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ABSTRACT: Background
Antithrombin resistance (ATR) is a congenital thrombotic predisposition caused by abnormal prothrombin (FII). Abnormal FII with ATR characteristics, when converted to thrombin (FIIa), shows a reduced affinity of binding to AT, resulting in reduced anti-FIIa and a thrombotic tendency. Data on the efficacy of anticoagulants in ATR are currently insufficient.Methods
Mouse models of ATR were generated to investigate the efficacy of anticoagulants. Because FII R596L, which causes ATR in humans, was considered to correspond to R593L in mice based on gene sequence analysis, knock-in mice that systemically express FII R593L were generated. First, the nature of ATR was confirmed by blood coagulation analysis. We then evaluated thrombotic tendency at the individual level u
SUBMITTER: Suzuki N
PROVIDER: S-EPMC12931876 | biostudies-literature | 2026 Jan
REPOSITORIES: biostudies-literature