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Fibroblast growth factor receptors a...
~
Tholpady, Sunil Shantigodu.
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Fibroblast growth factor receptors and calvarial development.
Record Type:
Electronic resources : Monograph/item
Title/Author:
Fibroblast growth factor receptors and calvarial development./
Author:
Tholpady, Sunil Shantigodu.
Description:
197 p.
Notes:
Source: Dissertation Abstracts International, Volume: 64-03, Section: B, page: 1045.
Contained By:
Dissertation Abstracts International64-03B.
Subject:
Biology, Cell. -
Online resource:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3083124
Fibroblast growth factor receptors and calvarial development.
Tholpady, Sunil Shantigodu.
Fibroblast growth factor receptors and calvarial development.
- 197 p.
Source: Dissertation Abstracts International, Volume: 64-03, Section: B, page: 1045.
Thesis (Ph.D.)--University of Virginia, 2003.
The fibroblast growth factor (FGF) signaling system plays an integral role in the formation of many structures. Mutations in the receptors mediating FGF activity are associated with severe consequences, as evidenced by dwarfing disorders and craniosynostotic syndromes. The preponderance of bony and cartilaginous deficits in these natural mutations point to the role FGFRs play in the development of these structures.Subjects--Topical Terms:
1017686
Biology, Cell.
Fibroblast growth factor receptors and calvarial development.
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197 p.
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Source: Dissertation Abstracts International, Volume: 64-03, Section: B, page: 1045.
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Adviser: Roy Ogle.
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Thesis (Ph.D.)--University of Virginia, 2003.
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The fibroblast growth factor (FGF) signaling system plays an integral role in the formation of many structures. Mutations in the receptors mediating FGF activity are associated with severe consequences, as evidenced by dwarfing disorders and craniosynostotic syndromes. The preponderance of bony and cartilaginous deficits in these natural mutations point to the role FGFRs play in the development of these structures.
520
$a
In this study, FGFR profiles were elucidated in cranial sutures, as well as bone and dural cells in vitro. Specific domains for FGFRs were found and their activities were tested both in vitro and in vivo. Dural cells are thought to be the endogenous secretors of FGFs, and varying concentrations of FGFs were used to mimic the in vivo situation of differential activation of bone cells as a function of distance from the dura. The experiments were designed so that the FGFs activated either the IgIIIb or IgIIIc splice variants of the FGFRs. FGFRI stimulation yielded a biphasic response curve with respect to bony differentiation. Proliferation was positively affected in a dose-dependent manner to IgIIIc activating ligands, with FGFR2 the apparent transducer of FGF signals to the intracellular milleu.
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These experiments coalesced a model in which centrally located FGFs acted upon FGFR2 to effect proliferation of osteoprogenitor cells within the suture. As these cells moved further from the morphogen gradient, FGFRI activation caused their differentiation. Thus, the spatial localization of FGFRI and FGFR2 allow for the proliferative and differentiative balance critical to suture preservation and function.
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School code: 0246.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3083124
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