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Ubiquitination and de-ubiquitination in the regulation of cell signalling
Reference
BBS/E/B/0000H081
Principal Investigator / Supervisor
Dr Peter Kilshaw
Co-Investigators /
Co-Supervisors
Institution
Babraham Institute
Department
Babraham Institute Department
Funding type
Research
Value (£)
8,768
Status
Completed
Type
Institute Project
Start date
01/05/2003
End date
30/09/2004
Duration
17 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 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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