F11 Conditional Knockout mouse models

Mouse F11, ortholog of human F11, encodes coagulation factor XI, a disulfide-linked homodimer in which each subunit contributes four apple domains and a trypsin-like catalytic domain; the apple modules dock high molecular weight kininogen, platelet GPIb, heparin, and the substrate factor IX. Factor XI is activated by factor XIIa during contact activation or, more relevant in vivo, by thrombin feedback on polyanionic surfaces, and factor XIa then cleaves factor IX to sustain intrinsic tenase and thrombin amplification. The therapeutic appeal is asymmetry: human factor XI deficiency causes only injury-related bleeding while mouse nulls are protected from arterial and venous thrombosis, uncoupling hemostasis from pathological clotting and underpinning abelacimab and milvexian development. Nulls are viable, so a conditional allele is not strictly required, though hepatocyte-restricted deletion clarifies the source. Humanized knockins are the appropriate design when antibodies or small molecules targeting human apple domains or the catalytic pocket are being tested.

Conditional deletion of F11 limits the genetic change to the lineage you choose. That helps in oncology, immunology, and metabolic work where systemic loss would muddy the read. After you confirm Cre specificity, crossing to F11 floxed stock yields usable cohorts.