Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH(2)-terminal kinases. - Wikidata - awgldk - TriplyDB

Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH(2)-terminal kinases.

Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH(2)-terminal kinases.

http://www.wikidata.org/entity/Q33857393

about

Helix-loop-helix protein p8, a transcriptional regulator required for cardiomyocyte hypertrophy and cardiac fibroblast matrix metalloprotease induction Stabilization of beta-catenin by a Wnt-independent mechanism regulates cardiomyocyte growth Complete inhibition of anisomycin and UV radiation but not cytokine induced JNK and p38 activation by an aryl-substituted dihydropyrrolopyrazole quinoline and mixed lineage kinase 7 small interfering RNA Dominant negative Ras attenuates pathological ventricular remodeling in pressure overload cardiac hypertrophy Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.Specific role of the extracellular signal-regulated kinase pathway in angiotensin II-induced cardiac hypertrophy in vitro c-Jun N-terminal kinase-interacting protein 1 inhibits gene expression in response to hypertrophic agonists in neonatal rat ventricular myocytes Targeted inhibition of calcineurin attenuates cardiac hypertrophy in vivo Pressure-independent enhancement of cardiac hypertrophy in natriuretic peptide receptor A-deficient mice Telomerase reverse transcriptase promotes cardiac muscle cell proliferation, hypertrophy, and survival Tachycardia-induced heart failure does not alter myocardial P-glycoprotein expression.MEKK1 is essential for cardiac hypertrophy and dysfunction induced by Gq.MEK and the inhibitors: from bench to bedside.Augmented cardiac hypertrophy in response to pressure overload in mice lacking ELTD1.Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectives Role of endothelin in the induction of cardiac hypertrophy in vitro.G protein-coupled receptor signalling in in vivo cardiac overload.Calcineurin and hypertrophic heart disease: novel insights and remaining questions.The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy.p21(CIP1) Controls proliferating cell nuclear antigen level in adult cardiomyocytes Emerging therapeutic targets in chronic heart failure: part I.Emerging therapeutic targets in chronic heart failure: part II.Garlic Oil Alleviates MAPKs- and IL-6-mediated Diabetes-related Cardiac Hypertrophy in STZ-induced DM Rats JNK modulates FOXO3a for the expression of the mitochondrial death and mitophagy marker BNIP3 in pathological hypertrophy and in heart failure.Tomoregulin-1 prevents cardiac hypertrophy after pressure overload in mice by inhibiting TAK1-JNK pathways.Phosphoinositide 3-kinase(p110alpha) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy.Glycogen synthase kinase-3beta is a negative regulator of cardiomyocyte hypertrophy Electrical and mechanical stimulation of cardiac cells and tissue constructs.The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth.Mitogen-activated protein kinases in heart development and diseases Regulator of G protein signalling 14 attenuates cardiac remodelling through the MEK-ERK1/2 signalling pathway.Stretch-induced regulation of angiotensinogen gene expression in cardiac myocytes and fibroblasts: opposing roles of JNK1/2 and p38alpha MAP kinases Deactivation of peroxisome proliferator-activated receptor-alpha during cardiac hypertrophic growth Role of mitogen-activated protein kinase in cardiac hypertrophy and heart failure Catecholamine-induced cardiac hypertrophy in rats is associated with the activation of p70 kinase and c-Jun NH(2)-terminal kinase 2.Designing heart performance by gene transfer.Cdc42 is an antihypertrophic molecular switch in the mouse heart.Role of the Wnt-Frizzled system in cardiac pathophysiology: a rapidly developing, poorly understood area with enormous potential.Signaling pathways and late-onset gene induction associated with renal mesangial cell hypertrophy.Wnt Signaling in Cardiac Disease.

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P2860

Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH(2)-terminal kinases.

http://www.wikidata.org/entity/Q33857393

description

1999 nî lūn-bûn

@nan

1999 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

1999 թվականի օգոստոսին հրատարակված գիտական հոդված

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1999年の論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年論文

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1999年论文

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name

Regulation of cardiac hypertro ...... /c-Jun NH(2)-terminal kinases.

@ast

Regulation of cardiac hypertro ...... /c-Jun NH(2)-terminal kinases.

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type

label

Regulation of cardiac hypertro ...... /c-Jun NH(2)-terminal kinases.

@ast

Regulation of cardiac hypertro ...... /c-Jun NH(2)-terminal kinases.

@en

prefLabel

Regulation of cardiac hypertro ...... /c-Jun NH(2)-terminal kinases.

@ast

Regulation of cardiac hypertro ...... /c-Jun NH(2)-terminal kinases.

@en

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Journal of Clinical Investigation

P1476

Regulation of cardiac hypertro ...... /c-Jun NH(2)-terminal kinases.

@en

P2093

Choukroun G

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Force T

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Fry S

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Guerrero JL

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Hajjar R

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Haq S

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Picard M

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Rosenzweig A

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del Monte F

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P2860

JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain

Transient cardiac expression of constitutively active Galphaq leads to hypertrophy and dilated cardiomyopathy by calcineurin-dependent and independent pathways

Structure of the DNA-binding domains from NFAT, Fos and Jun bound specifically to DNA

Transcription factors of the NFAT family: regulation and function

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

A calcineurin-dependent transcriptional pathway for cardiac hypertrophy

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

MAP kinase- and Rho-dependent signals interact to regulate gene expression but not actin morphology in cardiac muscle cells

The small GTP-binding proteins Rac1 and Cdc42 regulate the activity of the JNK/SAPK signaling pathway

The stress-activated protein kinase subfamily of c-Jun kinases

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391-398

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scholarly article

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10.1172/JCI6350

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4

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104

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1999-08-01T00:00:00Z

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10449431

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408523

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