Muscle LIM Protein: Master regulator of cardiac and skeletal muscle functions

被引:69
作者
Vafiadaki, Elizabeth [1 ]
Arvanitis, Demetrios A. [1 ]
Sanoudou, Despina [1 ,2 ]
机构
[1] Acad Athens, Biomed Res Fdn, Div Mol Biol, Athens 11527, Greece
[2] Univ Athens, Sch Med, Attikon Univ Hosp, Dept Internal Med 4, Athens, Greece
基金
美国国家卫生研究院;
关键词
MLP; Sarcomere; Muscle structure; Differentiation; Heart failure; Cardiomyopathies; Skeletal myopathies; CYSTEINE-RICH-PROTEIN; MLP-DEFICIENT MICE; DILATED CARDIOMYOPATHY; HEART-FAILURE; HYPERTROPHIC CARDIOMYOPATHY; DOMAIN PROTEINS; MYOGENIC DIFFERENTIATION; ACTIN CYTOSKELETON; GENE-EXPRESSION; ALPHA-ACTININ;
D O I
10.1016/j.gene.2015.04.077
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Muscle LIM Protein (MLP) has emerged as a key regulator of striated muscle physiology and pathophysiology. Mutations in cysteine and glycine-rich protein 3 (CSRP3), the gene encoding MLP, are causative of human cardiomyopathies, whereas altered expression patterns are observed in human failing heart and skeletal myopathies. In vitro and in vivo evidences reveal a complex and diverse functional role of MLP in striated muscle, which is determined by its multiple interacting partners and subcellular distribution. Experimental evidence suggests that MLP is implicated in both myogenic differentiation and myocyte cytoarchitecture, although the full spectrum of its intracellular roles still unfolds. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 7
页数:7
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