Hearts of these Prkca (protein kinase C, alpha) targeted mutation mice are hypercontractile, protecting them from heart failure induced by pressure overload. Homozygotes are viable, fertile, and have no overt phenotype. This strain may be useful in studies of heart failure.
Jeffery D. Molkentin, Cincinnati Children's Hospital
Hearts of these targeted mutation mice are hypercontractile, protecting them from heart failure induced by pressure overload. Homozygotes are viable, fertile, and have no overt phenotype. The targeted mutation eliminates expression, as determined by Western blot. This strain may be useful in studies of heart failure.
The exon encoding the ATP-binding region was replaced with a neomycin resistance cassette. A 129-derived embryonic stem (ES) cell line was used to create the mutation. Chimera's were crossed to C57BL/6 and the line was maintained on a mixed C57BL/6 and 129 background by the donating laboratory.
|Allele Name||targeted mutation 1, Jeffery D Molkentin|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Prkca, protein kinase C, alpha|
|Strain of Origin||129|
|Molecular Note||Homologous recombination was used to replace the exon encoding the ATP-binding cassette with a neomycin resistance gene. A lack of protein expression was confirmed by Western blot analysis.|
|Mutations Made By|| |
Jeffery Molkentin, Cincinnati Children's Hospital
When maintained as a live colony, heterozygotes or homozygotes may be bred.
When using the B6;129-Prkcatm1Jmk/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #009068 in your Materials and Methods section.