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Review
. 2015 Jul 15;566(1):1-7.
doi: 10.1016/j.gene.2015.04.077. Epub 2015 Apr 30.

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

Elizabeth Vafiadaki  1 , Demetrios A Arvanitis  1 , Despina Sanoudou  2
Affiliations
Review

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

Elizabeth Vafiadaki et al. Gene. .

Abstract

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.

Keywords: Cardiomyopathies; Differentiation; Heart failure; MLP; Muscle structure; Sarcomere; Skeletal myopathies.

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Conflict of interest statement

Conflict of interest

Authors have no conflict of interest.

Figures

Fig.1.
Fig.1.
Bioinformatical predictions of phosphorylation sites in MLP protein sequence. Graphical output showing multiple serine, threonine or tyrosine residues with predicted phosphorylation potential above the threshold. Bioinformatical analysis was performed using the publicly available NetPhos 2.0 Server (http://www.cbs.dtu.dk/services/NetPhos/) (Blom et al., 1999).
Fig.2.
Fig.2.
Diagrammatic representation of MLP illustrating the location of published human mutations. The positions of the two LIM domains (LIM1 and LIM2) as well as the nuclear localization signal (NLS) are indicated.
See this image and copyright information in PMC

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