pubmed-article:20855508 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20855508 | lifeskim:mentions | umls-concept:C0244756 | lld:lifeskim |
pubmed-article:20855508 | lifeskim:mentions | umls-concept:C0029433 | lld:lifeskim |
pubmed-article:20855508 | lifeskim:mentions | umls-concept:C0005508 | lld:lifeskim |
pubmed-article:20855508 | lifeskim:mentions | umls-concept:C0279266 | lld:lifeskim |
pubmed-article:20855508 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
pubmed-article:20855508 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:20855508 | pubmed:dateCreated | 2010-9-21 | lld:pubmed |
pubmed-article:20855508 | pubmed:abstractText | Extracellular regulation of signaling by transforming growth factor (TGF)-? family members is emerging as a key aspect of organ formation and tissue remodeling. In this study, we demonstrate that fibrillin-1 and -2, the structural components of extracellular microfibrils, differentially regulate TGF-? and bone morphogenetic protein (BMP) bioavailability in bone. Fibrillin-2-null (Fbn2(-/-)) mice display a low bone mass phenotype that is associated with reduced bone formation in vivo and impaired osteoblast maturation in vitro. This Fbn2(-/-) phenotype is accounted for by improper activation of latent TGF-? that selectively blunts expression of osterix, the transcriptional regulator of osteoblast maturation, and collagen I, the structural template for bone mineralization. Cultured osteoblasts from Fbn1(-/-) mice exhibit improper latent TGF-? activation as well, but mature faster because of increased availability of otherwise matrix-bound BMPs. Additional in vitro evidence excludes a direct role of microfibrils in supporting mineral deposition. Together, these findings identify the extracellular microfibrils as critical regulators of bone formation through the modulation of endogenous TGF-? and BMP signaling. | lld:pubmed |
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pubmed-article:20855508 | pubmed:language | eng | lld:pubmed |
pubmed-article:20855508 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20855508 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20855508 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20855508 | pubmed:month | Sep | lld:pubmed |
pubmed-article:20855508 | pubmed:issn | 1540-8140 | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:KarsentyGerar... | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:OnoRobert NRN | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:SakaiLynn YLY | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:RamirezFrance... | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:SmaldoneSilvi... | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:LevasseurRegi... | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:DucyPatriciaP | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:SengleGerhard... | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:CartaLucaL | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:Arteaga-Solis... | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:Lee-ArteagaSu... | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:NistalaHariki... | lld:pubmed |
pubmed-article:20855508 | pubmed:author | pubmed-author:SicilianoGabr... | lld:pubmed |
pubmed-article:20855508 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20855508 | pubmed:day | 20 | lld:pubmed |
pubmed-article:20855508 | pubmed:volume | 190 | lld:pubmed |
pubmed-article:20855508 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20855508 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20855508 | pubmed:pagination | 1107-21 | lld:pubmed |
pubmed-article:20855508 | pubmed:dateRevised | 2011-7-28 | lld:pubmed |
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