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Journal of Biochemistry Advance Access published online on January 2, 2009
Journal of Biochemistry, 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: Jianxin Gu, Box 103, No. 138 Yi Xue Yuan Road, Gene Research Center Shanghai Medical College of Fudan University Shanghai, People's Republic of China 200032 Email: jxgu{at}shmu.edu.cn Tel.: 86-21-54237704Fax: 86-21-64164489

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 CDK11p58negatively regulated cells.

Key Words: CDK11p58, Steroid, Estrogen receptor {alpha}, ubiquitin-proteasome, degradation


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