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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Atp2a2tm1.1Iemr
targeted mutation 1.1, Ole Sejersted
MGI:4415164
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Atp2a2tm1.1Iemr/Atp2a2+
Myl2tm1(cre)Krc/Myl2+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6Crl * C57BL/6J MGI:4415177
cn2
Atp2a2tm1.1Iemr/Atp2a2tm1.1Iemr
Tg(Myhca-cre)1Lrsn/0
involves: 129P2/OlaHsd * C57BL/6Crl * FVB MGI:4415178
cn3
Atp2a2tm1.1Iemr/Atp2a2tm1.1Iemr
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
involves: 129P2/OlaHsd * C57BL/6J * FVB/N MGI:4441305


Genotype
MGI:4415177
cn1
Allelic
Composition
Atp2a2tm1.1Iemr/Atp2a2+
Myl2tm1(cre)Krc/Myl2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6Crl * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atp2a2tm1.1Iemr mutation (0 available); any Atp2a2 mutation (76 available)
Myl2tm1(cre)Krc mutation (2 available); any Myl2 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit normal heart weight and cardiac function




Genotype
MGI:4415178
cn2
Allelic
Composition
Atp2a2tm1.1Iemr/Atp2a2tm1.1Iemr
Tg(Myhca-cre)1Lrsn/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6Crl * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atp2a2tm1.1Iemr mutation (0 available); any Atp2a2 mutation (76 available)
Tg(Myhca-cre)1Lrsn mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• although alive at E10.5, embryos die by E11.5




Genotype
MGI:4441305
cn3
Allelic
Composition
Atp2a2tm1.1Iemr/Atp2a2tm1.1Iemr
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (5 available); any A1cf mutation (39 available)
Atp2a2tm1.1Iemr mutation (0 available); any Atp2a2 mutation (76 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen-treated mice do not exhibit myocardial disarray or necrosis
• 4 and 7 weeks after tamoxifen treatment, left atrial diameter is increased compared to in Atp2a2tm1.1Iemr homozygotes
• after tamoxifen treatment
• after tamoxifen treatment
• tamoxifen-treated mice exhibit an increase in the time constant of isovolumetric pressure decay compared with Atp2a2tm1.1Iemr homozygotes
• 7 weeks after tamoxifen treatment, mice exhibit diastolic dysfunction compared with Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment
• 4 weeks after tamoxifen treatment, mice exhibit reduced contractile function compared with Atp2a2tm1.1Iemr homozygotes as determined by Doppler imaging
• at low stimulation frequency, cardiomyocytes from tamoxifen-treated mice exhibit reduced contraction magnitude compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• 7 weeks after tamoxifen treatment, fractional shortening is reduced compared to in Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment, end-diastolic pressure compared to in Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment, mice exhibit reduced maximum positive and minimum derivatives of the left ventricular pressure compared with Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment, anesthetized mice exhibit decreased heart rate compared with Atp2a2tm1.1Iemr homozygotes
• cardiomyocytes from tamoxifen-treated mice exhibit reduced magnitude of calcium ion transients and prolonged time to half decay of calcium ion transients compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• when stimulated at a 6 Hz frequency, cardiomyocytes from tamoxifen-treated mice exhibit shorter diastolic sarcomere length and a greater increase in the contractile response per unit during systole compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• during the slow decline of caffeine transients in the presence of nickel ions, cardiomyocytes from tamoxifen-treated mice exhibit shorter sarcomere length compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• 4 weeks after tamoxifen treatment, cardiomyocytes exhibit reduced sarcoplasmic reticulum calcium ion content compared with cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• 7 weeks after treatment with tamoxifen, mice exhibit reduced maximal rate of cardiomyocyte relaxation compared with Atp2a2tm1.1Iemr homozygotes
• 7 weeks after tamoxifen treatment

homeostasis/metabolism
• in tamoxifen-treated mice at 4 and 7 weeks

muscle
• 4 weeks after tamoxifen treatment, mice exhibit reduced contractile function compared with Atp2a2tm1.1Iemr homozygotes as determined by Doppler imaging
• at low stimulation frequency, cardiomyocytes from tamoxifen-treated mice exhibit reduced contraction magnitude compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• 7 weeks after tamoxifen treatment, fractional shortening is reduced compared to in Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment, end-diastolic pressure compared to in Atp2a2tm1.1Iemr homozygotes

growth/size/body
• after tamoxifen treatment





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory