Phenotypes associated with this allele

• Allele Symbol: Atp1a2^tm3Ling
• Allele Name: targeted mutation 3, Jerry B Lingrel
• Allele ID: MGI:3027260
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Atp1a2^tm3Ling/Atp1a2^tm3Ling	involves: 129S6/SvEvTac * Black Swiss	MGI:3027298
cx2	Atp1a1^tm2Ling/Atp1a1^tm2Ling Atp1a2^tm3Ling/Atp1a2^tm3Ling	involves: 129S6/SvEvTac * Black Swiss	MGI:3527479

Genotype
MGI:3027298

hm1

• Allelic Composition: Atp1a2^tm3Ling/Atp1a2^tm3Ling
• Genetic Background: involves: 129S6/SvEvTac * Black Swiss

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cardiovascular system

cardiovascular system phenotype ( J:87082 )

N • mice are viable, fertile, and exhibit normal cardiovascular function under normal conditions

abnormal cardiac muscle contractility ( J:87082 )

• the oubain-induced inotropy observed in wild-type mice does not occur in mutant oubain-treated hearts

muscle

abnormal cardiac muscle contractility ( J:87082 )

• the oubain-induced inotropy observed in wild-type mice does not occur in mutant oubain-treated hearts

Genotype
MGI:3527479

cx2

• Allelic Composition: Atp1a1^tm2Ling/Atp1a1^tm2Ling; Atp1a2^tm3Ling/Atp1a2^tm3Ling
• Genetic Background: involves: 129S6/SvEvTac * Black Swiss

cardiovascular system

increased cardiac muscle contractility ( J:95157 )

• ouabain, a glycoside poison that binds to and inhibits the sodium-potassium pump (inhibits Atp1a1 but not Atp1a2 in these mutants), increased cardiac contractility in isolated mutant hearts and resulted in greater positive inotropy than in wild-type

• 3-fold greater increase in the maximal rate of contraction and the rate of contraction at 40 mm Hg than in wild-type after ouabain infusion, however heart function and response of cardiac contraction to beta-adrenergic stimuli was normal under regular conditions (without ouabain)

muscle

increased cardiac muscle contractility ( J:95157 )

• ouabain, a glycoside poison that binds to and inhibits the sodium-potassium pump (inhibits Atp1a1 but not Atp1a2 in these mutants), increased cardiac contractility in isolated mutant hearts and resulted in greater positive inotropy than in wild-type

• 3-fold greater increase in the maximal rate of contraction and the rate of contraction at 40 mm Hg than in wild-type after ouabain infusion, however heart function and response of cardiac contraction to beta-adrenergic stimuli was normal under regular conditions (without ouabain)