Jumonji represses α-cardiac myosin heavy chain expression via inhibiting MEF2 activity
Copyright policy )Jumonji represses α-cardiac myosin heavy chain expression via inhibiting MEF2 activity
Expression of alpha-cardiac myosin heavy chain gene (alphaMHC) is developmentally regulated in normal embryonic hearts and down-regulated in cardiac myopathy and failing hearts. Jumonji (JMJ) has been shown to be critical for normal cardiovascular development and functions as a transcriptional repressor. Here, we demonstrate that JMJ represses alphaMHC expression through inhibition of myocyte enhancer factor 2 (MEF2) activity. In primary cardiomyocytes, overexpression of JMJ leads to marked reduction of endogenous alphaMHC expression. JMJ represses the synergistic activation of alphaMHC by MEF2 and thyroid hormone receptor (TR). Interestingly, JMJ inhibits transcriptional activities of all MEF2 isoforms, but not the TR-dependent activation. The transcriptional repression domain of JMJ interacts with the N-terminal part of MEF2A, resulting in the repression of MEF2A activities. These results suggest that JMJ represses alphaMHC expression via protein-protein interaction with MEF2A.
- University of Wisconsin–Oshkosh United States
- United States Food and Drug Administration United States
Myosin Heavy Chains, MEF2 Transcription Factors, Polycomb Repressive Complex 2, Gene Expression Regulation, Developmental, Nerve Tissue Proteins, Recombinant Proteins, Rats, DNA-Binding Proteins, Mice, Animals, Newborn, Myogenic Regulatory Factors, Animals, Myocytes, Cardiac, Cloning, Molecular, Cells, Cultured, Transcription Factors
Myosin Heavy Chains, MEF2 Transcription Factors, Polycomb Repressive Complex 2, Gene Expression Regulation, Developmental, Nerve Tissue Proteins, Recombinant Proteins, Rats, DNA-Binding Proteins, Mice, Animals, Newborn, Myogenic Regulatory Factors, Animals, Myocytes, Cardiac, Cloning, Molecular, Cells, Cultured, Transcription Factors
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