2014年4月23日我院张龙课题组在Protein Cell发表综述:The regulation of TGF-β/SMAD signaling by protein deubiquitination

时间:2014年04月23日 访问次数:1799

Protein Cell. 2014 Jul;5(7):503-17.

Juan Zhang, Xiaofei Zhang, Feng Xie, Zhengkui Zhang, Hans van Dam, Long Zhang*,Fangfang Zhou*
 
Abstract

Transforming growth factor-β (TGF-β) members are key cytokines that control embryogenesis and tissue homeostasis via transmembrane TGF-β type II (TβR II) and type I (TβRI) and serine/threonine kinases receptors. Aberrant activation of TGF-β signaling leads to diseases, including cancer. In advanced cancer, the TGF-β/SMAD pathway can act as an oncogenic factor driving tumor cell invasion and metastasis, and thus is considered to be a therapeutic target. The activity of TGF-β/SMAD pathway is known to be regulated by ubiquitination at multiple levels. As ubiquitination is reversible, emerging studies have uncovered key roles for ubiquitin-removals on TGF-β signaling components by deubiquitinating enzymes (DUBs). In this paper, we summarize the latest findings on the DUBs that control the activity of the TGF-β signaling pathway. The regulatory roles of these DUBs as a driving force for cancer progression as well as their underlying working mechanisms are also discussed.

全文链接:http://link.springer.com/article/10.1007%2Fs13238-014-0058-8