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Suggests that a total FXII deficiency does not affect embroyonic development and survival.
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Description: A genetically-transmissible factor (F) XII-inactivated allele has been produced in mice by targeted replacement of exons 3-8 of the FXII gene with the neomycin resistance gene. Interbreeding of these mice provided offspring homozygous for two inactivated FXII alleles (FXII-/-). Male and female FXII-deficient mice bred normally in all genotypic combinations of the heterozygous and homozygous states, and the offspring survived to adulthood, suggesting that a total FXII deficiency does not affect embroyonic development and survival. Neither FXII transcripts nor FXII antigen was found in various tissues of adult FXII-/- mice. No obvious unchallenged coagulopathies were present in FXII-/- adult mice, despite greatly prolonged activated partial thromboplastin times in this mouse cohort.