Ontology highlight
ABSTRACT: Rationale
Cardiac myocyte hypertrophy is the main compensatory response to chronic stress on the heart. p90 ribosomal S6 kinase (RSK) family members are effectors for extracellular signal-regulated kinases that induce myocyte growth. Although increased RSK activity has been observed in stressed myocytes, the functions of individual RSK family members have remained poorly defined, despite being potential therapeutic targets for cardiac disease.Objective
To demonstrate that type 3 RSK (RSK3) is required for cardiac myocyte hypertrophy.Methods and results
RSK3 contains a unique N-terminal domain that is not conserved in other RSK family members. We show that this domain mediates the regulated binding of RSK3 to the muscle A-kinase anchoring protein scaffold, defining a
SUBMITTER: Li J
PROVIDER: S-EPMC3537852 | biostudies-literature | 2013 Jan
REPOSITORIES: biostudies-literature