Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
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Kruppel-like factor 15 is a regulator of cardiomyocyte hypertrophy.Neuregulins promote survival and growth of cardiac myocytes. Persistence of ErbB2 and ErbB4 expression in neonatal and adult ventricular myocytesExpression cloning of cardiotrophin 1, a cytokine that induces cardiac myocyte hypertrophyAPEG-1, a novel gene preferentially expressed in aortic smooth muscle cells, is down-regulated by vascular injuryDisappearance of cyclin A correlates with permanent withdrawal of cardiomyocytes from the cell cycle in human and rat heartsInhibition of norepinephrine-induced cardiac hypertrophy in s100beta transgenic mice.Electrical stimulation of neonatal cardiac myocytes activates the NFAT3 and GATA4 pathways and up-regulates the adenylosuccinate synthetase 1 geneSmall molecule inhibitors targeting activator protein 1 (AP-1).The AP-1 transcription factor c-Jun prevents stress-imposed maladaptive remodeling of the heart.Multifaceted roles of miR-1s in repressing the fetal gene program in the heartSphingosine 1-Phosphate Receptors: Do They Have a Therapeutic Potential in Cardiac Fibrosis?Distinct functions of junD in cardiac hypertrophy and heart failureDifferential regulation of natriuretic peptide receptor messenger RNAs during the development of cardiac hypertrophy in the rat.The vascular smooth muscle alpha-actin gene is reactivated during cardiac hypertrophy provoked by load.Molecular approaches to cardiac development and hypertrophy.Molecular genetics and genomics of heart failure.fos/jun repression of cardiac-specific transcription in quiescent and growth-stimulated myocytes is targeted at a tissue-specific cis element.Role of transiently altered sarcolemmal membrane permeability and basic fibroblast growth factor release in the hypertrophic response of adult rat ventricular myocytes to increased mechanical activity in vitroExpression and functional assessment of a truncated cardiac troponin T that causes hypertrophic cardiomyopathy. Evidence for a dominant negative action.Transgenic expression of replication-restricted enteroviral genomes in heart muscle induces defective excitation-contraction coupling and dilated cardiomyopathy.S100B: a multifunctional role in cardiovascular pathophysiology.Cytokines and cardiac hypertrophy: roles of angiotensin II and basic fibroblast growth factor.Regulation of the mRNA-binding protein AUF1 by activation of the beta-adrenergic receptor signal transduction pathway.Cardiac actions of fibroblast growth factor 23.Control of cardiac gene transcription by fibroblast growth factors.Adaptation of cardiac structure by mechanical feedback in the environment of the cell: a model study.TGF-beta1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II.Chromatin immunoprecipitation of adult murine cardiomyocytes.The pathology of cardiac ischaemia: cellular and molecular aspects.Stimulation of proliferative events in the adult amphibian cardiac myocyte.Molecular analysis of TGF beta signal transduction. Dominant-inhibitory mutations of the type II and type I TGF beta receptor.Regulation of basic fibroblast growth factor (bFGF) and FGF receptors in the heart.Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: potential involvement of an autocrine/paracrine mechanism.Regulation of rat cardiac myocyte growth by a neuronal factor secreted by PC12 cells.Matrix remodelling in dilated cardiomyopathy entails the occurrence of oncofetal fibronectin molecular variants.Effects of an AT1 receptor antagonist, an ACE inhibitor and a calcium channel antagonist on cardiac gene expressions in hypertensive rats.Mechanical stretch induces hypertrophic responses in cardiac myocytes of angiotensin II type 1a receptor knockout mice.Constitutively active mutants of the alpha(1a)- and the alpha(1b)-adrenergic receptor subtypes reveal coupling to different signaling pathways and physiological responses in rat cardiac myocytes.Intracellular and Extracellular Effects of S100B in the Cardiovascular Response to Disease.TGF-beta(1) and prepro-ANP mRNAs are differentially regulated in exercise-induced cardiac hypertrophy.
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Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on January 1991
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
@en
Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
@nl
type
label
Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
@en
Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
@nl
prefLabel
Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
@en
Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
@nl
P1476
Growth factors, proto-oncogenes, and plasticity of the cardiac phenotype.
@en
P2093
Schneider MD
P304
P356
10.1146/ANNUREV.PH.53.030191.001143
P577
1991-01-01T00:00:00Z