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PROS encodes a vitamin K-dependent plasma protein that functions as a cofactor for the anticoagulant protease, activated protein C (APC) to inhibit blood coagulation. De plus, nous expédions PROS1 Anticorps (169) et PROS1 Protéines (20) et beaucoup plus de produits pour cette protéine.
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The present case combined with the review of the literature suggests that p.Arg451* in the PROS1 gene mainly leads to clinically evident thrombosis following trauma, surgery or serious comorbidities especially malignancy.
Protein S and Gas6 (Montrer GAS6 Kits ELISA) mediates phagocytosis of HIV-1-infected cells by bridging receptor tyrosine kinase (Montrer RET Kits ELISA) Mer (Montrer MERTK Kits ELISA) to phosphatidylserine exposed on infected cells.
these results suggest a novel pathogenic role of SPE B that initiates protein S degradation followed by the inhibition of apoptotic cell clearance by macrophages
Developed functional protein S assays that measure both the activated protein C (Montrer PROC Kits ELISA)- and TFPI (Montrer TFPI Kits ELISA)-cofactor activities of protein S in plasma, which are hardly if at all affected by the FV Leiden mutation.
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-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 (Montrer AXL Kits ELISA) expression
The prevalence of PS de fi ciency in the present study was higher than in Western countries and con (Montrer DISP1 Kits ELISA) 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).
An inhibitory role for PROS1 on BM-derived LCs. Collectively.
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 (Montrer INS Kits ELISA) sensitivity, and insulin (Montrer INS Kits ELISA) 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 (Montrer MERTK Kits ELISA) path represents an endogenous regulatory mechanism for SVZ cell phagocytic activity
Optimal TAM signaling requires coincident TAM ligand engagement of both its receptor and the phospholipid phosphatidylserine regulating TAM receptor tyrosine kinases Tyro3 (Montrer TYRO3 Kits ELISA), Axl (Montrer AXL Kits ELISA), and Mer (Montrer ERH Kits ELISA) and their ligands Gas6 (Montrer GAS6 Kits ELISA) and Protein S.
Data indicate that activated T cells express Pros1.
Results demonstrate that Protein S is a Mer (Montrer ERH Kits ELISA) ligand, and is active in Mer (Montrer ERH Kits ELISA)-driven phagocytosis in the retina.
A self-regulatory mechanism of Toll-like receptor signalling through the suppression of Gas6 (Montrer GAS6 Kits ELISA) and ProS expression is described.
Protein S controls hypoxic/ischemic blood-brain barrier disruption through the TAM receptor Tyro3 (Montrer TYRO3 Kits ELISA) and sphingosine 1-phosphate receptor1.
results demonstrate that ProS is a pleiotropic anticoagulant with activated Protein C (Montrer PROC Kits ELISA)-independent activities and highlight new roles for ProS in vascular development and homeostasis
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 plasma protein S
, vitamin K-dependent protein S