Prolylcarboxypeptidase Independently Activates Plasma Prekallikrein (Fletcher Factor)
نویسندگان
چکیده
منابع مشابه
Recombinant prolylcarboxypeptidase activates plasma prekallikrein.
The serine protease prolylcarboxypeptidase (PRCP), isolated from human umbilical vein endothelial cells (HUVECs), is a plasma prekallikrein (PK) activator. PRCP cDNA was cloned in pMT/BIP/V5-HIS-C, transfected into Schneider insect (S2) cells, and purified from serum-free media. Full-length recombinant PRCP (rPRCP) activates PK when bound to high-molecular-weight kininogen (HK). Recombinant PRC...
متن کاملPrekallikrein (Fletcher factor) deficiency.
One new case and 29 reported cases of hereditary prekallikrein (Fletcher factor) deficiency are reviewed. Abnormalities in the coagulation, fibrinolytic, complement, and kinin systems are described. These cases are discovered incidentally by prolonged partial thromboplastin times (PTTs) which correct with extended incubation in the presence of a contact activator. Prekallikrein levels are less ...
متن کاملIdentification of prolylcarboxypeptidase as the cell matrix-associated prekallikrein activator.
Investigations determined that the cell matrix-associated prekallikrein (PK) activator is prolylcarboxypeptidase. PK activation on human umbilical vein endothelial cell (HUVEC) matrix is inhibited by antipain (IC(50)=50 microM) but not anti-factor XIIa antibody, 3 mM benzamidine, 5 mM iodoacetic acid or iodoacetamide, or 3 mM N-ethylmaleimide. Corn trypsin inhibitor (IC(50)=100 nM) or Fmoc-amin...
متن کاملOverexpression of prolylcarboxypeptidase enhances plasma prekallikrein activation on Chinese hamster ovary cells.
Plasma prekallikrein (PK) complexes with its receptor, high-molecular-weight kininogen (HK), on human umbilical vein endothelial cells (HUVEC). When assembled on endothelial cells, PK is activated to plasma kallikrein independent of factor XIIa by the serine protease prolylcarboxypeptidase (PRCP, Km= 9 nM). PRCP was shown to be a PK activator when isolated from HUVEC (J Biol Chem 277: 17962-179...
متن کاملSevere prekallikrein (Fletcher factor) deficiency due to a compound heterozygosis (383Trp stop codon and Cys529Tyr).
We investigated a family with prekallikrein deficiency, using both standard coagulation tests and molecular biology techniques. The propositus was found to be a compound heterozygote for a Trp383 stop codon and a Cys529Tyr point mutation. The former mutation was located in exon 11, the latter in exon 14. The propositus inherited the first defect from his father and the second from his mother. B...
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ژورنال
عنوان ژورنال: Current Molecular Medicine
سال: 2014
ISSN: 1566-5240
DOI: 10.2174/1566524014666141015153519