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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 Kits (15) and many more products for this protein.
Showing 8 out of 9 products:
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 Proteins) interaction
The present study highlights that the GAS6 (show GAS6 Proteins)/ProS-TAM (show CCNA1 Proteins) system correlates in several ways with disease activity in systemic lupus erythematosus
genetic polymorphism affects endogenous thrombin (show F2 Proteins) 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 expression through a direct interaction with PFKP and ERK1/2 activation in coronary artery endothelial cells.
Data indicate that the protein S sex hormone-binding globulin (SHBG (show SHBG Proteins))-like domain was important for binding and enhancement of tissue factor pathway inhibitor (TFPI (show TFPI Proteins)).
miR (show MLXIP Proteins)-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 Proteins), and slowing thrombin (show F2 Proteins) generation.
Activated protein C (show PROC Proteins)(APC (show APC Proteins)) combined with protein S(PS) had significant antithrombotic effect. APC (show APC Proteins) combined with PS prolonged clotting time. Dependence on APC (show APC Proteins)-cofactor activity of PS for expression of anticoagulant activity by APC (show APC Proteins).
By revealing that neural stem-like cells act within the SVZ neurogenic niche as phagocytes and that the ProS/MerTK (show MERTK Proteins) path represents an endogenous regulatory mechanism for SVZ cell phagocytic activity
Optimal TAM (show CCNA1 Proteins) signaling requires coincident TAM (show CCNA1 Proteins) ligand engagement of both its receptor and the phospholipid phosphatidylserine regulating TAM (show CCNA1 Proteins) receptor tyrosine kinases Tyro3 (show TYRO3 Proteins), Axl (show AXL Proteins), and Mer (show ERH Proteins) and their ligands Gas6 (show GAS6 Proteins) and Protein S.
Data indicate that activated T cells express Pros1.
Results demonstrate that Protein S is a Mer (show ERH Proteins) ligand, and is active in Mer (show ERH Proteins)-driven phagocytosis in the retina.
A self-regulatory mechanism of Toll (show TLR4 Proteins)-like receptor signalling through the suppression of Gas6 (show GAS6 Proteins) and ProS expression is described.
Protein S controls hypoxic/ischemic blood-brain barrier disruption through the TAM (show CCNA1 Proteins) receptor Tyro3 (show TYRO3 Proteins) and sphingosine 1-phosphate receptor1.
results demonstrate that ProS is a pleiotropic anticoagulant with activated Protein C (show PROC Proteins)-independent activities and highlight new roles for ProS in vascular development and homeostasis
Pregnancy causes a decrease in APC (show APC Proteins) resistance in mice, which can be explained by the elevation of protein S levels and increased TFPI (show TFPI Proteins) 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