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Smad regulation in ...
Smad regulation in TGF-beta signal transduction
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- Moustakas, Aristidis (författare)
- Uppsala universitet,Ludwiginstitutet för cancerforskning
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- Souchelnytskyi, Serhiy (författare)
- Karolinska Institutet,Uppsala universitet,Ludwiginstitutet för cancerforskning
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- Heldin, Carl-Henrik (författare)
- Uppsala universitet,Ludwiginstitutet för cancerforskning
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(creator_code:org_t)
- The Company of Biologists, 2001
- 2001
- Engelska.
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Ingår i: Journal of Cell Science. - : The Company of Biologists. - 0021-9533 .- 1477-9137. ; 114:Pt 24, s. 4359-4369
- Relaterad länk:
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http://www.ncbi.nlm....
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Smad proteins transduce signals from transforming growth factor-beta (TGF-beta) superfamily ligands that regulate cell proliferation, differentiation and death through activation of receptor serine/threonine kinases. Phosphorylation of receptor-activated Smads (R-Smads) leads to formation of complexes with the common mediator Smad (Co-Smad), which are imported to the nucleus. Nuclear Smad oligomers bind to DNA and associate with transcription factors to regulate expression of target genes. Alternatively, nuclear R-Smads associate with ubiquitin ligases and promote degradation of transcriptional repressors, thus facilitating target gene regulation by TGF-beta. Smads themselves can also become ubiquitinated and are degraded by proteasomes. Finally, the inhibitory Smads (I-Smads) block phosphorylation of R-Smads by the receptors and promote ubiquitination and degradation of receptor complexes, thus inhibiting signalling.
Nyckelord
- Activin Receptors; Type I/*metabolism/physiology
- Animals
- DNA-Binding Proteins/physiology
- Humans
- Phosphoproteins/physiology
- Receptor Protein-Tyrosine Kinases/*metabolism/physiology
- Receptors; Transforming Growth Factor beta/*metabolism/physiology
- Research Support; Non-U.S. Gov't
- Signal Transduction/*physiology
- Trans-Activators/physiology
- Transforming Growth Factor beta/*physiology
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