Ontology highlight
ABSTRACT: Rationale
G protein-coupled receptor kinases (GRKs) are dynamic regulators of cellular signaling. GRK5 is highly expressed within myocardium and is upregulated in heart failure. Although GRK5 is a critical regulator of cardiac G protein-coupled receptor signaling, recent data has uncovered noncanonical activity of GRK5 within nuclei that plays a key role in pathological hypertrophy. Targeted cardiac elevation of GRK5 in mice leads to exaggerated hypertrophy and early heart failure after transverse aortic constriction (TAC) because of GRK5 nuclear accumulation.Objective
In this study, we investigated the role of GRK5 in physiological, swimming-induced hypertrophy (SIH).Methods and results
Cardiac-specific GRK5 transgenic mice and nontransgenic littermate control mice
SUBMITTER: Traynham CJ
PROVIDER: S-EPMC4825669 | biostudies-literature | 2015 Dec
REPOSITORIES: biostudies-literature