PROS1 / S, Recombinant Protein

PROS1, PROS

For Research Use Only. Not for use in diagnostic procedures.

Human Cells

> 95 % as determined by SDS-PAGE

Lyophilized from sterile PBS, pH 7.4

Samples are stable for up to twelve months from date of receipt at -70 degree C

Manufactured in an ISO 9001:2015 Certified Laboratory.

Small volumes of PROS1 / S recombinant protein vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Background: PROS1, also known as protein S, is a vitamin K-dependent plasma protein that functions as a cofactor for the anticoagulant protease, activated protein C (APC) to inhibit blood coagulation. PROS1 has two isoforms: a free, functionally active form and an inactive form complexed with C4b-binding protein. Besides its anticoagulant function, PROS1 also acts as an agonist for the tyrosine kinase receptors Tyro3, Axl, and Mer. The endothelium expresses Tyro3, Axl, and Mer and produces protein S. The interaction of protein S with endothelial cells and particularly its effects on angiogenesis have not yet been analyzed.

Description: A DNA sequence encoding the human PROS1 (P07225) (Met1-Ser676) was expressed with a polyhistidine tag at the C-terminus.

The recombinant human PROS1 consists of 663 amino acids and predicts a molecular mass of 74.1 KDa. It migrates as an approximately 69-89 KDa band in SDS-PAGE under reducing conditions.

75,123 Da

protein S (alpha)

vitamin K-dependent protein S

Vitamin K-dependent protein S

PROS  [Similar Products]

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. Alternative splicing results in multiple transcript variants encoding different isoforms that may undergo similar processing to generate mature protein. [provided by RefSeq, Oct 2015]

PROS1: Anticoagulant plasma protein; it is a cofactor to activated protein C in the degradation of coagulation factors Va and VIIIa. It helps to prevent coagulation and stimulating fibrinolysis. Defects in PROS1 are the cause of thrombophilia due to protein S deficiency, autosomal dominant (THPH5). A hemostatic disorder characterized by impaired regulation of blood coagulation and a tendency to recurrent venous thrombosis. However, many *****s with heterozygous disease may be asymptomatic. Based on the plasma levels of total and free PROS1 antigen as well as the serine protease-activated protein C cofactor activity, three types of PROS1D have been described: type I, characterized by reduced total and free PROS1 antigen levels together with reduced anticoagulant activity; type III, in which only free PROS1 antigen and PROS1 activity levels are reduced; and the rare type II which is characterized by normal concentrations of both total and free PROS1 antigen, but low cofactor activity. Defects in PROS1 are the cause of thrombophilia due to protein S deficiency, autosomal recessive (THPH6). A very rare and severe hematologic disorder resulting in thrombosis and secondary hemorrhage usually beginning in early infancy. Some affected individuals develop neonatal purpura fulminans, multifocal thrombosis, or intracranial hemorrhage.

Protein type: Secreted; Secreted, signal peptide

Chromosomal Location of Human Ortholog: 3q11.1

Cellular Component: endoplasmic reticulum membrane; extracellular region; extracellular space; Golgi lumen; Golgi membrane; plasma membrane

Molecular Function: endopeptidase inhibitor activity

Biological Process: blood coagulation; ER to Golgi vesicle-mediated transport; leukocyte migration; peptidyl-glutamic acid carboxylation; platelet degranulation; regulation of complement activation; signal peptide processing

Disease: Thrombophilia Due To Protein S Deficiency, Autosomal Dominant; Thrombophilia Due To Protein S Deficiency, Autosomal Recessive

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