Award details

Ubiquitination and de-ubiquitination in the regulation of cell signalling

ReferenceBBS/E/B/0000H081
Principal Investigator / Supervisor Dr Peter Kilshaw
Co-Investigators /
Co-Supervisors
Institution Babraham Institute
DepartmentBabraham Institute Department
Funding typeResearch
Value (£) 8,768
StatusCompleted
TypeInstitute Project
Start date 01/05/2003
End date 30/09/2004
Duration17 months

Abstract

Rejection of transplanted kidneys occurs when immune cells from the recipient attack the donor organ. Endothelial cells, which line the inner surface of blood vessels, constitute a barrier between the donor tissue and the recipient¿s circulating immune cells. The production of particular proteins by endothelial cells is known to alter their properties. Some molecules, such as NF-?B, trigger endothelial cells to become permissive to recipient immune cells, which leads to rejection. In contrast, endothelial cell production of a `protective¿ molecule called A20 has been associated with prolonged survival of transplanted organs. A20 is known to suppress the activity of the pro-inflammatory molecule NF-?B and also to prevent endothelial cell death. Our recent findings have revealed a new biological activity for A20 which may explain its protective effects

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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