These Cyp51flox/flox mutant mice possess loxP sites flanking exons 3-4 of the cytochrome P450, family 51 (Cyp51) gene. Mice that are homozygous for this allele are viable and fertile. CYP51 is an enzyme that catalyzes the oxidation of organic substances in metabolic processes such as cholesterol synthesis and drug metabolism. Inactivation of CYP51 is thought to give rise to a similar phenotype as mutation in the human gene POR (cytochrome P450 oxidoreductase) that has been associated with Antley-Bixler syndrome (ABS), characterized by skeletal, cardiac, and urogenital abnormalities. When these mutant mice are bred to mice that express tissue-specific Cre recombinase, resulting offspring will have exons 3-4 deleted in the cre-expressing tissues.
For examples, when bred to B6.FVB-Tg(EIIa-cre)C5379Lmgd/J mice (Stock No. 003724) with widespread cre expression, resulting offspring died at E15 due to heart failure, ventricle septum, and epicardial and vasculogenesis defects.
