HATs off to Hop: recruitment of a class I histone deacetylase incriminates a novel transcriptional pathway that opposes cardiac hypertrophy

被引：27

作者：

Hamamori, Y

Schneider, MD

机构：

[1] Baylor Coll Med, Ctr Cardiovasc Dev, Houston, TX 77030 USA

[2] Baylor Coll Med, Dept Med, Houston, TX 77030 USA

[3] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA

[4] Baylor Coll Med, Dept Mol Physiol & Biophys, Houston, TX 77030 USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2003年 / 112卷 / 06期

关键词：

D O I：

10.1172/JC1200319834

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

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 (see the related article beginning on page 863) 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.

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页码：824 / 826

页数：3

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