Journal article

Arresting inflammation: contributions of plasma membrane and endosomal signalling to neuropeptide-driven inflammatory disease

Fiore Cattaruzza, Daniel P Poole, Nigel W Bunnett

Biochemical Society Transactions | PORTLAND PRESS LTD | Published : 2013

Abstract

GPCR (G-protein-coupled receptor) signalling at the plasma membrane is under tight control. In the case of neuropeptides such as SP (substance P), plasma membrane signalling is regulated by cell-surface endopeptidases (e.g. neprilysin) that degrade extracellular neuropeptides, and receptor interaction with β-arrestins, which uncouple receptors from heterotrimeric G-proteins and mediate receptor endocytosis. By recruiting GPCRs, kinases and phosphatases to endocytosed GPCRs, β-arrestins assemble signalosomes that can mediate a second wave of signalling by internalized receptors. Endosomal peptidases, such as ECE-1 (endothelin-converting enzyme-1), can degrade SP in acidified endosomes, which ..

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University of Melbourne Researchers

Grants

Awarded by National Health and Medical Research Council (NHMRC)


Awarded by National Institutes of Health (NIH)


Awarded by NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES


Funding Acknowledgements

This work was supported by grants from the National Health and Medical Research Council (NHMRC) [grant number 633033] and National Institutes of Health (NIH) [grant number DK39957] to N.W.B.