HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Russo, A. Articles by Trejo, J. Search for Related Content PubMed PubMed Citation Articles by Russo, A. Articles by Trejo, J.

Proteases Display Biased Agonism at Protease-Activated Receptors: Location matters!

¹ Department of Pharmacology, University of North Carolina, Chapel Hill and
² Department of Pharmacology, University of California, San Diego

Protease-activated receptors (PARs) are G protein–coupled receptors (GPCRs) that transmit cellular responses begun by the actions of extracellular proteases. The activation of a PAR occurs by a unique mechanism whereby the extracellular N-terminal segment of the inactive receptor undergoes proteolytic cleavage, resulting in irreversible activation––unlike most GPCRs that are reversibly activated. PARs mediate cellular responses to coagulant proteases in various cell types localized within the vasculature. Additionally, PARs are expressed in other cell types and respond to a plethora of proteases. Recent studies have revealed that different proteases elicit distinct responses through the activation of the same PAR. This phenomenon appears to involve stabilization of distinct active PAR conformations that facilitates selectively coupling to different effectors and is localized to caveolae, a subtype of lipid rafts.

This article has been cited by other articles:

				M. B. Duncan and R. Kalluri Parstatin, a Novel Protease-Activated Receptor 1-Derived Inhibitor of Angiogenesis Mol. Interv., August 1, 2009; 9(4): 168 - 170. [Abstract] [Full Text] [PDF]