These mice carry a targeted knockout of the Dusp4 (dual specificity phosphatase 4; also called MKP2) gene and are useful in studies of cardiomyopathy.
Jeffery D. Molkentin, Cincinnati Children's Hospital
Mitogen-activated protein kinases (MAPKs) are activated in the heart by disease-inducing and stress-inducing stimuli, where they participate in hypertrophy, remodeling, contractility, and heart failure. A family of dual-specificity phosphatases (DUSPs) directly inactivates each of the MAPK terminal effectors, potentially serving a cardioprotective role.
These mice carry a targeted knockout of the Dusp4 (dual specificity phosphatase 4; also called MKP2) gene. RT-PCR confirms the deletion of the gene product in heart. Disruption of the single gene does not result in cardiomyopathy, but when combined with a Dusp1 targeted knockout, double null mice exhibit cardiomyopathy and increased mortality with aging.
Exons 2 and 3 were replaced with a neomycin cassette via homologous recombination in a 129-derived embryonic stem (ES) cells. This strain was maintained on a mixed C57BL/6-129 genetic background by the donating laboratory.
|Allele Name||targeted mutation 1, Jeffery D Molkentin|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Dusp4, dual specificity phosphatase 4|
|Strain of Origin||129|
|Molecular Note||Exons 2 and 3 were replaced with a neomycin cassette via homologous recombination. RT-PCR confirmed the absence of transcript expression in the heart.|
Homozygotes and heterozygotes are viable and fertile.
When using the B6;129-Dusp4tm1Jmol/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #023671 in your Materials and Methods section.