Menin, a tumor suppressor, represses JunD-mediated transcriptional activity by association with an mSin3A-histone deacetylase complex

被引：1
|
作者：
Kim, H
Lee, JE
Cho, EJ
Liu, JO
Youn, HD
机构：
[1] Seoul Natl Univ, Coll Med, Inst Canc Res, Dept Biochem & Mol Biol, Seoul 110799, South Korea
[2] Sungkyunkwan Univ, Coll Pharm, Suwon 440746, South Korea
[3] Johns Hopkins Univ, Sch Med, Dept Pharmacol, Baltimore, MD 21205 USA
[4] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA
来源：
CANCER RESEARCH | 2003年 / 63卷 / 19期
关键词：
D O I：
暂无
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Menin, a gene product of multiple endocrine neoplasia type I (MEN1), is known to act as a tumor suppressor to repress JunD, transcription factor. However, the mechanism by which Menin represses JunD transcriptional activity was still unclear. In this study, we found that Menin is a corepressor against JunD transcriptional activity via recruitment of histone deacetylases in an mSin3A-dependent manner. The amino acid search revealed that central domain of Menin includes a alpha-helical mSin3-interacting domain [SID (371-387)]. The SID mutation of Menin (L381P/A385P) abolished the interaction between mSin3A and paired amphipathic helix 2 domain of Menin and reduced its ability to repress JunD transcriptional activity, implicating that SID of Menin is important for recruiting an mSin3A-histone deacetylase complex to repress JunD transcriptional activity.
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页码：6135 / 6139
页数：5
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