F9-KO

The F9 gene is located on the X chromosome. In this F9 knockout mouse model, gRNAs were designed targeting Exon8 of F9 gene via CRISPR gene editing technology. Loss of F9 caused coagulopathy in mice. Mice that are homozygous for F9 knockout are viable, fertile and normal in size. Normal fighting in the cage may cause bleeding or even death due to massive internal hemorrhaging. After the tail cutting, wounds must be cauterized to prevent homozygous knockout mice from blood loss and death. This strain is a powerful model for studying coagulopathy, gene therapy methods and function of factor IX mutations. F9-KO mice (Stock No.NM-KO-18046）carry a knockout allele derived from the targeted deletion of exon 8. While F9-KO(2) mice (Stock No.NM-KO-200607) carrying the exon 1-8 deletion.

Fig 1. Generation of F9 mutant mouse strain. （Date source：Hum Genet. 2017;136(7):875-883. ）

Fig 2. Expression of F9 mRNA in the hepatic tissue of WT and KO mouse strains.（Date source：Hum Genet. 2017;136(7):875-883. ）

Fig 3. Concentration of FIX protein in the plasma of WT and KO mouse strains.（Date source：Hum Genet. 2017;136(7):875-883. ）

Data in c and d were acquired from 8 mice per group, and are shown as the mean ± the s.d.

Twotailed unpaired Student’s t tests were used to determine the P value.**P < 0.01

CRISPR/Cas9-mediated somatic and germline gene correction to restore hemostasis in hemophilia B mice
References：Springer Link