J
Jennifer S. Colvin
Researcher at Washington University in St. Louis
Publications - 14
Citations - 5629
Jennifer S. Colvin is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Fibroblast growth factor & Fibroblast growth factor receptor 3. The author has an hindex of 12, co-authored 14 publications receiving 5432 citations. Previous affiliations of Jennifer S. Colvin include University of Sydney.
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Journal ArticleDOI
Receptor specificity of the fibroblast growth factor family.
David M. Ornitz,Jingsong Xu,Jennifer S. Colvin,Donald G. McEwen,Craig A. MacArthur,François Coulier,Guangxia Gao,Mitchell Goldfarb +7 more
TL;DR: It is demonstrated that FGF 1 is the only FGF that can activate all FGF receptor splice variants and the relative activity of all the other members of the FGF family is determined.
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Skeletal overgrowth and deafness in mice lacking fibroblast growth factor receptor 3.
TL;DR: It is demonstrated that Fgfr3 is essential for normal endochondral ossification and inner ear development and Contrasts between the skeletal phenotype and achondroplasia suggest that activation of FGFR3 causes achondaplasia.
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Male-to-Female Sex Reversal in Mice Lacking Fibroblast Growth Factor 9
TL;DR: Male-to-female sex reversal in mice lacking Fibroblast growth factor 9 (Fgf9) is reported, demonstrating a novel role for FGF signaling in testicular embryogenesis and suggesting Fgfs may function in sex determination and reproductive system development in many species.
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Coordination of chondrogenesis and osteogenesis by fibroblast growth factor 18
TL;DR: It is demonstrated that FGF18 is expressed in the perichondrium and that mice homozygous for a targeted disruption of Fgf18 exhibit a growth plate phenotype similar to that observed in mice lacking Fgfr3 and an ossification defect at sites that express F gfr2, suggesting that F GF18 acts as a physiological ligand for FGFR3.
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Repression of hedgehog signaling and BMP4 expression in growth plate cartilage by fibroblast growth factor receptor 3
TL;DR: Findings support a model in which Fgfr3 is an upstream negative regulator of the hedgehog (Hh) signaling pathway, which may coordinate the growth and differentiation of chondrocytes with the growth of osteoprogenitor cells by simultaneously modulating Bmp4 and patched expression in both growth plate cartilage and in the perichondrium.