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Journal of Biochemistry Advance Access originally published online on January 2, 2009
Journal of Biochemistry 2009 145(3):331-343; doi:10.1093/jb/mvn177
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© The Authors 2009. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved

Repression of Estrogen Receptor alpha by CDK11p58 Through Promoting its Ubiquitin–Proteasome Degradation

Yanlin Wang, Hongliang Zong, Yayun Chi, Yi Hong, Yanzhong Yang, Weiying Zou, Xiaojing Yun and Jianxin Gu*

Gene Research Center, Shanghai Medical College and Institutes of Biomedical, Shanghai 200032, People's Republic of China

*To whom correspondence should be addressed. Tel: +86-21-54237704, Fax: +86-21-64164489, E-mail: jxgu{at}shmu.edu.cn

Received June 21, 2008; Accepted December 2, 2008


  Abstract

Estrogen receptor {alpha} (ER{alpha}) is a ligand-dependent transcription factor that mediates physiological responses to 17β-estradiol (E2). These responses of cells to estrogen are regulated in part by degradation of ER{alpha}. In this report, we found that CDK11p58 repressed ER{alpha} transcriptional activity. And we further demonstrated that ER{alpha} protein level was down-regulated by CDK11p58 in mammalian cells in a ligand independent manner. This effect could be abrogated by treatment with proteasome inhibitor MG132. Our results indicated that the ubiquitin/proteasome-mediated degradation of ER{alpha} was promoted by CDK11p58. Furthermore, the interaction between ER{alpha} and CDK11p58 was detected. This interaction was necessary for the polyubiquitination and degradation of ER{alpha}. On the contrary, the other isoform of CDK11, CDK11p110 and the kinase dead mutant of CDK11p58, D224N, did not associate with ER{alpha} and failed to reduce the ER{alpha} protein level. These data identified a new negative regulatory protein of ER{alpha} and provided a new pathway by which CDK11p58 negatively regulated cells.

Key Words: CDK11p58, degradation, estrogen receptor {alpha}, steroid, ubiquitin–proteasome

Abbreviations: ERa, estrogen receptor a; E2, 17b-estradiol; CDK, Cyclin-dependent kinase; AR, androgen receptor; CCND3, cyclin D3


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