Figure 1.
Engineering and analysis of inducible FX–deficient mice. (A) Mice containing an engineered f10 gene with loxP sequences surrounding exons 4 and 5. Upon activation of Cre-recombinase, both exons are excised. P1 and P2 indicate the locations of primers used for postinduction analysis. (B) Genomic DNA was isolated from liver of pI:pC–treated Cre+ and Cre–f10flox/flox mice. A virtually complete recombined F10 locus was observed in Cre+ mice. (C) A representative curve of RVV-X–induced FXa amidolytic activity over time in plasma from f10WT mice (n = 3) and f10low mice (n = 3). (D) Residual FX activity measured in RVV-X–induced activity assay. LOD of this assay is 0.5% FX. All mice having <1% FX activity are designated as f10low mice. (E) Survival curve of of pI:pC–treated f10WT mice and f10low mice (both n = 7). No differences in survival after 12 months were observed. LOD, limit of detection.

Engineering and analysis of inducible FX–deficient mice. (A) Mice containing an engineered f10 gene with loxP sequences surrounding exons 4 and 5. Upon activation of Cre-recombinase, both exons are excised. P1 and P2 indicate the locations of primers used for postinduction analysis. (B) Genomic DNA was isolated from liver of pI:pC–treated Cre+ and Cref10flox/flox mice. A virtually complete recombined F10 locus was observed in Cre+ mice. (C) A representative curve of RVV-X–induced FXa amidolytic activity over time in plasma from f10WT mice (n = 3) and f10low mice (n = 3). (D) Residual FX activity measured in RVV-X–induced activity assay. LOD of this assay is 0.5% FX. All mice having <1% FX activity are designated as f10low mice. (E) Survival curve of of pI:pC–treated f10WT mice and f10low mice (both n = 7). No differences in survival after 12 months were observed. LOD, limit of detection.

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