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MEF2AMocyte Enhancer Binding Factor-2A
References in periodicals archive ?
Requirement of MEF2A, C, and D for skeletal muscle regeneration.
miR-155 inhibits expression of the MEF2A protein to repress skeletal muscle differentiation.
MiR-155 acts as a prohypertrophic factor by abolishing the expression of Mef2A and Jarid2 in cardiomyocytes and inhibition of miR-155 improves the cardiac function from hypertrophy induced progressive heart failure [33].
Kong et al., "MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes," Molecular and Cellular Biology, vol.
In this article, we reviewed the current understanding of the MEF2A mutation and CAD, as well as MI.
MEF2A belongs to a family of four closely related transcription factors (MEF2-A, -B, -C, and -D) that are conserved from yeast to humans.[sup][2] The N termini of MEF2 proteins contain MADS and MEF2 domains.
Consistent with its potential involvement in vascular function, MEF2A is expressed at high concentrations in the endothelial and smooth muscle layers of the coronary arteries.
Among these 93 genes, MEF2A caught the authors' attention.
The phenotype of individuals that harbor the MEF2A mutation identified by Wang et al .
Identification of MEF2A mutations in families and patients with CAD and MI clearly links the MEF2 signaling pathway to an important human disease.
Transcription factor MEF2A mutations in patients with coronary artery disease.
Study on association of single nucleotide polymorphism of mef2a gene with carcass traits in chicken.