期刊
GENE
卷 569, 期 1, 页码 14-20出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.gene.2015.06.027
关键词
Myosin light chain-2 (MYL2/MLC-2); Cardiac muscle; Cardiac disease; Contraction; Sarcomere; Ventricular myosin light chain-2; Heart; Myosin light chain kinase; Cardiac torsion; Cardiac function; Phosphorylation
资金
- National Institutes of Health [GM089820, GM114833]
- Elsevier, the publisher of GENE
- NIH [5T32HL007444-31]
- NIH/NHLBI [HL09780, HL066100, HL106968, HL123626]
- American Heart Association [GRNT22940045]
Myosin light chain-2 (MYL2, also called MLC-2) is an similar to 19 kDa sarcomeric protein that belongs to the EF-hand calcium binding protein superfamily and exists as three major isoforms encoded by three distinct genes in mammalian striated muscle. Each of the three different MLC-2 genes (MLC-2f; fast twitch skeletal isoform, MLC-2v; cardiac ventricular and slow twitch skeletal isoform, MLC-2a; cardiac atrial isoform) has a distinct developmental expression pattern in mammals. Genetic loss-of-function studies in mice demonstrated an essential role for cardiac isoforms of MLC-2, MLC-2v and MLC-2a, in cardiac contractile function during early embryogenesis. In the adult heart, MLC-2v function is regulated by phosphorylation, which displays a specific 1 expression pattern (high in epicardium and low in endocardium) across the heart. These data along with new data from computational models, genetic mouse models, and human studies have revealed a direct role for MLC-2v phosphorylation in cross-bridge cycling kinetics, calcium-dependent cardiac muscle contraction, cardiac torsion, cardiac function and various cardiac diseases. This review focuses on the regulatory functions of MLC-2 in the embryonic and adult heart, with an emphasis on phosphotylation-driven actions of MLC-2v in adult cardiac muscle, which provide new insights into mechanisms regulating myosin cycling kinetics and human cardiac diseases. (C) 2015 Elsevier B.V. All rights reserved.
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