Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.69 (APC)
 16,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein C is an anticoagulant protein that circulates in blood as a zymogen of a serine protease. Recently the exogenous Protein C activator has been obtained from the venom of Agkistrodon Contortrix Contortrix. We also reported a functional assay method which activates Protein C with PROTAC and then measure the amidolytic activity with chromogenic substrate (S-2366) by COBAS FARA. At present, S-2366 (Glu-Pro-Arg-pNA), CBS 65-25 (Lys-Pro-Arg-pNA) and SPECTROZYME PCa (Lys-Pro-Arg-pNA) are used as the chromogenic substrate for activated Protein C. We studied which substrate is more suitable for amidolytic activity assay for Protein C by PROTAC in 99 patients under long-term Warfarin therapy and 29 as normal subjects. Our results indicate that SPECTROZYME PCa and CBS 65-25 are unsuitable for Protein C activity assay with PROTAC. Because change of absorbance was detected in Protein C deficient plasma and we couldn't gain good correlation between amidolytic activity of activated Protein C measured with these chromogenic substrates and antigenicity of Protein C by EIA. On the other hand, S-2366 is the most specific for activated Protein C and we also obtained good correlation against Protein C antigen.
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PMID:[Study of chromogenic substrate on protein C activity assay--in patients treated with warfarin]. 223 57

Although Virchow postulated 100 years ago that hypercoagulability states exist, it has only been in recent years that methods of documenting hypercoagulability have been developed. These clotting tendencies can be acquired or congenital. The common causes of acquired clotting tendencies include conditions which result in tissue and cellular damage, shock, transfusion reactions, and tissue necrosis. Certain drugs and drug reactions, and certain disease states which include blood dyscrasias and cancer are also associated with clotting problems. In certain diseases such as homocystinuria, hyperlipidemia, and lupus erythematosus, abnormal clotting tendencies may also develop. Important advances in the recognition of hypercoagulability have come with the documentation that congenital clotting abnormalities exist. Moreover, these abnormalities are proving to be more common than are congenital bleeding syndromes. Patients who appear to have spontaneous clotting manifestations and are under 40 years of age should be screened for one of these abnormalities. These congenital clotting tendencies can be classified as defects in thrombosis inhibitors, dysfibrinogenemias, or defects in fibrinolysis. The first thrombotic inhibitor defect recognized was antithrombin III deficiency which was reported in 1965. Subsequently, Protein C, Protein S, and Heparin cofactor II deficiencies have been recognized as contributing to thrombotic tendencies. Dysfibrinogenemias are relatively rare and most are associated with bleeding problems; however, 11% of the abnormal fibrinogens are associated with a clotting tendency. The reason appears to be that these fibrins are resistant to fibrinolysis. The most common defects which are associated with thrombotic tendencies appear, at the present time, to be due to defects in fibrinolysis. These include hypoplasminogenemia, decreases in plasminogen activator, increases in plasminogen activator inhibitor, and Factor XII deficiency.
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PMID:Acquired and congenital clotting syndromes. 223 69

Adrenocortical hormones have been used for nephrotic syndrome from 1950. But effects of these drugs in coagulation and fibrinolysis are unknown in detail. We studied the effect of prednisolone in a patient with nephrotic syndrome. Protein C increased remarkably after administration of prednisolone 40 mg/day and then decreased in parallel with the dose of prednisolone. Factor X increased more slowly than Protein C. On the other hand, we couldn't find increase of Protein S. Our results indicate that prednisolone have anticoagulant effect by promotion of production of Protein C.
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PMID:[A case of nephrotic syndrome with abnormally high level of protein C induced by prednisolone]. 226 77

We present a case of a 52-year-old woman suffering from an ischemic central retinal vein thrombosis with neovascular glaucoma of her left eye. Protein C activity was found to be reduced (32%). This supports the hypothesis that protein C may play a role in the pathogenesis of ocular vaso-occlusive disease, as protein C is an important inhibitor of hemostasis. Thus, we suggest to measure protein C in patients with preceding thromboembolic diseases or assumed disorders of coagulation.
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PMID:[Ischemic occlusion of the central retinal vein and protein C deficiency]. 229 11

Protein C is a vitamin K-dependent anticoagulant that functions by inhibiting the activity of factors Va and VIIIa. An inherited deficiency of this protein may enhance the risk of thrombosis. The first kindred with levels of protein C that averaged 50% of normal in association with recurrent thrombotic events were described in 1981. A black South African family with an inherited deficiency of this protein is reported.
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PMID:Protein C deficiency in a black South African family. A case report. 230 Aug 56

Protein C and antithrombin III represent main inhibitors of the plasmatic coagulation system. Due to the lack of practicable assays the clinical importance of protein C was only established during the last six years. In familial protein C deficiency 77% of patients present with recurrent venous thromboses, half of them below the age of 30. In addition to recurrent superficial thrombophlebitis more serious manifestations like deep vein thrombosis and pulmonary embolism have been described. Mesenteric vein thrombosis has been reported in only 5 cases all of which could be controlled by conservative treatment. In our patient protein C deficiency was discovered 10 years after the angiographic diagnosis of portal and mesenteric vein thrombosis. Thereafter, the patient complained of recurrent abdominal discomfort. Intestinal ischaemia due to mesenteric vein thrombosis required segmental resection twice. Postoperatively the patient was heparinized. After excluding a secondary protein C deficiency due to a lack in vitamin K, hepatic disease, or disseminated intravascular coagulation, long-term anticoagulation by dicumarol was implemented as therapy of first choice.
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PMID:[Protein C deficiency with recurrent infarct of the small intestine]. 231 54

In the neonatal rat submandibular gland, Type III cells contain a group of related proteins that we call the B1-immunoreactive proteins (B1-IP; 23.5, 26, and 27.5 kDa). Type I cells lack these, but synthesize a different protein, Protein C (89 kDa). With maturation of the gland, these neonatal cell types are no longer seen in the seromucous acini, which are no longer reactive for the B1-IP. Here, we report the ultrastructural immunocytochemical localization of the B1-IP and Protein C over the course of development. From their first appearance in the embryo, the B1-IP and Protein C are present in different cells which become morphologically typical Type I and III cells prior to birth. At all stages, Type I cells have strong Protein C labeling and no B1 labeling. By 3 days postpartum, ultrastructurally atypical Type III cells are seen (Type IIIP); these label for the B1-IP, but also show labeling with antibody to Protein C. In the next week, as mucous cells appear in the acini, these show both B1-IP and C labeling; the B1 marker is lost by 30 days postpartum, but adult mucous acinar cells continue to show Protein C reactivity. In view of the appearance of Protein C reactivity in neonatal Type IIIP and then in mucous cells, and the presence of B1 reactivity in early but not mature mucous cells, we suggest that Type III cells differentiate into mucous cells and that Type IIIP cells are intermediates in this transformation. We see no evidence for the differentiation of either Type III or mucous cells from Type I cells, although our data cannot rule out this possibility. In adult glands, cells with B1 labeling are seen in intercalated ducts. Cells that appear to be Type I cells are also present in these ducts and label for Protein C. Double labeling for B1-IP and Protein C demonstrated that the two markers were exclusively present in different cells within intercalated ducts. This is of considerable interest, as intercalated ducts have been reported to be the stem cell population for normal and trauma-induced cellular replacement.
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PMID:Localization of neonatal secretory proteins in different cell types of the rat submandibular gland from embryogenesis to adulthood. 233 73

The hemostatic response to acute exercise and increased atmospheric pressure was studied in 20 healthy male subjects (18-35 yr of age) exercised to volitional exhaustion on a cycle ergometer in a hyperbaric chamber at 3 atmospheres absolute (ATA). As a means of comparison, 6 of the 20 subjects were exercised in the same manner at 1 ATA. Similar increases in fibrinolytic activity (FA), Factor VIII activity (VIII:C), von Willebrand factor antigen (vWF:Ag) and plasma catecholamine levels were observed following acute exercise at 1 ATA and at 3 ATA. There were no changes in the levels of plasminogen, antithrombin III, Protein C or Fibrinopeptide A (FPA) with exercise either at 1 ATA or at 3 ATA. In addition, there were no changes in plasma catecholamine levels or any of the hemostatic variables measured when atmospheric pressure was increased from 1 ATA to 3ATA without exercise. These findings demonstrate that increasing atmospheric pressure from 1 ATA to 3 ATA does not alter the exercise-induced changes in hemostasis. Therefore, exercise or physical exertion at 3 ATA for a time period not to exceed 30 min does not perturb the hemostatic mechanism and increase the risk of bleeding or thrombosis.
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PMID:The effects of acute exercise and increased atmospheric pressure on the hemostatic mechanism and plasma catecholamine levels. 233 66

We describe a case of massive cerebral venous thrombosis following open heart surgery in a patient with a reduced level of Protein C (40% of mean level). Protein C deficiency is an inherited disorder which in the homozygous form may result in massive fatal venous thrombosis in the newborn. A Protein C level below 55% is highly suggestive of heterozygous deficiency and has been associated with a tendency to venous thrombosis although its clinical penetrance is variable. This is the first reported case of massive venous thrombosis in a patient following open heart surgery associated with Protein C deficiency.
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PMID:Protein C deficiency associated with massive cerebral thrombosis following open heart surgery. 234 85

Protein C (PC) is considered to be an important regulator of blood coagulation and fibrinolysis. During the production of monoclonal antibodies (MoAbs) against human PC in mouse ascitic fluid, one hybridoma was found to induce heavy thrombus in mice, resulting in severe hemorrhage. Intravenous infusion of the purified MoAb (PC01) from this hybridoma also caused thrombosis in mice. The crossreacting substance was then isolated from mouse plasma with PC01 immunoaffinity column, which was identified as mouse PC by several criteria. Mouse PC prolonged the activated partial thromboplastin time of mouse plasma, and PC01 neutralized this in vitro anti-coagulant activity. Therefore, heavy thrombosis observed in PC01-treated mice is likely to be ascribed to the defect of PC caused by PC01.
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PMID:Anti-protein C monoclonal antibody induces thrombus in mice. 234 79


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