Recombinant human protein C, protein S and thrombomodulin as antithrombotics

1994 ◽  
Vol 1 (3) ◽  
pp. 503-520 ◽  
Author(s):  
S. Betty Yan ◽  
Brian W. Grinnell
Keyword(s):  
Protein C ◽  
Protein S ◽  
Human Protein ◽  
C Protein ◽  
Recombinant Human Protein

A Procedure for Isolation of Human Protein C and Protein S as by-Products of the Purification of Factors VII, IX, X and Prothrombin

1983 ◽  
Vol 13 (3) ◽  
pp. 191-214 ◽  
Author(s):  
S. P. Bajaj ◽  
S. I. Rapaport ◽  
S. L. Maki ◽  
S. F. Brown
Keyword(s):  
Protein C ◽  
Protein S ◽  
Human Protein ◽  
By Products

Protein C, protein S and antithrombin III in children with portal vein obstruction

1997 ◽  
Vol 27 (1) ◽  
pp. 132-135 ◽  
Author(s):  
Claire Dubuisson ◽  
Catherine Boyer-Neumann ◽  
Martine Wolf ◽  
Dominique Meyer ◽  
Olivier Bernard
Keyword(s):  
Portal Vein ◽  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
C Protein ◽  
Portal Vein Obstruction

scholarly journals Thrombophilia And Arterial Ischemic Stroke

2017 ◽  
pp. 45
Author(s):  
A.A. Abrishamizadeh
Keyword(s):  
Ischemic Stroke ◽  
Vitamin K ◽  
Arterial Thrombosis ◽  
Protein C ◽  
Antithrombin Iii ◽  
Factor V Leiden ◽  
Protein S ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
C Protein

Ischemic stroke (IS) is a common cause of morbidity and mortality with significant socioeconomic impact especially when it affects young patients. Compared to the older adults, the incidence, risk factors, and etiology are distinctly different in younger IS. Hypercoagulable states are relatively more commonly detected in younger IS patients.Thrombophilic states are disorders of hemostatic mechanisms that result in a predisposition to thrombosis .Thrombophilia is an established cause of venous thrombosis. Therefore, it is tempting to assume that these disorders might have a similar relationship with arterial thrombosis. Despite this fact that 1-4 % of ischemic strokes are attributed to Thrombophillia, this   alone rarely causes arterial occlusions .Even in individuals with a positive thrombophilia screen and arterial thrombosis, the former might not be the primary etiological factor.Thrombophilic   disorders can be broadly divided into inherited or acquired conditions. Inherited thrombophilic states include deficiencies of natural anticoagulants such as protein C, protein S, and antithrombin III (AT III) deficiency, polymorphisms causing resistance to activated protein C(Factor V Leiden mutation), and disturbance in the clotting balance (prothrombin gene 20210G/A variant). Of all the inherited  thrombophilic disorders, Factor V Leiden mutation is perhaps the commonest cause. On the contrary, acquired thrombophilic disorders are more common and include conditions such as the antiphospholipid syndrome, associated with lupus anticoagulant and anticardiolipin antibodies.The more useful and practical approach of ordering various diagnostic tests for the uncommon thrombophilic states tests should be determined by a detailed clinical history, physical examination, imaging studies and evaluating whether an underlying hypercoagulable state appears more likely.The laboratory thrombophilia   screening should be comprehensive and avoid missing the coexisting defect and It is important that a diagnostic search protocol includes tests for both inherited and acquired thrombophilic disorders.Since the therapeutic approach (anticoagulation and thrombolytic therapy) determines the clinical outcomes, early diagnosis of the thrombophilic  disorders plays an important role. Furthermore, the timing of test performance of some of the  thrombophilic  defects (like protein C, protein S, antithrombin III and fibrinogen levels) is often critical since these proteins can behave as acute phase reactants and erroneously elevated levels of these factors may be observed in patients with acute thrombotic events. On the other hand, the plasma levels of vitamin K-dependent proteins (protein C, protein S and APC resistance) may not be reliable in patients taking vitamin K antagonists. Therefore, it is suggested that plasma-based assays for these disorders should be repeated3 to 6 months after the initial thrombotic episode to avoid false-positive results and avoid unnecessary prolonged   anticoagulation therapy. The assays for these disorders are recommended after discontinuation of oral anticoagulant treatment or heparin for at least 2 weeks.    

A Scalable Method for the Purification of Recombinant Human Protein C from the Milk of Transgenic Swine

1994 ◽  
pp. 501-507 ◽  
Author(s):  
W. N. Drohan ◽  
T. D. Wilkins ◽  
E. Latimer ◽  
D. Zhou ◽  
W. Velander ◽  
...  
Keyword(s):  
Protein C ◽  
Human Protein ◽  
Transgenic Swine ◽  
Recombinant Human Protein

scholarly journals Participation of endothelial cells in the protein C-protein S anticoagulant pathway: the synthesis and release of protein S.

1986 ◽  
Vol 102 (5) ◽  
pp. 1971-1978 ◽  
Author(s):  
D Stern ◽  
J Brett ◽  
K Harris ◽  
P Nawroth
Keyword(s):  
Endothelial Cells ◽  
Vessel Wall ◽  
Protein C ◽  
Protein S ◽  
Calcium Flux ◽  
Ionophore A23187 ◽  
Intracellular Protein ◽  
Major Band ◽  
C Protein ◽  
Morphological Studies

The protein C-protein S anticoagulant pathway is closely linked to the endothelium. In this paper the synthesis and release of the vitamin K-dependent coagulation factor protein S is demonstrated. Western blotting, after SDS PAGE of Triton X-100 extracts of bovine aortic endothelial cells grown in serum-free medium, demonstrated the presence of protein S. A single major band was observed at Mr approximately 75,000, closely migrating with protein S purified from plasma absent from cells treated with cycloheximide. Metabolic labeling of endothelial cells with [35S]methionine confirmed de novo synthesis of protein S. Using a radioimmunoassay, endothelium was found to release 180 fmol/10(5) cells per 24 h and contain 44 fmol/10(5) cells of protein S antigen. Protein S released from endothelium was functionally active and could promote activated protein C-mediated factor Va inactivation on the endothelial cell surface. Warfarin decreased secretion of protein S antigen by greater than 90% and increased intracellular accumulation by almost twofold. Morphological studies demonstrated intracellular protein S was in the Golgi complex, concentrated at the trans face, rough endoplasmic reticulum, lysosomes, and in vesicles at the periphery. In contrast, protein S was not found in vascular fibroblasts or smooth muscle cells. A pool of intracellular protein S could be released rapidly by the calcium ionophore A23187 (5 microM). This effect was dependent on the presence of calcium in the culture medium and could be blocked by LaCl3, which suggests that cytosolic calcium flux may be responsible for protein S release. These results demonstrate that endothelial cells, but not the subendothelial cells of the vessel wall, can synthesize and release protein S, which indicates a new mechanism by which the inner lining of the vessel wall can contribute to the prevention of thrombotic events.

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