Pathological cardiac hypertrophy involves auto/paracrine mediators acting through Gq/11-coupled receptors. A novel signaling route stimulated by βγ-subunits of Gq/11 results in the autophosphorylation of ERK1/2 on a new site and the nuclear retention of ERK1/2, thereby activating hypertrophic gene programs
The increase in protein activity and upregulation of G-protein coupled receptor kinase 2 (GRK2) is a...
The terminally differentiated adult cardiac myocyte cannot undergo cellular division. Growth of the ...
The heart initially compensates for hypertension-mediated pressure overload by enhancing its contrac...
Pathological cardiac hypertrophy involves auto/paracrine mediators acting through Gq/11-coupled rece...
Pathological cardiac hypertrophy involves auto/paracrine mediators acting through G(q/11)-coupled re...
Cardiac hypertrophy is an adaptive and compensatory mechanism preserving cardiac output during detri...
Cardiac hypertrophy is the result of increased myocardial cell size responding to an increased workl...
Background The role of the Galphaq/11-mediated signal transduction pathway in angiotensin II ( Ang I...
<div><p>The increase in protein activity and upregulation of G-protein coupled receptor kinase 2 (GR...
RATIONALE: Mitogen-activated protein kinase (MAPK) pathways provide a critical connection between ex...
AbstractMitogen-activated protein kinases (MAPKs) are involved in the regulation of cardiac hypertro...
Cardiac hypertrophy is a well-established risk factor for cardiovascular morbidity and mortality. Ac...
Heart failure is a leading cause of death that develops subsequent to deleterious hyper-trophic card...
AbstractOBJECTIVESUsing a transgenic mouse model of myocardial-targeted overexpression of the wild-t...
Hormones and neurotransmitters may mediate common responses through receptors that couple to the sam...
The increase in protein activity and upregulation of G-protein coupled receptor kinase 2 (GRK2) is a...
The terminally differentiated adult cardiac myocyte cannot undergo cellular division. Growth of the ...
The heart initially compensates for hypertension-mediated pressure overload by enhancing its contrac...
Pathological cardiac hypertrophy involves auto/paracrine mediators acting through Gq/11-coupled rece...
Pathological cardiac hypertrophy involves auto/paracrine mediators acting through G(q/11)-coupled re...
Cardiac hypertrophy is an adaptive and compensatory mechanism preserving cardiac output during detri...
Cardiac hypertrophy is the result of increased myocardial cell size responding to an increased workl...
Background The role of the Galphaq/11-mediated signal transduction pathway in angiotensin II ( Ang I...
<div><p>The increase in protein activity and upregulation of G-protein coupled receptor kinase 2 (GR...
RATIONALE: Mitogen-activated protein kinase (MAPK) pathways provide a critical connection between ex...
AbstractMitogen-activated protein kinases (MAPKs) are involved in the regulation of cardiac hypertro...
Cardiac hypertrophy is a well-established risk factor for cardiovascular morbidity and mortality. Ac...
Heart failure is a leading cause of death that develops subsequent to deleterious hyper-trophic card...
AbstractOBJECTIVESUsing a transgenic mouse model of myocardial-targeted overexpression of the wild-t...
Hormones and neurotransmitters may mediate common responses through receptors that couple to the sam...
The increase in protein activity and upregulation of G-protein coupled receptor kinase 2 (GRK2) is a...
The terminally differentiated adult cardiac myocyte cannot undergo cellular division. Growth of the ...
The heart initially compensates for hypertension-mediated pressure overload by enhancing its contrac...
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