Format

Send to

Choose Destination
See comment in PubMed Commons below
Congest Heart Fail. 2011 Nov-Dec;17(6):269-82. doi: 10.1111/j.1751-7133.2011.00266.x. Epub 2011 Nov 9.

Mitochondrial protein phosphorylation as a regulatory modality: implications for mitochondrial dysfunction in heart failure.

Author information

1
Department of Medicine, Division of Cardiology, The Johns Hopkins University, Baltimore, MD 21205-2195, USA. bor@jhmi.edu

Abstract

Phosphorylation of mitochondrial proteins has been recognized for decades, and the regulation of pyruvate- and branched-chain α-ketoacid dehydrogenases by an atypical kinase/phosphatase cascade is well established. More recently, the development of new mass spectrometry-based technologies has led to the discovery of many novel phosphorylation sites on a variety of mitochondrial targets. The evidence suggests that the major classes of kinase and several phosphatases may be present at the mitochondrial outer membrane, intermembrane space, inner membrane, and matrix, but many questions remain to be answered as to the location, timing, and reversibility of these phosphorylation events and whether they are functionally relevant. The authors review phosphorylation as a mitochondrial regulatory strategy and highlight its possible role in the pathophysiology of cardiac hypertrophy and failure.

PMID:
22103918
PMCID:
PMC4067253
DOI:
10.1111/j.1751-7133.2011.00266.x
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley Icon for PubMed Central
    Loading ...
    Support Center