| pubmed-article:9094310 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9094310 | lifeskim:mentions | umls-concept:C0079427 | lld:lifeskim |
| pubmed-article:9094310 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:9094310 | lifeskim:mentions | umls-concept:C0694891 | lld:lifeskim |
| pubmed-article:9094310 | lifeskim:mentions | umls-concept:C1325410 | lld:lifeskim |
| pubmed-article:9094310 | lifeskim:mentions | umls-concept:C0205099 | lld:lifeskim |
| pubmed-article:9094310 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:9094310 | lifeskim:mentions | umls-concept:C1363844 | lld:lifeskim |
| pubmed-article:9094310 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:9094310 | pubmed:dateCreated | 1997-5-29 | lld:pubmed |
| pubmed-article:9094310 | pubmed:abstractText | The invertebrate and vertebrate Smad proteins have recently been identified as important mediators of the responses to transforming growth factor beta (TGF-beta) and related factors. We have previously shown that Smad3 and Smad4 (the product of the tumor suppressor gene DPC 4) strongly synergize as mediators of TGF-beta signaling, and that inactive carboxy-terminally truncated mutants of either Smad act as dominant-negative inhibitors of the natural TGF-beta response. The finding that Smad4, unlike Smad3, does not interact with the TGF-beta receptor, coupled with the distinct structural features of Smad4, raises the possibility that Smad4 cooperates not only with Smad3, but also with Smad1 and Smad2 to mediate signaling by TGF-beta family members. | lld:pubmed |
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| pubmed-article:9094310 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9094310 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9094310 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9094310 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:9094310 | pubmed:issn | 0960-9822 | lld:pubmed |
| pubmed-article:9094310 | pubmed:author | pubmed-author:DerynckRR | lld:pubmed |
| pubmed-article:9094310 | pubmed:author | pubmed-author:ZhangYY | lld:pubmed |
| pubmed-article:9094310 | pubmed:author | pubmed-author:MusciTT | lld:pubmed |
| pubmed-article:9094310 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9094310 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:9094310 | pubmed:volume | 7 | lld:pubmed |
| pubmed-article:9094310 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9094310 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9094310 | pubmed:pagination | 270-6 | lld:pubmed |
| pubmed-article:9094310 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9094310 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9094310 | pubmed:articleTitle | The tumor suppressor Smad4/DPC 4 as a central mediator of Smad function. | lld:pubmed |
| pubmed-article:9094310 | pubmed:affiliation | Department of Growth and Development, University of California at San Francisco, San Francisco, California 94143-0640, USA. | lld:pubmed |
| pubmed-article:9094310 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9094310 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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