Ventricular expression of a MLC-2v-ras fusion gene induces cardiac hypertrophy and selective diastolic dysfunction in transgenic mice.
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Heart-specific activation of LTK results in cardiac hypertrophy, cardiomyocyte degeneration and gene reprogramming in transgenic miceExpression of a beta-adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted miceSmall G proteins in the cardiovascular system: physiological and pathological aspectsThe Role of ERK1/2 in the Development of Diabetic CardiomyopathyAltered focal adhesion regulation correlates with cardiomyopathy in mice expressing constitutively active rac1Dominant negative Ras attenuates pathological ventricular remodeling in pressure overload cardiac hypertrophyHypoxia-inducible factor-dependent degeneration, failure, and malignant transformation of the heart in the absence of the von Hippel-Lindau proteinMitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.Targeted overexpression of ornithine decarboxylase enhances beta-adrenergic agonist-induced cardiac hypertrophyThe in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathyRole of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy17 beta-estradiol attenuates pressure overload-induced myocardial hypertrophy through regulating caveolin-3 protein in ovariectomized female ratsPak1 as a novel therapeutic target for antihypertrophic treatment in the heartThe ral exchange factor rgl2 promotes cardiomyocyte survival and inhibits cardiac fibrosisA novel putative protein-tyrosine phosphatase contains a BRO1-like domain and suppresses Ha-ras-mediated transformation.Guanine nucleotide exchange factor-like factor (Rlf) induces gene expression and potentiates alpha 1-adrenergic receptor-induced transcriptional responses in neonatal rat ventricular myocytes.Opposing effects of Jun kinase and p38 mitogen-activated protein kinases on cardiomyocyte hypertrophyA Ras-dependent pathway regulates RNA polymerase II phosphorylation in cardiac myocytes: implications for cardiac hypertrophy.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.Meeting Koch's postulates for calcium signaling in cardiac hypertrophy.Hydrogen sulfide anion regulates redox signaling via electrophile sulfhydrationA cardiac-enriched microRNA, miR-378, blocks cardiac hypertrophy by targeting Ras signaling.Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice.Atrial chamber-specific expression of sarcolipin is regulated during development and hypertrophic remodeling.Statins and myocardial remodelling: cell and molecular pathways.On the physiological importance of endoproteolysis of CAAX proteins: heart-specific RCE1 knockout mice develop a lethal cardiomyopathy.Crosstalk between mitogen-activated protein kinases and mitochondria in cardiac diseases: therapeutic perspectivesCardiac hypertrophy and failure: lessons learned from genetically engineered mice.MEK-ERK pathway modulation ameliorates disease phenotypes in a mouse model of Noonan syndrome associated with the Raf1(L613V) mutationCapacity for resolution of Ras-MAPK-initiated early pathogenic myocardial hypertrophy modeled in mice.Cyclosporine attenuates cardiomyocyte hypertrophy induced by RAF1 mutants in Noonan and LEOPARD syndromes.Molecular mechanism of size control in development and human diseases.Ablation of p21-activated kinase-1 in mice promotes isoproterenol-induced cardiac hypertrophy in association with activation of Erk1/2 and inhibition of protein phosphatase 2AA novel pleiotropic effect of statins: prevention of cardiac hypertrophy by cholesterol-independent mechanismsInteractions between Ras1, dMyc, and dPI3K signaling in the developing Drosophila wing.Statins and myocardial hypertrophy.Regional dysfunction correlates with myofiber disarray in transgenic mice with ventricular expression of rasStatin therapy for cardiac hypertrophy and heart failureStatins and the myocardium
P2860
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P2860
Ventricular expression of a MLC-2v-ras fusion gene induces cardiac hypertrophy and selective diastolic dysfunction in transgenic mice.
description
1995 nî lūn-bûn
@nan
1995年の論文
@ja
1995年学术文章
@wuu
1995年学术文章
@zh
1995年学术文章
@zh-cn
1995年学术文章
@zh-hans
1995年学术文章
@zh-my
1995年学术文章
@zh-sg
1995年學術文章
@yue
1995年學術文章
@zh-hant
name
Ventricular expression of a ML ...... ysfunction in transgenic mice.
@en
Ventricular expression of a ML ...... ysfunction in transgenic mice.
@nl
type
label
Ventricular expression of a ML ...... ysfunction in transgenic mice.
@en
Ventricular expression of a ML ...... ysfunction in transgenic mice.
@nl
prefLabel
Ventricular expression of a ML ...... ysfunction in transgenic mice.
@en
Ventricular expression of a ML ...... ysfunction in transgenic mice.
@nl
P2093
P2860
P356
P1476
Ventricular expression of a ML ...... ysfunction in transgenic mice.
@en
P2093
P2860
P304
23173-23178
P356
10.1074/JBC.270.39.23173
P407
P577
1995-09-01T00:00:00Z