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Cardiovascular Research Advance Access first published online on March 11, 2009
This version [Corrected Proof] published online on April 2, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp087
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Nuclear and mitochondrial signalling Akts in cardiomyocytes

Shigeki Miyamoto1, Marta Rubio2 and Mark A. Sussman2,*

1 Department of Pharmacology, University of California, La Jolla, San Diego, CA 92093-0636, USA
2 Department of Biology, SDSU Heart Institute, San Diego State University, NLS 426, 5500 Campanile Drive, San Diego, CA 92182, USA

* Corresponding author. Tel: +1 619 594 2983; +1 619 594 2610. E-mail address: sussman{at}heart.sdsu.edu

Biological actions resulting from phosphoinositide synthesis trigger multiple downstream signalling cascades by recruiting proteins with pleckstrin homology domains, including phosphoinositide-dependent kinase-1 and protein kinase B (also known as Akt). Retrospectively, more attention has been focused on the plasma membrane-associated interactions of these molecules and resulting cytoplasmic target activation. The complex biological activities exerted by Akt activation suggest, however, that more subtle and complex subcellular control mechanisms are involved. This review examines the regulation of Akt activity from the perspective of subcellular compartmentalization and focuses specifically upon the actions of Akt activation downstream from phosphoinositide synthesis that influence cell biology by altering nuclear signalling leading to Pim-1 kinase induction as well as hexokinase phosphorylation that, together with Akt, serves to preserve mitochondrial integrity.

KEYWORDS Heart; Cardiomyocyte; Akt; PKB; Mitochondria; Pim-1; Kinase; Nucleus

Time for primary review: 19 days


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