastolic dysfunction in mice with chronic pressure overload.Pacing-induced cardiomyopathy: pathophysiological insights through matrix metalloproteinases.c-Jun N-terminal kinases (JNK) antagonize cardiac growth through cross-talk with calcineurin-NFAT signaling.H-Ras Isoform Mediates Protection Against Pressure Overload-Induced Cardiac Dysfunction in Part Through Activation of AKT.Endogenous muscle atrophy F-box mediates pressure overload-induced cardiac hypertrophy through regulation of nuclear factor-kappaB.The CRM1 nuclear export receptor controls pathological cardiac gene expression.Phosphorylation of Bad at Thr-201 by JNK1 promotes glycolysis through activation of phosphofructokinase-1.Nix-mediated apoptosis links myocardial fibrosis, cardiac remodeling, and hypertrophy decompensation.Nicotinamide phosphoribosyltransferase regulates cell survival through NAD+ synthesis in cardiac myocytes.Nifedipine inhibits cardiac hypertrophy and left ventricular dysfunction in response to pressure overload.Protein kinase g iα inhibits pressure overload-induced cardiac remodeling and is required for the cardioprotective effect of sildenafil in vivo.Proapoptotic Rassf1A/Mst1 signaling in cardiac fibroblasts is protective against pressure overload in mice.TGF-beta1 improves cardiac performance via up-regulation of laminin receptor 37/67 in adult ventricular cardiomyocytes.MEF2 transcriptional activity maintains mitochondrial adaptation in cardiac pressure overload.

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P2860

The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy.

http://www.wikidata.org/entity/Q34793636

description

2002 nî lūn-bûn

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2002 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2002 թվականի հուլիսին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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The MEKK1-JNK pathway plays a ...... t mediate cardiac hypertrophy.

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The MEKK1-JNK pathway plays a ...... t mediate cardiac hypertrophy.

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The MEKK1-JNK pathway plays a ...... t mediate cardiac hypertrophy.

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The MEKK1-JNK pathway plays a ...... t mediate cardiac hypertrophy.

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Journal of Clinical Investigation

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Chull Hong

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Dorothy E Vatner

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Gary L Johnson

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Gen Takagi

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Guiping Yang

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Jill Warden

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Jing Liu

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Olivier Montagne

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Qian Wang

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Stephen F Vatner

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P2860

The TNF receptor 1-associated protein TRADD signals cell death and NF-kappa B activation

MEKK1 suppresses oxidative stress-induced apoptosis of embryonic stem cell-derived cardiac myocytes

Signal transduction by the JNK group of MAP kinases

A divergence in the MAP kinase regulatory network defined by MEK kinase and Raf

Cardiac hypertrophy induced by mitogen-activated protein kinase kinase 7, a specific activator for c-Jun NH2-terminal kinase in ventricular muscle cells

Role of MEKK1 in cell survival and activation of JNK and ERK pathways defined by targeted gene disruption

Specific role of the extracellular signal-regulated kinase pathway in angiotensin II-induced cardiac hypertrophy in vitro

Mekk3 is essential for early embryonic cardiovascular development

Double-outlet right ventricle and overriding tricuspid valve reflect disturbances of looping, myocardialization, endocardial cushion differentiation, and apoptosis in TGF-beta(2)-knockout mice

Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy

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2

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Junichi Sadoshima

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12122119

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151048

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