Protein kinase cascades in the regulation of cardiac hypertrophy - Test2 - elhamkhani - TriplyDB

Protein kinase cascades in the regulation of cardiac hypertrophy

Protein kinase cascades in the regulation of cardiac hypertrophy

http://www.wikidata.org/entity/Q24518494

about

Helix-loop-helix protein p8, a transcriptional regulator required for cardiomyocyte hypertrophy and cardiac fibroblast matrix metalloprotease induction Signaling effectors underlying pathologic growth and remodeling of the heart Targeting G protein coupled receptor-related pathways as emerging molecular therapies Mechanisms of altered Ca²⁺ handling in heart failure Repair Injured Heart by Regulating Cardiac Regenerative Signals The critical role of Akt in cardiovascular function The beta-catenin/T-cell factor/lymphocyte enhancer factor signaling pathway is required for normal and stress-induced cardiac hypertrophy Myosin regulatory light chain phosphorylation attenuates cardiac hypertrophy Cardiac myosin light chain kinase is necessary for myosin regulatory light chain phosphorylation and cardiac performance in vivo Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.Cardiac tissue-restricted deletion of plakoglobin results in progressive cardiomyopathy and activation of {beta}-catenin signaling Computer-aided targeting of the PI3K/Akt/mTOR pathway: toxicity reduction and therapeutic opportunities Effect of hypoxia and aging on PKC delta-mediated SC-35 phosphorylation in rat myocardial tissue Curcumin prevents and reverses murine cardiac hypertrophy Repression of miR-142 by p300 and MAPK is required for survival signalling via gp130 during adaptive hypertrophy Induction of manganese superoxide dismutase by nuclear translocation and activation of SIRT1 promotes cell survival in chronic heart failure Nuclear localization of protein kinase C-alpha induces thyroid hormone receptor-alpha1 expression in the cardiomyocyte Activating transcription factor 3 deficiency promotes cardiac hypertrophy, dysfunction, and fibrosis induced by pressure overload Inpp5f is a polyphosphoinositide phosphatase that regulates cardiac hypertrophic responsiveness Regulator of G protein signaling 2 mediates cardiac compensation to pressure overload and antihypertrophic effects of PDE5 inhibition in mice Skeletal muscle contractile protein function is preserved in human heart failure Glucose regulation of load-induced mTOR signaling and ER stress in mammalian heart.PARP-inhibitor treatment prevents hypertension induced cardiac remodeling by favorable modulation of heat shock proteins, Akt-1/GSK-3β and several PKC isoforms.CapZ dynamics are altered by endothelin-1 and phenylephrine via PIP2- and PKC-dependent mechanisms.Myocyte-restricted focal adhesion kinase deletion attenuates pressure overload-induced hypertrophy Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction.Cardiomyocyte PDGFR-beta signaling is an essential component of the mouse cardiac response to load-induced stress.Melusin gene (ITGB1BP2) nucleotide variations study in hypertensive and cardiopathic patients.Mammalian target of rapamycin is a critical regulator of cardiac hypertrophy in spontaneously hypertensive rats.MicroRNA-133a protects against myocardial fibrosis and modulates electrical repolarization without affecting hypertrophy in pressure-overloaded adult hearts Oxidative Stress-Induced Afterdepolarizations and Protein Kinase C Signaling MAFbx/Atrogin-1 is required for atrophic remodeling of the unloaded heart.Genome-wide expression patterns in physiological cardiac hypertrophy.Sirtuin1-p53, forkhead box O3a, p38 and post-infarct cardiac remodeling in the spontaneously diabetic Goto-Kakizaki rat Receptor interacting protein 3 suppresses vascular smooth muscle cell growth by inhibition of the phosphoinositide 3-kinase-Akt axis.Phosphorylation of TRPC6 channels at Thr69 is required for anti-hypertrophic effects of phosphodiesterase 5 inhibition Molecular Signals Elicited by GPCR Agonists in Hypertension, Cardiovascular Remodeling: Are MMPs and ADAMs Elusive Therapeutic Targets?Etanercept protects rat cardiomyocytes against hypertrophy by regulating inflammatory cytokines secretion and cell apoptosis Glycogen synthase kinase-3beta regulates post-myocardial infarction remodeling and stress-induced cardiomyocyte proliferation in vivo Motility, survival, and proliferation.

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P2860

Protein kinase cascades in the regulation of cardiac hypertrophy

http://www.wikidata.org/entity/Q24518494

description

2005 nî lūn-bûn

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2005 թուականի Մարտին հրատարակուած գիտական յօդուած

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2005 թվականի մարտին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年论文

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name

Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Journal of Clinical Investigation

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Protein kinase cascades in the regulation of cardiac hypertrophy

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Gerald W Dorn

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Thomas Force

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P2860

Restoration of contractile function in isolated cardiomyocytes from failing human hearts by gene transfer of SERCA2a.

Protein kinase Calpha negatively regulates systolic and diastolic function in pathological hypertrophy

mTOR controls cell cycle progression through its cell growth effectors S6K1 and 4E-BP1/eukaryotic translation initiation factor 4E

GSK-3: tricks of the trade for a multi-tasking kinase

Cardiotrophic effects of protein kinase C epsilon: analysis by in vivo modulation of PKCepsilon translocation

Transgenic overexpression of constitutively active protein kinase C epsilon causes concentric cardiac hypertrophy

Loss of a gp130 cardiac muscle cell survival pathway is a critical event in the onset of heart failure during biomechanical stress

Stabilization of beta-catenin by a Wnt-independent mechanism regulates cardiomyocyte growth

PKCepsilon activation induces dichotomous cardiac phenotypes and modulates PKCepsilon-RACK interactions and RACK expression

The genetic basis for cardiomyopathy: from mutation identification to mechanistic paradigms

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405501

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10.1172/JCI24178

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3

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115

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7969699

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15765134

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1052008

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