HATs off to Hop: recruitment of a class I histone deacetylase incriminates a novel transcriptional pathway that opposes cardiac hypertrophy.
Histone acetylation, regulated by two antagonistic enzymes - histone acetyltransferases (HATs) and histone deacetylases (HDACs) - results in transcriptional changes and also plays a critical role in cardiac development and disease. A new study shows that overexpression of the atypical transcriptional corepressor homeodomain-only protein (Hop) causes cardiac hypertrophy via recruitment of a class I HDAC. In contrast to the body of work on transcriptional mechanisms that drive cardiac hypertrophy, including class II HDACs, this report elucidates a novel growth-suppressing transcriptional pathway in cardiac muscle that opposes hypertrophic growth.
Hamamori
Yasuo
Y
Center for Cardiovascular Development, Baylor College of Medicine, One Baylor Plaza, Room 506D, Houston, Texas 77030, USA.
Schneider
Michael D
MD
D000123:Acetyltransferases / Q000378:metabolism*; D000818:Animals; D006332:Cardiomegaly / Q000188:drug therapy / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D051548:Histone Acetyltransferases; D006655:Histone Deacetylases / Q000145:classification / Q000378:metabolism*; D018398:Homeodomain Proteins / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D012097:Repressor Proteins / Q000378:metabolism*; D029701:Saccharomyces cerevisiae Proteins / Q000378:metabolism*; D014158:Transcription, Genetic
D004791:Enzyme Inhibitors; D018398:Homeodomain Proteins; D012097:Repressor Proteins; D029701:Saccharomyces cerevisiae Proteins; D000123:Acetyltransferases; D051548:Histone Acetyltransferases; D006655:Histone Deacetylases