Antithrombin III (ATIII) is a small glycoprotein produced by the liver that functions as a serine protease inhibitor to block coagulation.
Antithrombin III is a 58kDa glycoprotein synthesized in the liver. It has two domains, a heparin-binding domain and target protease binding domain.
Immunogen
human antithrombin III
Application
Anti-Antithrombin III antibody has been used in western blotting and antigenic assay.
Biochem/physiol Actions
Antithrombin III is a serine protease inhibitor which affects many intrinsic and extrinsic blood coagulation pathways. It inactivates the function of thrombin and factor X in blood. Severe sepsis is caused due to lack of antithrombin III.
Physical form
Lyophilized from 0.01 M phosphate buffered saline, pH 7.2
Reconstitution
Reconstitute with 2 mL deionized water.
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Antithrombin deficiency, the most severe congenital thrombophilia, might be underestimated, as some pathogenic variants are not detected by routine functional methods. We have identified 2 new SERPINC1 variants, p.Glu227Lys and p.Asn224His, in 4 unrelated thrombophilic patients with early and recurrent
High-dose antithrombin III in severe sepsis: a randomized controlled trial
Warren B L, et al.
JAMA : The Journal of the American Medical Association, 286(15), 1869-1878 (2001)
American journal of hematology, 97(2), 216-225 (2021-11-21)
Antithrombin deficiency, the most severe thrombophilia, might be underestimated, since it is only investigated in cases with consistent functional deficiency or family history. We have analyzed 444 consecutive, unrelated cases, from 1998 to 2021, with functional results supporting antithrombin deficiency
The lack of physiological parity between 2D cell culture and in vivo culture has led to the development of more organotypic models, such as organoids. Organoid models have been developed for a number of tissues, including the liver. Current organoid
Clot-bound thrombin is protected from inhibition by heparin-antithrombin III but is susceptible to inactivation by antithrombin III-independent inhibitors.
Weitz J I, et al.
The Journal of Clinical Investigation, 86(2), 385-391 (1990)
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