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The role of palmitoylation in Y1 receptor inactivation and signalling specificity

Reference	C12870
Principal Investigator / Supervisor	Professor Helen Cox
Co-Investigators / Co-Supervisors	Dr Nicholas Holliday
Institution	King's College London
Department	GKT School of Biomedical Sciences
Funding type	Research
Value (£)	196,279
Status	Completed
Type	Research Grant
Start date	01/01/2000
End date	01/07/2003
Duration	42 months

Abstract

We have found that both the native Y1 receptor and a C337S mutant (lacking the putative C terminal palmitoylation site) attenuate chloride secretion via Gi proteins in stably transfected epithelial clones; however, Y1 (C337S) receptors are resistant to desensitisation. This project will further investigate the C337S phenotype and the wider role of palmitoylation by molecular, biochemical and functional approaches. Studies will include an assessment of Y1 and Y1 (C337S) receptor efficacies, and the generation of new mutants which target phosphorylation sites near to Cys337 (i.e. Ser341 or Thr348) and a potential acylation consensus sequence (FQRDL). Antisense techniques and Y1-Gi alpha fusion constructs will provide new insights into Y1/Y1 (C337S) receptor coupling specificity and trafficking of receptor signals by two native peptides, neuropeptide Y and peptide YY.

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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