These Kcnj12 knock-out mice exhibit a reduction in inwardly rectifying potassium ion currents in cardiac ventribular myocytes.
Thomas Schwarz, Harvard University
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern blot analysis of cardiac tissue or Southern blot analysis. Cardiac ventribular myocytes isolated from homozygotes exhibit a 50% reduction in inwardly rectifying potassium ion currents under physiological and elevated extracellular potassium ion concentration levels. This mutant mouse strain may be useful in studies of potassium ion dependent cardiac electrophysiology.
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt the entire open reading frame. The construct was electroporated into 129-derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts.
|Allele Name||targeted mutation 1, Thomas L Schwarz|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Kcnj12, potassium inwardly-rectifying channel, subfamily J, member 12|
|Strain of Origin||(129X1/SvJ x 129S1/Sv)F1-Kitl+|
|Molecular Note||The entire open reading frame of the endogenous gene was replaced with a neomycin selection cassette.|
|Mutations Made By|| |
Joshua Zaritsky, Harvard University
The resulting chimeric animals were crossed to FVB mice, and then backcrossed to the same for 10 generations.
When using the Kir2.2- mouse strain in a publication, please cite the originating article(s) and include JAX stock #005059 in your Materials and Methods section.