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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 (101) and PROS1 Kits (24) and many more products for this protein.
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Human PROS1 Protein expressed in HEK-293 Cells - ABIN2729817
Kariolis, Miao, Jones, Kapur, Mathews, Giaccia, Cochran: An engineered Axl 'decoy receptor' effectively silences the Gas6-Axl signaling axis. in Nature chemical biology 2014
Taken together, our gain-of-function, loss-of-function analyses suggest that PROS may facilitate cell proliferation and promote castration resistance in human castration-resistant PCa (show FLVCR1 Proteins)-like cells via its apoptosis-regulating property.
we identify PROS1 as a driver of Oral Squamous Cell Carcinoma tumor growth and a modulator of AXL (show AXL Proteins) expression
The prevalence of PS de fi ciency in the present study was higher than in Western countries and con (show DISP1 Proteins) fi rms the high prevalence of PS de fi ciency in Asian populations
Patients with type 2 diabetes had significantly lower circulating free protein S than healthy control subjects
In the present study, gene analysis of six unrelated Japanese families diagnosed with congenital protein S deficiency identified five missense mutations in the PROS1 gene - c.757C>T (Ala139Val; A139V), c.1346 G>T (Cys449Phe; C449F), c.1352G>A (Arg451Gln; R451Q), c.1424G>T (Cys475Phe; C475F) and c.1574C>T (Ala525Val; A525V) - and one frameshift mutation, c.2135delA (Asp599ThrfsTer13; D599TfsTer13).
The odds ratio of developing idiopathic fatal pulmonary embolism as a variant carrier for PROS1 is 56.4 (95% CI, 5.3-351.1; P = 0.001).
described a novel PROS1 frameshift mutation, c.74dupA, in a hereditary protein S deficiency family. Interestingly, both of the proband and his mother carried the mutation and had a protein S deficiency, however, only the proband suffered a pulmonary embolism while his mother had no history of any thrombosis, suggesting that a triggering event might have been involved in the thrombus formation.
PROS1 may play an important role in the development of glioblastoma multiforme through cellular proliferation, migration and invasion as well as apoptosis.
analysis of genotype phenotype correlation in PROS1 in a large cohort of adults with suspicion of inherited quantitative protein S deficiency
The immunoabsorption of PON1 (show PON1 Proteins) from plasma significantly reduced protein S anti-coagulant activity.
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).
This study identifies a duple role for PROS1 in stem-cell quiescence and as a pro-neurogenic factor, and highlights a unique segregation of increased stem cell proliferation from enhanced neuronal differentiation.
Mice overexpressing protein S showed significant improvements in blood glucose level, glucose tolerance, insulin (show INS Proteins) sensitivity, and insulin (show INS Proteins) secretion compared with wild-type counterparts. diabetic protein S transgenic mice developed significantly less severe diabetic glomerulosclerosis than controls.
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