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| Non-Smad TGF-beta signals |
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| Author(s): Moustakas A, Heldin CH |
| Source: JOURNAL OF CELL SCIENCE Volume: 118 Issue: 16 Pages: 3573-3584 Published: AUG 15 2005 |
| Times Cited: 218 References: 144 |
| Abstract: 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 beta (TGF-beta) superfamily members to the nucleus. However, growing biochemical and developmental evidence supports the notion that alternative, non-Smad pathways also participate in TGF-beta signalling. Non-Smad signalling proteins have three general mechanisms by which they contribute to physiological responses to TGF-beta: (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-beta 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-beta 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. |
| Document Type: Editorial Material |
| Language: English |
| Reprint Address: Moustakas, A (reprint author), Uppsala Univ, Ctr Biomed, Ludwig Inst Canc Res, Box 595, SE-75124 Uppsala, Sweden |
Addresses:
1. Uppsala Univ, Ctr Biomed, Ludwig Inst Canc Res, SE-75124 Uppsala, Sweden |
| Publisher: COMPANY OF BIOLOGISTS LTD, BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND |
| Subject Category: Cell Biology |
| IDS Number: 964OW |
| ISSN: 0021-9533 |
| DOI: 10.1242/jcs.02554 |
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