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

Hyungsoo Kim, Ji Eun Lee, Eun Jung Cho, Jun O. Liu, Hong Duk Youn

Research output: Contribution to journalArticlepeer-review

Abstract

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 α-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.

Original languageEnglish (US)
Pages (from-to)6135-6139
Number of pages5
JournalCancer Research
Volume63
Issue number19
StatePublished - Oct 1 2003

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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