Menin, a tumor suppressor, represses JunD-mediated transcriptional activity by association with an mSin3A-histone deacetylase complex.
Copyright policy )Menin, a tumor suppressor, represses JunD-mediated transcriptional activity by association with an mSin3A-histone deacetylase complex.
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.
- Seoul National University Korea (Republic of)
Transcriptional Activation, Proto-Oncogene Proteins c-jun, Molecular Sequence Data, Transfection, Histone Deacetylases, Repressor Proteins, Sin3 Histone Deacetylase and Corepressor Complex, Proto-Oncogene Proteins, Humans, Amino Acid Sequence, HeLa Cells
Transcriptional Activation, Proto-Oncogene Proteins c-jun, Molecular Sequence Data, Transfection, Histone Deacetylases, Repressor Proteins, Sin3 Histone Deacetylase and Corepressor Complex, Proto-Oncogene Proteins, Humans, Amino Acid Sequence, HeLa Cells
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