pubmed-article:16105881 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16105881 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
pubmed-article:16105881 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:16105881 | pubmed:issue | Pt 16 | lld:pubmed |
pubmed-article:16105881 | pubmed:dateCreated | 2005-8-17 | lld:pubmed |
pubmed-article:16105881 | pubmed:abstractText | 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. | lld:pubmed |
pubmed-article:16105881 | pubmed:language | eng | lld:pubmed |
pubmed-article:16105881 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16105881 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16105881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16105881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16105881 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16105881 | pubmed:month | Aug | lld:pubmed |
pubmed-article:16105881 | pubmed:issn | 0021-9533 | lld:pubmed |
pubmed-article:16105881 | pubmed:author | pubmed-author:HeldinCarl-He... | lld:pubmed |
pubmed-article:16105881 | pubmed:author | pubmed-author:MoustakasAris... | lld:pubmed |
pubmed-article:16105881 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16105881 | pubmed:day | 15 | lld:pubmed |
pubmed-article:16105881 | pubmed:volume | 118 | lld:pubmed |
pubmed-article:16105881 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16105881 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16105881 | pubmed:pagination | 3573-84 | lld:pubmed |
pubmed-article:16105881 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
pubmed-article:16105881 | pubmed:meshHeading | pubmed-meshheading:16105881... | lld:pubmed |
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pubmed-article:16105881 | pubmed:meshHeading | pubmed-meshheading:16105881... | lld:pubmed |
pubmed-article:16105881 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:16105881 | pubmed:articleTitle | Non-Smad TGF-beta signals. | lld:pubmed |
pubmed-article:16105881 | pubmed:affiliation | Ludwig Institute for Cancer Research, Biomedical Center, Uppsala University, Box 595, SE 751 24 Uppsala, Sweden. aris.moustakas@licr.uu.se | lld:pubmed |
pubmed-article:16105881 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16105881 | pubmed:publicationType | Review | lld:pubmed |
pubmed-article:16105881 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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