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Imprinting of Igf2: role of repressors and silencers and relevance to Beckwith-Wiedemann cancer syndrome

Reference	BBS/E/B/21966373
Principal Investigator / Supervisor	Professor Wolf Reik
Co-Investigators / Co-Supervisors
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	130,929
Status	Completed
Type	Institute Project
Start date	02/01/1998
End date	31/01/2001
Duration	37 months

Abstract

We inherit a set of genes from our mother and from our father. For most, both copies are equally active irrespective of their parentage. A few genes defy this expectation: only one copy of an imprinted gene is normally expressed. Consequently, developmental processes in which imprinted genes function are especially susceptible to the effect of mutation, for example, problems in imprinting give rise to disturbances in fetal growth and predispose to some cancers. The molecular means by which one copy of an imprinted gene is silenced are poorly understood.One of the genes which is important for growth of babies in the womb is Igf2. If this gene is not properly shut off in children and in adults, it may be able to cause cancers. We are studying a regulatory region in Igf2 which may be required for shutting off the gene. We are altering this region to see whether Igf2 is regulated differently, and whether these mice have a higher risk of developing cancer. This model may lead to important diagnostic and therapeutic applications.

Summary

unavailable

Committee	Closed Committee - Genes & Developmental Biology (GDB)
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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