These mitochondrial cyclophilin knockout mice may be useful in studying mitochondrial-driven cell death, as well as brain and cardiac injury.
Jeffery D. Molkentin, Cincinnati Children's Hospital
Mitochondria isolated from the livers, hearts, and brains of homozygous targeted mutant mice are resistant to swelling and permeability transition in vitro. Hepatocytes and fibroblasts are largely protected from Ca2+-overload and oxidative stress-induced cell death. Mice are protected from ischaemia/reperfusion-induced cell death in vivo. This strain may be useful in studies of mitochondrial-driven cell death.
The first three coding exons were replaced with a neomycin resistance cassette. A 129-dervived emabryonic stem (ES) cell line was used to create the mutation. Chimeras were crossed to C57BL/6 and the strain was maintained on a mixed C57BL/6 and 129 genetic background by the donating laboratory.
|Allele Name||targeted mutation 1, Jeffery D Molkentin|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Ppif, peptidylprolyl isomerase F (cyclophilin F)|
|Strain of Origin||129|
|Molecular Note||A neomycin resistance gene replaced the first three coding exons. Western blot of cardiac protein extracts from mutants demonstrated the lack of protein.|
|Mutations Made By|| |
Jeffery Molkentin, Cincinnati Children's Hospital
When maintained as a live colony, homozygotes or heterozygotes may be bred. Homozygotes are smaller than wildtype mice and are prone to obesity as they age.
When using the Ppif- mouse strain in a publication, please cite the originating article(s) and include JAX stock #009071 in your Materials and Methods section.