pubmed-article:11927558 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11927558 | lifeskim:mentions | umls-concept:C0014653 | lld:lifeskim |
pubmed-article:11927558 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
pubmed-article:11927558 | lifeskim:mentions | umls-concept:C0292688 | lld:lifeskim |
pubmed-article:11927558 | lifeskim:mentions | umls-concept:C0560187 | lld:lifeskim |
pubmed-article:11927558 | lifeskim:mentions | umls-concept:C1442792 | lld:lifeskim |
pubmed-article:11927558 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:11927558 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:11927558 | pubmed:dateCreated | 2002-4-2 | lld:pubmed |
pubmed-article:11927558 | pubmed:abstractText | The generation of mice lacking specific components of the transforming growth factor-beta (TGF-beta) signal tranduction pathway shows that TGF-beta is a key player in the development and physiology of the cardiovascular system. Both pro- and anti-angiogenic properties have been ascribed to TGF-beta, for which the molecular mechanisms are unclear. Here we report that TGF-beta can activate two distinct type I receptor/Smad signalling pathways with opposite effects. TGF-beta induces phosphorylation of Smad1/5 and Smad2 in endothelial cells and these effects can be blocked upon selective inhibition of ALK1 or ALK5 expression, respectively. Whereas the TGF-beta/ALK5 pathway leads to inhibition of cell migration and proliferation, the TGF-beta/ALK1 pathway induces endothelial cell migration and proliferation. We identified genes that are induced specifically by TGF-beta-mediated ALK1 or ALK5 activation. Id1 was found to mediate the TGF-beta/ALK1-induced (and Smad-dependent) migration, while induction of plasminogen activator inhibitor-1 by activated ALK5 may contribute to the TGF-beta-induced maturation of blood vessels. Our results suggest that TGF-beta regulates the activation state of the endothelium via a fine balance between ALK5 and ALK1 signalling. | lld:pubmed |
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pubmed-article:11927558 | pubmed:language | eng | lld:pubmed |
pubmed-article:11927558 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11927558 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11927558 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11927558 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11927558 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11927558 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11927558 | pubmed:month | Apr | lld:pubmed |
pubmed-article:11927558 | pubmed:issn | 0261-4189 | lld:pubmed |
pubmed-article:11927558 | pubmed:author | pubmed-author:ten... | lld:pubmed |
pubmed-article:11927558 | pubmed:author | pubmed-author:Valdimarsdott... | lld:pubmed |
pubmed-article:11927558 | pubmed:author | pubmed-author:ItohSusumuS | lld:pubmed |
pubmed-article:11927558 | pubmed:author | pubmed-author:GoumansMarie-... | lld:pubmed |
pubmed-article:11927558 | pubmed:author | pubmed-author:RosendahlAlex... | lld:pubmed |
pubmed-article:11927558 | pubmed:author | pubmed-author:SiderasPascha... | lld:pubmed |
pubmed-article:11927558 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11927558 | pubmed:day | 2 | lld:pubmed |
pubmed-article:11927558 | pubmed:volume | 21 | lld:pubmed |
pubmed-article:11927558 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11927558 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11927558 | pubmed:pagination | 1743-53 | lld:pubmed |
pubmed-article:11927558 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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