activated protein c resistance/protease

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Decrease in protein C inhibitor activity and acquired APC resistance during normal pregnancy.

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BACKGROUND Since protein C inhibitor (PCI) inhibits activated protein C (APC) and a number of proteases, one would expect lower concentrations of PCI in a hypercoagulable state due to increased consumption of the inhibitor. Normal pregnancy is associated with a state of activated hemostasis, where

Preliminary Data From the Study of Coagulative Profile of HIV Infected Individuals Suggest a Role For Point Mutations in the Gene in Protein S Deficiency in Individuals Undergoing Highly Antiretroviral Therapy.

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UNASSIGNED HIV infection is a known prothrombotic condition but factors involved are still controversial. A role for antiretrovirals, especially protease inhibitors, was advocated. UNASSIGNED The study aimed to analyze the levels of anticoagulant proteins in virally suppressed HIV-infected subjects

Proteolysis of protein C in pooled normal plasma and purified protein C by activated protein C (APC).

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Protein C is a vitamin-K dependent zymogen of the anti-coagulant serine protease activated protein C (APC). In this paper, we report four lines of evidence that APC can activate protein C in pooled normal plasma, and purified protein C. First, the addition of APC to protein C-deficient plasma

Progress in the understanding of the protein C anticoagulant pathway.

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A natural anticoagulant pathway denoted the protein C system provides specific and efficient control of blood coagulation. Protein C is the key component of the system and circulates in the blood as a zymogen to an anticoagulant serine protease. Activation of protein C is achieved on the surface of

Factor V.

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Factor V is a single chain glycoprotein that plays an essential role in the regulation of blood coagulation. After initiation of coagulation, factor V is converted into factor Va through limited proteolysis. Factor Va acts as protein cofactor in the prothrombin-activating complex, which is comprised

Survival advantage of heterozygous factor V Leiden carriers in murine sepsis.

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BACKGROUND The high allelic frequency of the prothrombotic Leiden polymorphism in human blood coagulation factor V (FV) has been speculated to reflect positive selection during evolution. Heterozygous Leiden carriers enrolled in the placebo arm of the PROWESS sepsis trial and heterozygous Leiden

Venous thrombosis and changes of hemostatic variables during cross-sex hormone treatment in transsexual people.

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The incidence of venous thrombosis associated with estrogen treatment in male-to-female (M-->F) transsexuals is considerably higher with administration of oral ethinyl estradiol (EE) than with transdermal (td) 17-beta-estradiol (E(2)). To find an explanation for the different thrombotic risks of

Protein Z levels and central retinal vein or artery occlusion.

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OBJECTIVE Central retinal vein occlusion (CRVO) and central retinal artery occlusion (CRAO) are common disorders associated with risk factors for atherosclerosis. Protein Z is a cofactor for the inactivation of activated factor X (Xa) by the protein Z dependent protease inhibitor. Protein Z

Mutation in blood coagulation factor V associated with resistance to activated protein C.

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Activated protein C (APC) is a serine protease with potent anticoagulant properties, which is formed in blood on the endothelium from an inactive precursor. During normal haemostasis, APC limits clot formation by proteolytic inactivation of factors Va and VIIIa (ref. 2). To do this efficiently the

Possible mechanisms contributing to oxidative inactivation of activated protein C: molecular dynamics study.

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Activated protein C (APC) is a serine protease, an effector enzyme of the natural anticoagulant pathway. APC is approved for treatment of severe sepsis characterized by the increased concentrations of H(2)O(2) and hypochlorite. We found that treatment of APC with these oxidants markedly inhibits the

The cytoprotective protein C pathway.

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Protein C is best known for its mild deficiency associated with venous thrombosis risk and severe deficiency associated with neonatal purpura fulminans. Activated protein C (APC) anticoagulant activity involves proteolytic inactivation of factors Va and VIIIa, and APC resistance is often caused by

Venous thrombosis among patients with AIDS.

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Thrombosis has been considered an uncommon complication in patients with AIDS. In a 42-month period, 28 adult male homosexuals with AIDS experienced 34 thrombotic events. All but three received HAART regimen, two a successful round of double nucleoside analog therapy, and one patient received no

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