期刊
CELL RESEARCH
卷 19, 期 1, 页码 21-35出版社
INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/cr.2008.308
关键词
lysosome; phosphorylation; proteasome; Smad; SUMO; TGF beta; ubiquitin
类别
资金
- Ludwig Institute for Cancer Research
- Atlantic Philanthropies/Ludwig Institute for Cancer Research Clinical Discovery Program
- Swedish Cancer Society
- Swedish Research Council
- Marie Curie Research Training Network (RTN) EpiPlastCarcinoma
- Network of Excellence ENFIN under the European Union FP6 program
Transforming growth factor beta (TGF beta) controls cellular behavior in embryonic and adult tissues. TGF beta 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 TGF beta are presented. We discuss how the activity and duration of TGF beta receptor/Smad signaling can be regulated by post-translational modifications that affect the stability of key proteins in the pathway. We highlight links between these mechanisms and human diseases, such as tissue fibrosis and cancer.
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