RGS4 causes increased mortality and reduced cardiac hypertrophy in response to pressure overload. - Wikidata - awgldk - TriplyDB

RGS4 causes increased mortality and reduced cardiac hypertrophy in response to pressure overload.

RGS4 causes increased mortality and reduced cardiac hypertrophy in response to pressure overload.

http://www.wikidata.org/entity/Q33857945

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Generation and characterization of Rgs4 mutant mice The aorta and heart differentially express RGS (regulators of G-protein signalling) proteins that selectively regulate sphingosine 1-phosphate, angiotensin II and endothelin-1 signalling Deregulation of RGS2 in cardiovascular diseases Synthetic heterovalent inhibitors targeting recognition E3 components of the N-end rule pathway PGC-1alpha deficiency causes multi-system energy metabolic derangements: muscle dysfunction, abnormal weight control and hepatic steatosis Regulators of G-protein signaling in the heart and their potential as therapeutic targets.Beta-catenin overexpression reduces myocardial infarct size through differential effects on cardiomyocytes and cardiac fibroblasts Statins as antioxidant therapy for preventing cardiac myocyte hypertrophy The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy Activator of G protein signaling 8 (AGS8) is required for hypoxia-induced apoptosis of cardiomyocytes: role of G betagamma and connexin 43 (CX43)Inactivation of focal adhesion kinase in cardiomyocytes promotes eccentric cardiac hypertrophy and fibrosis in mice.Regulator of G protein signaling 2 mediates cardiac compensation to pressure overload and antihypertrophic effects of PDE5 inhibition in mice PDGF-dependent regulation of regulator of G protein signaling-5 expression and vascular smooth muscle cell functionality.Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction.Impaired contractile function and calcium handling in hearts of cardiac-specific calcineurin b1-deficient mice Rescue of cardiomyopathy in peroxisome proliferator-activated receptor-alpha transgenic mice by deletion of lipoprotein lipase identifies sources of cardiac lipids and peroxisome proliferator-activated receptor-alpha activators Adiponectin-mediated modulation of hypertrophic signals in the heart Human cord blood progenitors with high aldehyde dehydrogenase activity improve vascular density in a model of acute myocardial infarction.RGS4 and RGS5 are in vivo substrates of the N-end rule pathway An RGS4-mediated phenotypic switch of bronchial smooth muscle cells promotes fixed airway obstruction in asthma A neurostimulant para-chloroamphetamine inhibits the arginylation branch of the N-end rule pathway.Hypertension and prolonged vasoconstrictor signaling in RGS2-deficient mice.The role of the Grb2-p38 MAPK signaling pathway in cardiac hypertrophy and fibrosis.Regulation of GPCR signaling in hypertension.A critical role for PPARalpha-mediated lipotoxicity in the pathogenesis of diabetic cardiomyopathy: modulation by dietary fat content.Cardiomyocyte-specific deficiency of ketone body metabolism promotes accelerated pathological remodeling.Hypoxic induction of the regulator of G-protein signalling 4 gene is mediated by the hypoxia-inducible factor pathway.The critical role of Astragalus polysaccharides for the improvement of PPARα [ correction of PPRAα]-mediated lipotoxicity in diabetic cardiomyopathy Dual roles of modulatory calcineurin-interacting protein 1 in cardiac hypertrophy.14-3-3 proteins block apoptosis and differentially regulate MAPK cascades Chronic inhibition of pyruvate dehydrogenase in heart triggers an adaptive metabolic response.Transcriptional coactivators PGC-1alpha and PGC-lbeta control overlapping programs required for perinatal maturation of the heart Identification of transcription factor E3 (TFE3) as a receptor-independent activator of Gα16: gene regulation by nuclear Gα subunit and its activator.Vascular failure: a hypothesis.Inhibition of hypertrophy is a good therapeutic strategy in ventricular pressure overload.A novel mouse model of lipotoxic cardiomyopathy.A finer tuning of G-protein signaling through regulated control of RGS proteins.GLUT4, GLUT1, and GLUT8 are the dominant GLUT transcripts expressed in the murine left ventricle.R4 RGS proteins: regulation of G-protein signaling and beyond.Developmental adaptation of the mouse cardiovascular system to elastin haploinsufficiency

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P2860

RGS4 causes increased mortality and reduced cardiac hypertrophy in response to pressure overload.

http://www.wikidata.org/entity/Q33857945

description

1999 nî lūn-bûn

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1999 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

1999 թվականի սեպտեմբերին 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

RGS4 causes increased mortalit ...... response to pressure overload.

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RGS4 causes increased mortalit ...... response to pressure overload.

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RGS4 causes increased mortalit ...... response to pressure overload.

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RGS4 causes increased mortalit ...... response to pressure overload.

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RGS4 causes increased mortalit ...... response to pressure overload.

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RGS4 causes increased mortalit ...... response to pressure overload.

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Journal of Clinical Investigation

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RGS4 causes increased mortalit ...... response to pressure overload.

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P2093

A J Muslin

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A Kovacs

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C Weinheimer

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D P Kelly

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J H Rogers

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K J Blumer

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M Courtois

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P Tamirisa

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P2860

Inhibition of G-protein-mediated MAP kinase activation by a new mammalian gene family

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

Expression of a beta-adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted mice

Structure of RGS4 bound to AlF4--activated G(i alpha1): stabilization of the transition state for GTP hydrolysis

Regulation of polyphosphoinositide-specific phospholipase C activity by purified Gq.

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

Interaction of human retinal RGS with G-protein alpha-subunits

EGL-10 regulates G protein signaling in the C. elegans nervous system and shares a conserved domain with many mammalian proteins

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

GAIP and RGS4 are GTPase-activating proteins for the Gi subfamily of G protein alpha subunits

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567-576

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10.1172/JCI6713

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5

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104

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12811986

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10487771

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408537

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