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BBSRC Quota Studentship: Regulation of DUSP5 and DUSP6 expression in RAS and BRAF-dependent tumour cells

ReferenceBBS/E/B/0000L953
Principal Investigator / Supervisor Dr Simon Cook
Co-Investigators /
Co-Supervisors
Institution Babraham Institute
DepartmentBabraham Institute Department
Funding typeResearch
Value (£) 12,923
StatusCompleted
TypeInstitute Project
Start date 01/10/2003
End date 30/09/2007
Duration48 months

Abstract

KRAS and BRAF are human proto-oncogenes that are mutated in human tumours and lead to hyperactivation of the ERK1/2 signalling pathway. ERK1/2 are protein kinases that phosphorylate key substrates to promote gene expression, cell proliferation and cell survival. ERK1/2 are themselves activated by phosphorylation catalysed by a protein kinase called MEK1. ERK1/2 are inactivated by removal of these activating phosphates and this is catalysed by one of a number of phosphatases. Two of these phosphatases, called DUSP5 and DUSP6, are absolutely specific for ERK1/2 in cells. The expression of DUSP5 and DUSP6 can be increased in response to ERK1/2 activation as part of a self-regualting feedback mechanism. This project will investigate the degree to which this operates in human tumour cells which exhibit activation of the ERK1/2 pathway.

Summary

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