Phospho-control of TGF-β superfamily signaling  

作　　者：Katharine H Wrighton Xia Lin Xin-Hua Feng 

机构地区：[1]Michael E. DeBakey Department of Surgery, Department of Molecular & Cellular Biology and Dan L. Duncan Cancer Center,Baylor College of Medicine, Houston, TX 77030, USA

出　　处：《Cell Research》2009年第1期8-20,共13页细胞研究（英文版）

摘　　要：Members of the transforming growth factor-β （TGF-β） family control a broad range of cellular responses in metazoan organisms via autocrine, paracrine, and endocrine modes. Thus, aberrant TGF-β signaling can play a key role in the pathogenesis of several diseases, including cancer. TGF-β signaling pathways are activated by a short phospho-cascade, from receptor phosphorylation to the subsequent phosphorylation and activation of downstream signal transducers called R-Smads. R-Smad phosphorylation state determines Smad complex assembly/disassembly, nuclear import/export, transcriptional activity and stability, and is thus the most critical event in TGF-β signaling. Dephosphorylation of R-Smads by specific phosphatases prevents or terminates TGF-β signaling, highlighting the need to consider Smad （de）phosphorylation as a tightly controlled and dynamic event. This article illustrates the es- sential roles of reversible phosphorylation in controlling the strength and duration of TGF-β signaling and the ensu- ing physiological responses.

关 键 词：SMAD PHOSPHORYLATION PHOSPHATASE TGF-β signaling 

分 类 号：R4[医药卫生—临床医学]