Factor XII Knockout Mice
This Factor XII (F12) knockout mouse model was created by targeted disruption of F12 using programed nuclease. Mutations are confirmed by PCR genotyping and Sanger sequencing. The complete absence of FXII protein in the plasma of homozygous mice is confirmed by Western Blot. This mouse model will be useful for cardiovascular and neurological studies.
Strain Background: C57B6SJL
Protein: Coagulation Factor XII
Synonyms: FXII, Hageman Factor
Targeted Exon: Exon 8-12
Mutation: Large deletions on Exon 8-12
Our mutant mice are from an ongoing colony made in-house at our state of the art facility in the U.S.A and available immediately. No waiting for cryo recovery or costly breeding.
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- In humans, patients with FXII deficiency have no risk of bleeding, which is consistent with the observation of normal hemostatic capacity in murine FXII KO model. Given the benefit of no associated bleeding risks, targeting FXII is a promising therapeutic strategy to prevent thrombosis along with anti-inflammatory properties[1-2].
- Depletion of FXII has been shown to improve cognitive impairment in Alzheimer disease mice. This FXII KO mouse model will be useful for studying neurodegeneration disease.
- Kenne E, Nickel KF, Long AT, Fuchs TA, Stavrou EX, Stahl FR, et al. Factor XII: a novel target for safe prevention of thrombosis and inflammation. J Intern Med. 2015. 278(6):571–85. http://www.ncbi.nlm.nih.gov/pubmed/26373901
- Nickel KF, Long AT, Fuchs TA, Butler LM, Renné T. Factor XII as a Therapeutic Target in Thromboembolic and Inflammatory Diseases Highlights. Arterioscler Thromb Vasc Biol. 2017. 37(1):13–20. http://www.ncbi.nlm.nih.gov/pubmed/27834692
- Chen Z-L, Revenko AS, Singh P, MacLeod AR, Norris EH, Strickland S. Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice. Blood. 2017. 129(18):2547–56. http://www.ncbi.nlm.nih.gov/pubmed/28242605