Asset Details
Do you wish to reserve the book?
Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
Do you wish to request the book?
Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
2017
Overview
Acute hormone secretion triggered by G protein-coupled receptor (GPCR) activation underlies many fundamental physiological processes. GPCR signalling is negatively regulated by β-arrestins, adaptor molecules that also activate different intracellular signalling pathways. Here we reveal that TRV120027, a β-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1R), stimulates acute catecholamine secretion through coupling with the transient receptor potential cation channel subfamily C 3 (TRPC3). We show that TRV120027 promotes the recruitment of TRPC3 or phosphoinositide-specific phospholipase C (PLCγ) to the AT1R-β-arrestin-1 signalling complex. Replacing the C-terminal region of β-arrestin-1 with its counterpart on β-arrestin-2 or using a specific TAT-P1 peptide to block the interaction between β-arrestin-1 and PLCγ abolishes TRV120027-induced TRPC3 activation. Taken together, our results show that the GPCR-arrestin complex initiates non-desensitized signalling at the plasma membrane by coupling with ion channels. This fast communication pathway might be a common mechanism of several cellular processes.
Angiotensin II type 1 receptor (AT1R)-mediated acute catecholamine release is modulated by β-arrestin. Here the authors show that β-arrestin-1 recruits the Ca
2+
channel TRPC3 and the PLCγ to the AT1R-β-arrestin complex, triggering G protein-independent calcium influx and catecholamine secretion.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 14/19
/ 14/35
/ 82/80
/ Animals
/ beta-Arrestin 1 - metabolism
/ beta-Arrestin 2 - metabolism
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Ligands
/ Medicine
/ Oligopeptides - pharmacology
/ Peptides
/ Phospholipase C gamma - metabolism
/ Plasma
/ Proteins
/ Pyrrolidinones - pharmacology
/ Receptor, Angiotensin, Type 1 - agonists
/ Receptor, Angiotensin, Type 1 - metabolism
/ Science
