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PROS1 encodes a vitamin K-dependent plasma protein that functions as a cofactor for the anticoagulant protease, activated protein C (APC) to inhibit blood coagulation. Additionally we are shipping PROS1 Antibodies (75) and PROS1 Proteins (9) and many more products for this protein.
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A PROS1 c.1486_1490delGATTA mutation on exon 12. appeared to be the primary cause of thrombosis in the family of the present study.
analysis of the amino acid residues in the laminin G domains of protein S involved in tissue factor pathway inhibitor (show TFPI ELISA Kits) interaction
The present study highlights that the GAS6 (show GAS6 ELISA Kits)/ProS-TAM (show CCNA1 ELISA Kits) system correlates in several ways with disease activity in systemic lupus erythematosus
genetic polymorphism affects endogenous thrombin (show F2 ELISA Kits) potential among FV Leiden carriers
Identical large duplication mutation of PROS1 was detected in 3 unrelated patients with thrombophilia from hereditary protein S deficiency.
Anti-human protein S antibody induces tissue factor (show F3 ELISA Kits) expression through a direct interaction with PFKP (show PFKP ELISA Kits) and ERK1/2 (show MAPK1/3 ELISA Kits) activation in coronary artery endothelial cells.
Data indicate that the protein S sex hormone-binding globulin (SHBG (show SHBG ELISA Kits))-like domain was important for binding and enhancement of tissue factor pathway inhibitor (TFPI (show TFPI ELISA Kits)).
miR (show MLXIP ELISA Kits)-494 is involved in the mechanism of estrogen-mediated downregulation of PS expression
This is the first report of a large deletion of PROS1 from exon 1 through 12 in Polish patients with deep-vein thrombosis.
PS exerts anticoagulant cofactor activity with TFPIalpha from any physiological pool, likely by localizing TFPIalpha to membrane surfaces, stabilizing its interaction with membrane-bound FXa (show F10 ELISA Kits), and slowing thrombin (show F2 ELISA Kits) generation.
Activated protein C (show PROC ELISA Kits)(APC (show APC ELISA Kits)) combined with protein S(PS) had significant antithrombotic effect. APC (show APC ELISA Kits) combined with PS prolonged clotting time. Dependence on APC (show APC ELISA Kits)-cofactor activity of PS for expression of anticoagulant activity by APC (show APC ELISA Kits).
By revealing that neural stem-like cells act within the SVZ neurogenic niche as phagocytes and that the ProS/MerTK (show MERTK ELISA Kits) path represents an endogenous regulatory mechanism for SVZ cell phagocytic activity
Optimal TAM (show CCNA1 ELISA Kits) signaling requires coincident TAM (show CCNA1 ELISA Kits) ligand engagement of both its receptor and the phospholipid phosphatidylserine regulating TAM (show CCNA1 ELISA Kits) receptor tyrosine kinases Tyro3 (show TYRO3 ELISA Kits), Axl (show AXL ELISA Kits), and Mer (show ERH ELISA Kits) and their ligands Gas6 (show GAS6 ELISA Kits) and Protein S.
Data indicate that activated T cells express Pros1.
Results demonstrate that Protein S is a Mer (show ERH ELISA Kits) ligand, and is active in Mer (show ERH ELISA Kits)-driven phagocytosis in the retina.
A self-regulatory mechanism of Toll (show TLR4 ELISA Kits)-like receptor signalling through the suppression of Gas6 (show GAS6 ELISA Kits) and ProS expression is described.
Protein S controls hypoxic/ischemic blood-brain barrier disruption through the TAM (show CCNA1 ELISA Kits) receptor Tyro3 (show TYRO3 ELISA Kits) and sphingosine 1-phosphate receptor1.
results demonstrate that ProS is a pleiotropic anticoagulant with activated Protein C (show PROC ELISA Kits)-independent activities and highlight new roles for ProS in vascular development and homeostasis
Pregnancy causes a decrease in APC (show APC ELISA Kits) resistance in mice, which can be explained by the elevation of protein S levels and increased TFPI (show TFPI ELISA Kits) activity in plasma.
This gene encodes a vitamin K-dependent plasma protein that functions as a cofactor for the anticoagulant protease, activated protein C (APC) to inhibit blood coagulation. It is found in plasma in both a free, functionally active form and also in an inactive form complexed with C4b-binding protein. Mutations in this gene result in autosomal dominant hereditary thrombophilia. An inactive pseudogene of this locus is located at an adjacent region on chromosome 3.
vitamin K-dependent protein S
, protein Sa
, vitamin K-dependent plasma protein S
, vitamin K-dependent protein S preproprotein