| pubmed-article:15452148 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15452148 | lifeskim:mentions | umls-concept:C0083867 | lld:lifeskim |
| pubmed-article:15452148 | lifeskim:mentions | umls-concept:C1332712 | lld:lifeskim |
| pubmed-article:15452148 | lifeskim:mentions | umls-concept:C1416962 | lld:lifeskim |
| pubmed-article:15452148 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:15452148 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15452148 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:15452148 | pubmed:dateCreated | 2004-9-28 | lld:pubmed |
| pubmed-article:15452148 | pubmed:abstractText | Bone morphogenetic protein 7 (BMP-7) regulates cellular metabolism in embryonic and adult tissues. Signal transduction occurs through the activation of intracellular Smad proteins. In this paper, using a yeast two-hybrid screen, Smad1 was found to interact with the cytoplasmic domain of CD44, a receptor for the extracellular matrix macromolecule hyaluronan. Coimmunoprecipitation experiments confirmed the interaction of Smad1 with full-length CD44-interactions that did not occur when CD44 receptors truncated within the cytoplasmic domain were tested. Chondrocytes overexpressing a truncated CD44 on a background of endogenous full-length CD44 no longer exhibited Smad1 nuclear translocation upon BMP-7 stimulation. Further, pretreatment of chondrocytes with Streptomyces hyaluronidase to disrupt extracellular hyaluronan-cell interactions inhibited BMP-7-mediated Smad1 phosphorylation, nuclear translocation of Smad1 or Smad4, and SBE4-luciferase reporter activation. These results support a functional link between the BMP signaling cascade and CD44. Thus, changes in hyaluronan-cell interactions may serve as a means to modulate cellular responsiveness to BMP. | lld:pubmed |
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| pubmed-article:15452148 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15452148 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15452148 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15452148 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15452148 | pubmed:issn | 0021-9525 | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:KnudsonWarren... | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:KnudsonCheryl... | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:PetersonRicha... | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:WangWeihuaW | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:RouscheKathle... | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:Hollingsworth... | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:ThomasRaymond... | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:AndhareRoma... | lld:pubmed |
| pubmed-article:15452148 | pubmed:author | pubmed-author:GrossfieldJam... | lld:pubmed |
| pubmed-article:15452148 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15452148 | pubmed:day | 27 | lld:pubmed |
| pubmed-article:15452148 | pubmed:volume | 166 | lld:pubmed |
| pubmed-article:15452148 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15452148 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15452148 | pubmed:pagination | 1081-91 | lld:pubmed |
| pubmed-article:15452148 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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