Mice with a severe deficiency in protein C display prothrombotic and proinflammatory phenotypes and compromised maternal reproductive capabilities
J. Clin. Invest. Angelina J. Lay, et al. 115:1552 doi:10.1172/JCI24030 [Go to this article.]

Figure 1
Generation of low-PC transgenic mice. (A) Schematic diagram showing relevant features of the low PC DNA construct. A 12.5-kb fragment of an inactivated (by partial promoter deletion FVII gene and an 18-kb fragment of an inactive (by exon 1 deletion) FX gene were cloned upstream and downstream, respectively, of the PC cDNA/polyA sequences. Expression of PC was driven by the FX promoter contained within the complete intergenic region (IGR) of the FVII-FX chromosomal segment. (B) Low-PC potential founders were identified by PCR analysis. The sense and antisense primers spanned exons 4 and 6 of the PC gene, respectively, amplifying a 497-bp fragment for the WT allele and a 284-bp fragment for the mPC cDNA that is derived from the transgene. (C) Low-PC transgenic mice from various lines were evaluated by Southern blot analysis of KpnI-digested genomic DNA. The Southern probe in A hybridized to a 2.7-kb fragment of the WT FVII gene in addition to various PC transgene fragments (asterisks), the sizes of which are dependent on sites of PC transgene integration. The 3.7-kb band shows that at least 1 tandem repeat of the transgene has occurred in each mouse line.