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Control of cell cycle and apoptosis in cortical progenitors by FGF receptor 3

Reference	BBS/B/08736
Principal Investigator / Supervisor	Dr Tomoko Iwata
Co-Investigators / Co-Supervisors
Institution	University of Glasgow
Department	Institute of Cancer Studies
Funding type	Research
Value (£)	209,270
Status	Completed
Type	Research Grant
Start date	12/07/2004
End date	11/07/2007
Duration	36 months

Abstract

Our preliminary observation shows that a gain-of-function mutation of the Fibroblast Growth Factors Receptor 3 (Fgfr3) in mice causes a dramatic increase in the neocortex thickness. Fgfr3 is expressed in the embryonic neuroepithelium where cortical progenitors are produced. The function of Fgfr3 in cortex progenitors has not been investigated so far. In this study, we will identify how activated Fgfr3 regulates cell cycle kinetics and apoptosis in the Fgfr3-positive population of cortical progenitors using a combination of histology, cell biology, and biochemical approaches. The project will set the basis for a better understanding of molecular mechanisms controlling of cortical progenitor proliferation and differentiation by FGF.

Summary

unavailable

Committee	Closed Committee - Biochemistry & Cell Biology (BCB)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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