Document Detail

The endothelial cell protein C receptor. Inhibition of activated protein C anticoagulant function without modulation of reaction with proteinase inhibitors.
MedLine Citation:
PMID:  8663474     Owner:  NLM     Status:  MEDLINE    
A soluble form of the endothelial cell protein C receptor (EPCR) was analyzed for the ability to modulate the functional properties of protein C and activated protein C (APC). In a plasma clotting system initiated with factor Xa, EPCR blocked the anticoagulant activity of APC in a dose-dependent fashion. EPCR had no influence on clotting in the absence of APC. Consistent with the plasma results, EPCR slowed the proteolytic inactivation of factor Va by slowing both of the key proteolytic cleavages in the heavy chain of factor Va. EPCR did not prevent protein C activation by the soluble thrombin-thrombomodulin complex, did not alter the inactivation of APC by alpha1-antitrypsin or protein C inhibitor, and did not influence the kinetics of peptide paranitroanilide substrate cleavage significantly. We conclude that EPCR binds to an exosite on APC that selectively modulates the enzyme specificity in a manner reminiscent of the influence of thrombomodulin on thrombin.
L M Regan; D J Stearns-Kurosawa; S Kurosawa; J Mollica; K Fukudome; C T Esmon
Related Documents :
3930684 - Crohn's disease activity: assessment by factor viii coagulation proteins.
7309234 - Protein a effect on alternative pathway complement activation and opsonization of staph...
23213374 - 3d-structured illumination microscopy provides novel insight into architecture of human...
16479444 - Disorders of coagulation in stroke.
7518224 - Intracellular processing and antigenic maturation of measles virus hemagglutinin protein.
15044734 - A new, structurally nonredundant, diverse data set of protein-protein interfaces and it...
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  271     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  1996 Jul 
Date Detail:
Created Date:  1996-09-12     Completed Date:  1996-09-12     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  17499-503     Citation Subset:  IM    
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, University of Oklahoma Health Sciences Center, Oklahoma City, 73104, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Amidohydrolases / metabolism
Anticoagulants / metabolism*,  pharmacology
Blood Coagulation*
Blood Coagulation Factors*
Endothelium, Vascular / metabolism*
Factor Va / antagonists & inhibitors
Protease Inhibitors / pharmacology*
Protein C / antagonists & inhibitors,  metabolism*
Receptors, Cell Surface / metabolism*
Recombinant Proteins / metabolism
Grant Support
Reg. No./Substance:
0/Anticoagulants; 0/Blood Coagulation Factors; 0/Protease Inhibitors; 0/Protein C; 0/Receptors, Cell Surface; 0/Recombinant Proteins; 0/activated protein C receptor; 65522-14-7/Factor Va; EC 3.5.-/Amidohydrolases

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

Previous Document:  Metabolic stress opens K+ channels in hepatoma cells through a Ca2+- and protein kinase calpha-depen...
Next Document:  The endothelial cell protein C receptor. Cell surface expression and direct ligand binding by the so...