个人信息Personal Information
教授
博士生导师
硕士生导师
任职 : 教授
性别:男
毕业院校:九州大学理学部
学位:博士
所在单位:生物工程学院
学科:生物化学与分子生物学. 细胞生物学. 生药学
办公地点:生物楼603
联系方式:邮编:116024 大连市高新区凌工路2号 大连理工大学生物楼603 电话:0411-84706105
电子邮箱:wuhj@dlut.edu.cn
SUMOylation of AhR modulates its activity and stability through inhibiting its ubiquitination
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论文类型:期刊论文
发表时间:2012-12-01
发表刊物:JOURNAL OF CELLULAR PHYSIOLOGY
收录刊物:Scopus、SCIE、PubMed
卷号:227
期号:12
页面范围:3812-3819
ISSN号:0021-9541
摘要:Aryl hydrocarbon receptor (AhR) is a transcription factor that belongs to the basic helixloophelix (bHLH) Per-Arnt-Sim homology domain (PAS) family. AhR can be activated by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (2, 3, 7, 8-TCDD) and once activated, it promotes the abnormal expression of cytochrome P450, leading to several diseases, including cancer. In this study, we showed that AhR is subjected to post-translational modification by SUMOylation and this modification could be reversed by SENP1. Two SUMOylation sites were identified, one in the bHLH domain (K63) and the other in the TAD domain (K510) of AhR. Substitution of either K63 or K510 with arginine resulted in reduced SUMOylation for AhR. Treatment of MCF-7 cells with TCDD led to a reduced level of SUMOylated AhR in a time-dependent manner, and this occurred mainly in the nucleus. SUMOylation of AhR enhanced its stability through inhibiting its ubiquitination. Moreover, SUMOylation also repressed the transactivation activity of AhR and this could be reversed by TCDD. These results suggested that SUMOylation of AhR might play an important role in the regulation of its function, and TCDD may activate the transcriptional activity of AhR through downregulating its SUMOylation. J. Cell. Physiol. 227: 38123819, 2012. (c) 2012 Wiley Periodicals, Inc.