ArticleHemaSphere2026
Functional, biochemical, and clinical characterization of natural mutations affecting arginine residues in the heparin-binding site of antithrombin.
Article in HemaSphere, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Arginine residues in antithrombin are essential for heparin binding and for the activation of this key anticoagulant serpin. Mutations affecting these residues may cause antithrombin deficiency, specifically Type II heparin-binding site (HBS) defects, and increase the risk of thrombosis. However, previous alanine-scanning mutagenesis and crystallographic studies have yielded conflicting results regarding the specific residues involved in heparin binding. Our aim was to characterize natural variants affecting arginine residues in antithrombin. Genetic, biochemical, and functional characterization of antithrombin was done in 663 unrelated patients, most with antithrombin deficiency. Recombinant expression of the variants was performed in two different N-glycosylation backgrounds. We identified nine
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