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P13K and Vav-dependent regulation of Rac activation reactive oxygen species production and phagocytosis by neutrophils

Reference	BBS/B/01979
Principal Investigator / Supervisor	Professor Len Stephens
Co-Investigators / Co-Supervisors	Professor Edwin Chilvers, Dr Phillip Hawkins, Professor Klaus Okkenhaug, Dr Martin Turner
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	219,477
Status	Completed
Type	Research Grant
Start date	13/04/2004
End date	12/04/2007
Duration	36 months

Abstract

Neutrophils are a vital part of the immune system because of their ability to hunt-down, phagocytose and kill pathogenic bacteria and fungi. These processes are co-ordinated by a family of neutrophil receptors that act to either prime or elicit phagocytic uptake and subsequent intracellular digestion of opsonised particles and/or localised extracellular release of degradative agents. Key amongst these degradative agents are reactive oxygen species (ROS) because of their intrinsic cyto-toxicity and ability to initiate the mobilisation of proteases. The signalling downstream of the receptors that control these response, is poorly understood. PI3Ks and Rac proteins have already been implicated and our preliminary data indicates Vav proteins are involved. Within the context of multiple forms of all 3 of these families being present in neutrophils we propose to study the roles of specific molecules from these families in the delivery of ROS formation and phagocytosis.

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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