Regulation of cardiac hypertrophic signaling by prolyl isomerase Pin1.

ABSTRACT:

Rationale

Cardiac hypertrophy results from the complex interplay of differentially regulated cascades based on the phosphorylation status of involved signaling molecules. Although numerous critical regulatory kinases and phosphatases have been identified in the myocardium, the intracellular mechanism for temporal regulation of signaling duration and intensity remains obscure. In the nonmyocyte context, control of folding, activity, and stability of proteins is mediated by the prolyl isomerase Pin1, but the role of Pin1 in the heart is unknown.

Objective

To establish the role of Pin1 in the heart.

Methods and results

Here, we show that either genetic deletion or cardiac overexpression of Pin1 blunts hypertrophic responses induced by transaortic constriction and consequ

SUBMITTER: Toko H 

PROVIDER: S-EPMC3742109 | biostudies-literature | 2013 Apr

REPOSITORIES: biostudies-literature