DEVELOPMENTAL NEUROSCIENCEHDAC3 augments the autoregulation of neuroD gene in P19 cellsFang, Hong-Bo; Mi, Yang; Zhang, Ye; Wu, Ning-Hua; Shen, Yu-FeiAuthor Information National Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China Correspondence to Yu-Fei Shen or Ye Zhang, 5 Dongdan Santiao, Beijing 100005, China Tel: +86 10 6529 5939; fax: +86 10 6526 9665; e-mail: firstname.lastname@example.org; email@example.com; firstname.lastname@example.org Received 28 May 2009 accepted 29 July 2009 NeuroReport: January 6th, 2010 - Volume 21 - Issue 1 - p 19-23 doi: 10.1097/WNR.0b013e3283315aec Buy SDC Metrics Abstract NeuroD, a basic helix–loop–helix transcription factor, is capable of converting embryonic epidermal cells into neuronal cells. However, whether histone deacetylases (HDACs) are involved in the autoregulation of neuroD or not is unclear. In this study, neuroD expression was found to be significantly increased in the all-trans retinoid acid-treated P19 cells. Meanwhile, neuroD could itself enhance its promoter activity and mRNA expression. By using specific inhibitors to histone modification enzymes, HDAC3 was identified to specifically augment the autoactivation of neuroD in P19 cells. The data suggest that the elevation of HDAC3 and neuroD in all-trans retinoid acid-treated cells exponentially increases the neuroD expression and mediates an early commitment of P19 cells for neuronal differentiation. © 2010 Lippincott Williams & Wilkins, Inc.