The transcriptional enhancer factor (TEF) multigene family is primarily functional in muscle-specific genes through binding to MCAT elements that activate or repress transcription of many genes in response to physiological and pathological stimuli. Among the TEF family, TEF-1, RTEF-1, and DTEF-1 are critical regulators of cardiac and smooth muscle-specific genes during cardiovascular development and cardiac disorders including cardiac hypertrophy. Emerging evidence suggests that in addition to functioning as muscle-specific transcription factors, members of the TEF family may be key mediators of gene expression induced by hypoxia in endothelial cells by virtue of its multidomain organization, potential for post-translational modifications, and interactions with numerous transcription factors, which represent a cell-selective control mediator of nuclear signaling. We review the recent literature demonstrating the involvement of the TEF family of transcription factors in the regulation of differential gene expression in cardiovascular physiology and pathology.
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