A family of transcription factors in the MADS superfamily that bind to the MEF2 locus present in most muscle-specific genes. MEF-2A is calcium-regulated and promotes cell survival during development and induction of myogenesis, whereas MEF2C may be more involved with maintenance of the differentiated state. Mutations in MEF2A are responsible for autosomal dominant coronary artery disease with acute myocardial infarction. MEF2B is important in the regulation of T-cell apoptosis, normally inactive because bound to cabin1 but released when T-cell receptor activation increases intracellular calcium. MEF2C is expressed in skeletal muscle, spleen, brain, and various myeloid cells. In monocytic cells MEF2C has its transactivation activity enhanced by LPS acting through the MAP kinase p38 and is itself regulated by myeloid-specific microRNA-223 (miR223). MEF2D is present in undifferentiated myoblasts and in the cerebellum and cerebrum of developing mouse brains, suggesting that it may be involved in the early stages of differentiation of both nerves and muscles.
Subjects: Medicine and Health.