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Transgenic Galphaq overexpression induces cardiac contractile failure in mice

Transgenic Galphaq overexpression induces cardiac contractile failure in mice

http://www.wikidata.org/entity/Q36302328

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Protein kinase cascades in the regulation of cardiac hypertrophy Intrinsic-mediated caspase activation is essential for cardiomyocyte hypertrophy Transient cardiac expression of constitutively active Galphaq leads to hypertrophy and dilated cardiomyopathy by calcineurin-dependent and independent pathways Deregulation of RGS2 in cardiovascular diseases Scaffold Proteins Regulating Extracellular Regulated Kinase Function in Cardiac Hypertrophy and Disease An experimental approach to study the function of mitochondria in cardiomyopathy Gap junction modulation and its implications for heart function Molecular mechanisms that differentiate apoptosis from programmed necrosis Prospects for gene transfer for clinical heart failure Nuclear compartmentalization of α1-adrenergic receptor signaling in adult cardiac myocytes Gene therapy targets in heart failure: the path to translation The cell biology of disease: cellular mechanisms of cardiomyopathy."Freeze, Don't Move": How to Arrest a Suspect in Heart Failure - A Review on Available GRK2 Inhibitors PKCepsilon activation induces dichotomous cardiac phenotypes and modulates PKCepsilon-RACK interactions and RACK expression Protein kinase C epsilon induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism Fibroblast growth factor-2 mediates pressure-induced hypertrophic response Targeted overexpression of ornithine decarboxylase enhances beta-adrenergic agonist-induced cardiac hypertrophy Acyloxy nitroso compounds inhibit LIF signaling in endothelial cells and cardiac myocytes: evidence that STAT3 signaling is redox-sensitive Effects of G-protein mutations on skin color The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy PKC alpha regulates the hypertrophic growth of cardiomyocytes through extracellular signal-regulated kinase1/2 (ERK1/2)Akt-mediated cardiomyocyte survival pathways are compromised by G alpha q-induced phosphoinositide 4,5-bisphosphate depletion Regulation of myocardial function by histidine-rich, calcium-binding protein Embryonic cardiomyocyte hypoplasia and craniofacial defects in G alpha q/G alpha 11-mutant mice.Phospholipase Cε hydrolyzes perinuclear phosphatidylinositol 4-phosphate to regulate cardiac hypertrophy Serotonin 2B receptor is required for heart development Regulator of G protein signaling 2 mediates cardiac compensation to pressure overload and antihypertrophic effects of PDE5 inhibition in mice Deletion of low molecular weight protein tyrosine phosphatase (Acp1) protects against stress-induced cardiomyopathy.Conditional expression of a Gi-coupled receptor causes ventricular conduction delay and a lethal cardiomyopathy.Cardiac-specific genetic inhibition of nuclear factor-κB prevents right ventricular hypertrophy induced by monocrotaline.Deep mRNA sequencing for in vivo functional analysis of cardiac transcriptional regulators: application to Galphaq.MicroRNA-133a protects against myocardial fibrosis and modulates electrical repolarization without affecting hypertrophy in pressure-overloaded adult hearts Cytosolic H2O2 mediates hypertrophy, apoptosis, and decreased SERCA activity in mice with chronic hemodynamic overload.Cardiac-specific overexpression of RhoA results in sinus and atrioventricular nodal dysfunction and contractile failure.Regulation of cardiac hypertrophy in vivo by the stress-activated protein kinases/c-Jun NH(2)-terminal kinases.RGS4 causes increased mortality and reduced cardiac hypertrophy in response to pressure overload.Heterotrimeric G proteins in heart disease.PDE5 inhibitor efficacy is estrogen dependent in female heart disease.Meeting Koch's postulates for calcium signaling in cardiac hypertrophy.MEKK1 is essential for cardiac hypertrophy and dysfunction induced by Gq.

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Transgenic Galphaq overexpression induces cardiac contractile failure in mice

http://www.wikidata.org/entity/Q36302328

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1997 nî lūn-bûn

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1997年の論文

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1997年学术文章

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1997年学术文章

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1997年学术文章

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1997年学术文章

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1997年學術文章

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1997年學術文章

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1997年學術文章

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name

Transgenic Galphaq overexpression induces cardiac contractile failure in mice

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Transgenic Galphaq overexpression induces cardiac contractile failure in mice

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type

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Transgenic Galphaq overexpression induces cardiac contractile failure in mice

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Transgenic Galphaq overexpression induces cardiac contractile failure in mice

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prefLabel

Transgenic Galphaq overexpression induces cardiac contractile failure in mice

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Transgenic Galphaq overexpression induces cardiac contractile failure in mice

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Proceedings of the National Academy of Sciences of the United States of America

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Transgenic Galphaq overexpression induces cardiac contractile failure in mice

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D D D'Angelo

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G P Boivin

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G W Dorn

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Y Sakata

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P2860

Nuclear localization and regulation of erk- and rsk-encoded protein kinases

G protein diversity: a distinct class of alpha subunits is present in vertebrates and invertebrates

Differential regulation of protein kinase C isoforms in isolated neonatal and adult rat cardiomyocytes

Characterization of protein kinase C isotype expression in adult rat heart. Protein kinase C-epsilon is a major isotype present, and it is activated by phorbol esters, epinephrine, and endothelin

Regulation of cardiac gene expression during myocardial growth and hypertrophy: molecular studies of an adaptive physiologic response

Protooncogene induction and reprogramming of cardiac gene expression produced by pressure overload

Differential activation of protein kinase C isoforms by endothelin-1 and phenylephrine and subsequent stimulation of p42 and p44 mitogen-activated protein kinases in ventricular myocytes cultured from neonatal rat hearts

Cardiac function in mice overexpressing the beta-adrenergic receptor kinase or a beta ARK inhibitor

Autocrine release of angiotensin II mediates stretch-induced hypertrophy of cardiac myocytes in vitro

A mouse model of familial hypertrophic cardiomyopathy

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