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The Hippo Tumor Pathway Promotes TAZ Degradation by Phosphorylating a Phosphodegron and Recruiting the SCFβ-TrCP E3 Ligase.

J Biol Chem.. 2010-11;  285(48):37159 - 37169
Chen-Ying Liu, Zheng-Yu Zha, Xin Zhou, Heng Zhang, Wei Huang, Di Zhao, Tingting Li, Siew Wee Chan, Chun Jye Lim, Wanjin Hong, Shimin Zhao, Yue Xiong, Qun-Ying Lei, and Kun-Liang Guan. Key Laboratory of Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology School of Medicine.
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摘要

The TAZ transcription co-activator promotes cell proliferation and epithelial-mesenchymal transition. TAZ is inhibited by the Hippo tumor suppressor pathway, which promotes TAZ cytoplasmic localization by phosphorylation. We report here that TAZ protein stability is controlled by a phosphodegron recognized by the F-box protein β-TrCP and ubiquitylated by the SCF/CRL1(β-TrCP) E3 ligase. The interaction between TAZ and β-TrCP is regulated by the Hippo pathway. Phosphorylation of a phosphodegron in TAZ by LATS primes it for further phosphorylation by CK1 and subsequent binding by β-TrCP. Therefore, the Hippo pathway negatively regulates TAZ function by both limiting its nuclear accumulation and... More

关键词

Breast Cancer; E3 Ubiquitin Ligase; Protein Degradation; Protein Phosphorylation; Transcription Coactivators; Hippo Pathway; TAZ