Regulating the stability of TGFβ receptors and Smads  

作　　者：Peter Lonn Anita Moren Erna Raja Markus Dahl Aristidis Moustakas 

机构地区：[1]Ludwig Institute for Cancer Research, Uppsala University, Box 595, Biomedical Center, SE- 751 24 Uppsala, Sweden

出　　处：《Cell Research》2009年第1期21-35,共15页细胞研究（英文版）

摘　　要：Transforming growth factor β （TGFβ） controls cellular behavior in embryonic and adult tissues. TGFβ binding to serine/threonine kinase receptors on the plasma membrane activates Smad molecules and additional signaling proteins that together regulate gene expression. In this review, mechanisms and models that aim at explaining the coordination between several components of the signaling network downstream of TGFβ are presented. We discuss how the activity and duration of TGFβ receptor/Smad signaling can be regulated by post-translational modifications that affect the stability of key proteins in the pathway. We highlight finks between these mechanisms and human diseases, such as tissue fibrosis and cancer.

关 键 词：LYSOSOME phosphorylation PROTEASOME Smad SUMO TGFΒ UBIQUITIN 

分 类 号：R4[医药卫生—临床医学]