Adrenergic receptor stimulation of the mitogen-activated protein kinase cascade and cardiac hypertrophy.
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Phosphorylation and activation of mitogen- and stress-activated protein kinase-1 in adult rat cardiac myocytes by G-protein-coupled receptor agonists requires both extracellular-signal-regulated kinase and p38 mitogen-activated protein kinaseCardiac hypertrophy with preserved contractile function after selective deletion of GLUT4 from the heartNew advances in beta-blocker therapy in heart failureTargeted overexpression of ornithine decarboxylase enhances beta-adrenergic agonist-induced cardiac hypertrophyRole of protein kinase C in the signal pathways that link Na+/K+-ATPase to ERK1/2Obesity is associated with impaired ventricular protein kinase C-MAP kinase signaling and altered ANP mRNA expression in the heart of adult Zucker ratsMaximal beta3-adrenergic regulation of lipolysis involves Src and epidermal growth factor receptor-dependent ERK1/2 activation.AFos dissociates cardiac myocyte hypertrophy and expression of the pathological gene programDeactivation of the sympathetic nervous system in patients with chronic congestive heart failure.Monophosphothreonyl extracellular signal-regulated kinases 1 and 2 (ERK1/2) are formed endogenously in intact cardiac myocytes and are enzymically active.Melatonin protects against myocardial hypertrophy induced by lipopolysaccharide.Cardiac hypertrophy induced by sustained beta-adrenoreceptor activation: pathophysiological aspects.Role of mitogen-activated protein kinase in cardiac hypertrophy and heart failureβ-adrenergic receptor responsiveness in aging heart and clinical implications.Beta-adrenergic receptors, from their discovery and characterization through their manipulation to beneficial clinical application.The transcriptional co-activators CBP and p300 are activated via phenylephrine through the p42/p44 MAPK cascade.β-Adrenergic signaling stimulates osteoclastogenesis via reactive oxygen species.The C-terminal domain of c-fos is required for activation of an AP-1 site specific for jun-fos heterodimers.Beta 3- and alpha1-adrenergic Erk1/2 activation is Src- but not Gi-mediated in Brown adipocytes.The role of Ca2+/calmodulin-dependent protein kinase II and calcineurin in TNF-α-induced myocardial hypertrophy.Mitogen-activated protein kinase phosphatase 1 inhibits the stimulation of gene expression by hypertrophic agonists in cardiac myocytes.Activation of mitogen-activated protein kinases (p38-MAPKs, SAPKs/JNKs and ERKs) by the G-protein-coupled receptor agonist phenylephrine in the perfused rat heart.Alterations of cardiac ERK1/2 expression and activity due to volume overload were attenuated by the blockade of RAS.Signal-transducing function of Na+-K+-ATPase is essential for ouabain's effect on [Ca2+]i in rat cardiac myocytes.Beta-adrenergic receptor-mediated DNA synthesis in cardiac fibroblasts is dependent on transactivation of the epidermal growth factor receptor and subsequent activation of extracellular signal-regulated kinases.Alpha(1)-AR-induced positive inotropic response in heart is dependent on myosin light chain phosphorylation.delta-Opioid receptor stimulation enhances the growth of neonatal rat ventricular myocytes via the extracellular signal-regulated kinase pathway.Cross-talk between alpha(1B)-adrenergic receptor (alpha(1B)AR) and interleukin-6 (IL-6) signaling pathways. Activation of alpha(1b)AR inhibits il-6-activated STAT3 in hepatic cells by a p42/44 mitogen-activated protein kinase-dependent mechanism.The induction of cardiac ornithine decarboxylase by β2 -adrenergic agents is associated with calcium channels and phosphorylation of ERK1/2.Different roles of alpha1-adrenoceptor subtypes in mediating cardiomyocyte protein synthesis in neonatal rats.Strain-dependent beta-adrenergic receptor function influences myocardial responses to isoproterenol stimulation in mice.p38 mitogen-activated protein kinase (MAPK) is activated by noradrenaline and serves a cardioprotective role, whereas adrenaline induces p38 MAPK dephosphorylation.The MEKK-JNK pathway is stimulated by alpha1-adrenergic receptor and ras activation and is associated with in vitro and in vivo cardiac hypertrophy.Phosphodiesterase inhibition promotes the transition from compensated hypertrophy to cardiac dilatation in rats.A beta1-adrenergic receptor CaM kinase II-dependent pathway mediates cardiac myocyte fetal gene induction.Oncogenic src, raf, and ras stimulate a hypertrophic pattern of gene expression and increase cell size in neonatal rat ventricular myocytes.Investigating β-adrenergic-induced cardiac hypertrophy through computational approach: classical and non-classical pathways.Multiple signal transduction pathways link Na+/K+-ATPase to growth-related genes in cardiac myocytes. The roles of Ras and mitogen-activated protein kinases.Activation pattern of MAPK signaling in the hearts of trained and untrained rats following a single bout of exercise.Natriuretic peptide receptor-C-mediated attenuation of vascular smooth muscle cell hypertrophy involves Gqα/PLCβ1 proteins and ROS-associated signaling.
P2860
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P2860
Adrenergic receptor stimulation of the mitogen-activated protein kinase cascade and cardiac hypertrophy.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年論文
@yue
1996年論文
@zh-hant
1996年論文
@zh-hk
1996年論文
@zh-mo
1996年論文
@zh-tw
1996年论文
@wuu
1996年论文
@zh
1996年论文
@zh-cn
name
Adrenergic receptor stimulatio ...... scade and cardiac hypertrophy.
@en
Adrenergic receptor stimulatio ...... scade and cardiac hypertrophy.
@nl
type
label
Adrenergic receptor stimulatio ...... scade and cardiac hypertrophy.
@en
Adrenergic receptor stimulatio ...... scade and cardiac hypertrophy.
@nl
prefLabel
Adrenergic receptor stimulatio ...... scade and cardiac hypertrophy.
@en
Adrenergic receptor stimulatio ...... scade and cardiac hypertrophy.
@nl
P2093
P2860
P356
P1433
P1476
Adrenergic receptor stimulatio ...... scade and cardiac hypertrophy.
@en
P2093
J Gillespie-Brown
M B Andersson
P E Glennon
P H Sugden
S J Fuller
P2860
P304
P356
10.1042/BJ3140115
P407
P478
314 ( Pt 1)
P577
1996-02-01T00:00:00Z