Document Detail


Allosteric modulation of protease-activated receptor signaling.
MedLine Citation:
PMID:  22681248     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The protease-activated receptors (PARs) are G protein-coupled receptors (GPCRs) that are uniquely activated by proteolysis. PARs mediate hemostasis, thrombosis, inflammation, embryonic development and progression of certain malignant cancers. The family of PARs include four members: PAR1, PAR2, PAR3 and PAR4. PARs harbor a cryptic ligand sequence within their N-terminus that is exposed following proteolytic cleavage. The newly formed PAR Nterminus functions as a tethered ligand that binds intramolecularly to the receptor to trigger transmembrane signaling. This unique mechanism of activation would indicate that regardless of the activating protease, cleavage of PARs would unmask a tethered ligand sequence that would induce a similar active receptor conformation and signaling response. However, this is not the case. Recent studies demonstrate that PARs can be differentially activated by synthetic peptide agonists, proteases or through dimerization, that ultimately result in distinct cellular responses. In some cases, allosteric modulation of PARs involves compartmentalization in caveolae, plasma membrane microdomains enriched in cholesterol. Here, we discuss some mechanisms that lead to allosteric modulation of PAR signaling.
Authors:
I Canto; U J K Soh; J Trejo
Related Documents :
10942778 - Antiproliferative properties of sphingosine 1-phosphate in human hepatic myofibroblasts...
16383308 - Real-time monitoring of morphological changes in living cells by electronic cell sensor...
22725608 - Deciphering µ-opioid receptor phosphorylation and dephosphorylation in hek293 cells.
12084918 - Characterization of an orphan g protein-coupled receptor localized in the dorsal root g...
8301598 - Inhibition by capsazepine of resiniferatoxin- and capsaicin-induced contractions of gui...
19906028 - Translating 5-ht receptor pharmacology.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Mini reviews in medicinal chemistry     Volume:  12     ISSN:  1875-5607     ISO Abbreviation:  Mini Rev Med Chem     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-07-04     Completed Date:  2012-10-24     Revised Date:  2012-11-06    
Medline Journal Info:
Nlm Unique ID:  101094212     Medline TA:  Mini Rev Med Chem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  804-11     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, School of Medicine, University of California, San Diego, Biomedical Sciences Building, Room 3044A, 9500 Gilman Drive, La Jolla, CA 92093-0636, USA. joanntrejo@ucsd.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Allosteric Regulation
Cell Transformation, Neoplastic / metabolism
Embryonic Development / physiology
Hemostasis / drug effects,  physiology
Humans
Peptides / pharmacology
Protein Isoforms / metabolism
Protein Multimerization
Protein Structure, Tertiary
Proteolysis / drug effects
Receptors, Proteinase-Activated / metabolism*
Signal Transduction / drug effects,  physiology*
Thrombin / metabolism*
Thrombosis / metabolism,  physiopathology
Grant Support
ID/Acronym/Agency:
GM090689/GM/NIGMS NIH HHS; HL073328/HL/NHLBI NIH HHS; R01 GM090689/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Peptides; 0/Protein Isoforms; 0/Receptors, Proteinase-Activated; EC 3.4.21.5/Thrombin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Cadaveric analysis of an accelerometer-based portable navigation device for distal femoral cutting b...
Next Document:  Functional selectivity in GPCR heterocomplexes.