Non-Smad TGF-{beta} signals

Moustakas, Aristidis (author): Uppsala universitet,Ludwiginstitutet för cancerforskning

Heldin, Carl-Henrik (author): Uppsala universitet,Ludwiginstitutet för cancerforskning

(creator_code:org_t)

The Company of Biologists, 2005
2005
English.
In: Journal of Cell Science. - : The Company of Biologists. - 0021-9533 .- 1477-9137. ; 118:Pt 16, s. 3573-3584

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Abstract Subject headings

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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