Non-Smad TGF-β signals
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- Aristidis Moustakas
- Ludwig Institute for Cancer Research, Biomedical Center, Uppsala University, Box 595, SE 751 24 Uppsala, Sweden
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- Carl-Henrik Heldin
- Ludwig Institute for Cancer Research, Biomedical Center, Uppsala University, Box 595, SE 751 24 Uppsala, Sweden
Abstract
<jats:p>During the past 10 years, it has been firmly established that Smad pathways are central mediators of signals from the receptors for transforming growth factor β (TGF-β) superfamily members to the nucleus. However, growing biochemical and developmental evidence supports the notion that alternative, non-Smad pathways also participate in TGF-β signalling. Non-Smad signalling proteins have three general mechanisms by which they contribute to physiological responses to TGF-β: (1) non-Smad signalling pathways directly modify (e.g. phosphorylate) the Smads and thus modulate the activity of the central effectors; (2) Smads directly interact and modulate the activity of other signalling proteins (e.g. kinases), thus transmitting signals to other pathways; and (3) the TGF-β receptors directly interact with or phosphorylate non-Smad proteins, thus initiating parallel signalling that cooperates with the Smad pathway in eliciting physiological responses. Thus, non-Smad signal transducers under the control of TGF-β provide quantitative regulation of the signalling pathway, and serve as nodes for crosstalk with other major signalling pathways, such as tyrosine kinase, G-protein-coupled or cytokine receptors.</jats:p>
Journal
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- Journal of Cell Science
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Journal of Cell Science 118 (16), 3573-3584, 2005-08-15
The Company of Biologists
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Details 詳細情報について
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- CRID
- 1360292619454581248
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- NII Article ID
- 80017564307
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- ISSN
- 14779137
- 00219533
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- Data Source
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- Crossref
- CiNii Articles