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Phenotypes Associated with This Genotype
Genotype
MGI:5779906
cn1
Allelic
Composition
Mcutm1.1Jmol/Mcutm1.1Jmol
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * 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)
Mcutm1.1Jmol mutation (2 available); any Mcu mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• hearts of tamoxifen-treated mice exhibit normal cardiac adaptation to long-term stress induced by transverse aortic constriction
• tamoxifen-treated mice exhibit inhibited acute cardiac mitochondrial calcium uptake compared with control cells
• at 18 weeks, cardiac myocytes from tamoxifen-treated mice challenged with calcium exhibit a severely blunted compared with control cells
• cardiac myocytes from tamoxifen-treated mice exhibit lower sodium-induced calcium efflux rates compared with control cells
• cardiac mitochondria from mice treated with tamoxifen and dobutamine fail to exhibit an increase in calcium unlike control mitochondria
• however, mice exhibit normal baseline mitochondrial calcium levels, response to Ru360, and elevated calcium levels in the mitochondrial following sustained dobutamine treatment
• tamoxifen-treated mice subjected to dobutamine (the beta-adrenergic receptor agonist) exhibit lesser short-term increase in the maximal rate of cardiac pressure compared with control mice
• however, sustained administration of dobutamine at 32 ng/g/min induced similar ventricular pressure
• cardiomyocytes from tamoxifen treated mice fail to exhibit an increase in mitochondrial oxygen consumption and ATP utilization compared with control mice
• however, baseline mitochondrial oxygen consumption and ATP utilization are normal
• in tamoxifen treated mice

homeostasis/metabolism
• under the short warm-up/high-intensity sprinting regimen, tamoxifen-treated mice exhibit reduced running capacity compared with control mice
• however, the difference is lost with a longer warm-up period
• in tamoxifen treated mice

behavior/neurological
• under the short warm-up/high-intensity sprinting regimen, tamoxifen-treated mice exhibit reduced running capacity compared with control mice
• however, the difference is lost with a longer warm-up period

cellular
• in cardiomyocytes from tamoxifen treated mice in response to ionomycin

muscle
• tamoxifen-treated mice exhibit inhibited acute cardiac mitochondrial calcium uptake compared with control cells
• at 18 weeks, cardiac myocytes from tamoxifen-treated mice challenged with calcium exhibit a severely blunted compared with control cells
• cardiac myocytes from tamoxifen-treated mice exhibit lower sodium-induced calcium efflux rates compared with control cells
• cardiac mitochondria from mice treated with tamoxifen and dobutamine fail to exhibit an increase in calcium unlike control mitochondria
• however, mice exhibit normal baseline mitochondrial calcium levels, response to Ru360, and elevated calcium levels in the mitochondrial following sustained dobutamine treatment
• tamoxifen-treated mice subjected to dobutamine (the beta-adrenergic receptor agonist) exhibit lesser short-term increase in the maximal rate of cardiac pressure compared with control mice
• however, sustained administration of dobutamine at 32 ng/g/min induced similar ventricular pressure
• in cardiomyocytes from tamoxifen treated mice in response to ionomycin


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
03/18/2025
MGI 6.24
The Jackson Laboratory