Journal
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
Volume 8, Issue 8, Pages -Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a022053
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Funding
- Ludwig Institute for Cancer Research
- Swedish Cancer Society
- Swedish Research Council
- Network of Excellence ENFIN under the European Union FP6 program
- Initial Training Network IT-Liver under the European Union FP7 program
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Transforming growth factor beta (TGF-beta) family members signal via heterotetrameric complexes of type I and type II dual specificity kinase receptors. The activation and stability of the receptors are controlled by posttranslational modifications, such as phosphorylation, ubiquitylation, sumoylation, and neddylation, as well as by interaction with other proteins at the cell surface and in the cytoplasm. Activation of TGF-beta receptors induces signaling via formation of Smad complexes that are translocated to the nucleus where they act as transcription factors, as well as via non-Smad pathways, including the Erk1/2, JNK and p38 MAP kinase pathways, and the Src tyrosine kinase, phosphatidylinositol 30-kinase, and Rho GTPases.
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