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Non-Smad TGF-β signals

Moustakas, Aristidis, Heldin, Carl-Henrik·2005·Journal of Cell Science
DOI 10.1242/jcs.02554
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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 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.

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  • Dab2 modulates the non-canonical pathways of TGF-beta by suppressing Ras/MAPK activation.

    “Therefore, it was concluded that Dab2 modulates the non-canonical pathways of TGF-beta by suppressing Ras/MAPK activation”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Moustakas and Heldin, 2005

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Metadata

Authors
Moustakas, A., & Heldin, C.-H.
Affiliations
Ludwig Institute for Cancer Research, Biomedical Center, Uppsala University, Box 595, SE 751 24 Uppsala, Sweden
Venue
Journal of Cell Science
Publisher
The Company of Biologists
Published
2005-08-15
Volume
118
Issue
16
Pages
3573-3584
ISSN
  • 1477-9137
  • 0021-9533
DOI
10.1242/jcs.02554
Cited by
958
References
2
Language
en

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