MEF2A


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MEF2A

A gene on chromosome 15q26 that encodes a DNA-binding transcription factor, which activates an array of muscle-specific, growth factor-induced and stress-induced genes. It plays a role in muscle development, neuronal differentiation, cell growth control and apoptosis.

Molecular pathology
MEF2A mutations have been linked to autosomal dominant coronary artery disease 1 with myocardial infarction.
References in periodicals archive ?
A immunostaining study with an antibody for MEF2A revealed that the MEF2A protein is highly expressed in the endothelium.
It is important to point out, the recent discovery of MEF2A as a disease-causing gene for CAD and MI and its high expression in the endothelium lead us to hypothesize that an early trigger for the pathogenesis of CAD and MI may be dysfunction or abnormal development of the endothelium, which increases susceptibility of the coronary arteries to inflammation, leading to the development of CAD and MI.
In conclusion, MEF2A may play an important role in cardiovascular biology, and rare variants inMEF2A may influence its activity as a transcription factor in vitro , but the genetic evidence available to date does not demonstrate that these mutations play a causal role in CAD and/or MI in humans.
Mutation of MEF2A in an inherited disorder with features of coronary artery disease.
Structure of the MADS-box/MEF2 domain of MEF2A bound to DNA and its implication for myocardin recruitment.
Association of MEF2A gene polymorphisms with coronary artery disease.
Lack of association between the MEF2A gene and coronary artery disease in Iranian families.
Assessment of MEF2A mutations in myocardial infarction in Japanese patients.
Association and functional analyses of MEF2A as a susceptibility gene for premature myocardial infarction and coronary artery disease.
Structural changes in exon 11 of MEF2A are not related to sporadic coronary artery disease in Han Chinese population.
Variants in exon 11 of MEF2A gene and coronary artery disease: evidence from a case-control study, systematic review, and meta-analysis.