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Non-Smad TGF-{beta}...
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Moustakas, AristidisUppsala universitet,Ludwiginstitutet för cancerforskning
(författare)
Non-Smad TGF-{beta} signals
- Artikel/kapitelEngelska2005
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The Company of Biologists,2005
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printrdacarrier
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LIBRIS-ID:oai:DiVA.org:uu-74131
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-74131URI
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https://doi.org/10.1242/jcs.02554DOI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:art swepub-publicationtype
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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.
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Heldin, Carl-HenrikUppsala universitet,Ludwiginstitutet för cancerforskning(Swepub:uu)carlheld
(författare)
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Uppsala universitetLudwiginstitutet för cancerforskning
(creator_code:org_t)
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Ingår i:Journal of Cell Science: The Company of Biologists118:Pt 16, s. 3573-35840021-95331477-9137
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