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Phenotypes Associated with This Genotype
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kcnj8tm1Sse mutation (0 available); any Kcnj8 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
• homozygous null mice died prematurely between 5 and 6 weeks after birth due to myocardial ischemia
• homozygous mutant mice were found dead within 24 hours of displaying normal behavior and activity levels ("sudden cardiac death")

cardiovascular system
• electrophysiological measurements of ventricular myocytes exhibited no abnormalities in the plasma membrane of homozygous null cardiomyocytes relative to wild-type
• in addition, flavoprotein oxidation measurements revealed normal plasma membrane ATP-sensitive K+ current channels in homozygous null cardiomyocytes
• representative ECGs generated by radio telemetry revealed spontaneous ST elevations and atrioventricular blocks of various degrees in homozygous null mice
• in contrast to the normal electrophysiological properties of homozygous null cardiomyocytes, vascular smooth-muscle KATP channels were defective in mutant aortas
• homozygous null aortic smooth-muscle cells failed to generate a vasodilation response to pinacidil (a K+ channel opener) both in vivo (blood pressure decrease) and in vitro (vasorelaxation of aortic rings), indicating dysregulation of the vascular tonus
• administration of the ergot alkaloid methylergometrine, a vasoconstrictive agent, elicited ST elevation followed by cardiac death in mutant mice but not in wild-type mice, resulting in hypercontractility of coronary arteries and a phenotype similar to Prinzmetal (or variant) angina in humans
• notably, some homozygous null mice exhibited spontaneous coronary spasm under basal conditions

Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
MGI 6.12
The Jackson Laboratory