CAC1 negatively regulates RARα activity through cooperation with HDAC.
作者： MinO Moon , Soo-Jong Um , Eun-Joo Kim
DOI: 10.1016/J.BBRC.2012.08.142
关键词:
摘要: Retinoic acid (RA) plays pleiotropic roles in cellular differentiation and animal development. RA responses are mediated by transcriptional activation the retinoic receptor (RAR) retinoid X (RXR) cooperation with various types of coregulators at RA-responsive gene promoters. Here, we identified CDK2-associated cullin (CAC1) as a novel type RARα coregulator that interacts inhibits its activity. The CoRNR box CAC1 is required for binding to inactivation RARα. In addition, cooperates histone deacetylases (HDACs) suppress RARα, probably associating HDAC. Finally, depletion increases RA-induced neuronal P19 cells, response accompanied significant upregulation marker nestin. From these results, suggest corepressor HDACs involved regulation differentiation.
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