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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 Kits (24) and PROS1 Proteins (10) and many more products for this protein.
Showing 10 out of 101 products:
Human Polyclonal PROS1 Primary Antibody for IHC, IHC (p) - ABIN4892115
Ten Kate, Platteel, Mulder, Terpstra, Nicolaes, Reitsma, van der Steege, van der Meer: PROS1 analysis in 87 pedigrees with hereditary protein S deficiency demonstrates striking genotype-phenotype associations. in Human mutation 2008
Show all 2 Pubmed References
Human Polyclonal PROS1 Primary Antibody for IHC, IHC (p) - ABIN4347906
Kato, Nicholson, Neiman, Rantalainen, Holmes, Barrett, Uhlén, Nilsson, Spector, Schwenk: Variance decomposition of protein profiles from antibody arrays using a longitudinal twin model. in Proteome science 2011
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 Antibodies)-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 Antibodies) expression
The prevalence of PS de fi ciency in the present study was higher than in Western countries and con (show DISP1 Antibodies) 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 Antibodies) from plasma significantly reduced protein S anti-coagulant activity.
Activated protein C (show PROC Antibodies)(APC (show APC Antibodies)) combined with protein S(PS) had significant antithrombotic effect. APC (show APC Antibodies) combined with PS prolonged clotting time. Dependence on APC (show APC Antibodies)-cofactor activity of PS for expression of anticoagulant activity by APC (show APC Antibodies).
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 Antibodies) sensitivity, and insulin (show INS Antibodies) 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 Antibodies) path represents an endogenous regulatory mechanism for SVZ cell phagocytic activity
Optimal TAM (show CCNA1 Antibodies) signaling requires coincident TAM (show CCNA1 Antibodies) ligand engagement of both its receptor and the phospholipid phosphatidylserine regulating TAM (show CCNA1 Antibodies) receptor tyrosine kinases Tyro3 (show TYRO3 Antibodies), Axl (show AXL Antibodies), and Mer (show ERH Antibodies) and their ligands Gas6 (show GAS6 Antibodies) and Protein S.
Data indicate that activated T cells express Pros1.
Results demonstrate that Protein S is a Mer (show ERH Antibodies) ligand, and is active in Mer (show ERH Antibodies)-driven phagocytosis in the retina.
A self-regulatory mechanism of Toll (show TLR4 Antibodies)-like receptor signalling through the suppression of Gas6 (show GAS6 Antibodies) and ProS expression is described.
Protein S controls hypoxic/ischemic blood-brain barrier disruption through the TAM (show CCNA1 Antibodies) receptor Tyro3 (show TYRO3 Antibodies) and sphingosine 1-phosphate receptor1.
results demonstrate that ProS is a pleiotropic anticoagulant with activated Protein C (show PROC Antibodies)-independent activities and highlight new roles for ProS in vascular development and homeostasis
Pregnancy causes a decrease in APC (show APC Antibodies) resistance in mice, which can be explained by the elevation of protein S levels and increased TFPI (show TFPI Antibodies) 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