| pubmed-article:15863035 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15863035 | lifeskim:mentions | umls-concept:C0816871 | lld:lifeskim |
| pubmed-article:15863035 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:15863035 | lifeskim:mentions | umls-concept:C0016026 | lld:lifeskim |
| pubmed-article:15863035 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:15863035 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15863035 | pubmed:dateCreated | 2005-5-2 | lld:pubmed |
| pubmed-article:15863035 | pubmed:abstractText | Mutations in fibroblast growth factor receptors (Fgfrs) are the etiology of many craniosynostosis and chondrodysplasia syndromes in humans. The phenotypes associated with these human syndromes and the phenotypes resulting from targeted mutagenesis in the mouse have defined essential roles for FGF signaling in both endochondral and intramembranous bone development. In this review, I will focus on the role of FGF signaling in chondrocytes and osteoblasts and how FGFs regulate the growth and development of endochondral bone. | lld:pubmed |
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