Analysis Tools
normal phenotype
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• mice are viable and fertile; used for cre reporter expression analysis
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Allele Symbol Allele Name Allele ID |
Gt(ROSA)26Sortm3(CAG-EYFP)Hze targeted mutation 3, Hongkui Zeng MGI:3809521 |
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| Summary |
3 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are viable and fertile; used for cre reporter expression analysis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• hearts show re-expression of fetal cardiac genes
• however, heart development proceeds normally
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• hypertrophic cardiomyocytes are seen in the right ventricle free wall as early as 15 days after birth
• however, aberrant proliferation of or apoptosis of cardiomyocytes is not seen and there is no evidence of increased DNA damage
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• lesions contain degenerating cardiomyocytes
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• hearts at 6 weeks and 6 months of age exhibit white surface scars localized to the subepicardial region of the ventricular free walls; lesions contain degenerating cardiomyocytes and a large degree of collagen deposition indicating focal replacement fibrosis localized to the subepicardial myocardium
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• mice show increased arterial elastance at 6 months of age, which is a measure of arterial load
• the slope of the end-diastolic pressure-volume relationship, which describes diastolic function, is elevated
• however, no effect is seen on the slope of end-systolic pressure-volume relationship, which describes the maximal developed ventricular pressure at any given ventricular volume
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• mice show decreased stroke work at 6 months
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• at 6 months of age
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• at 6 months of age
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• mice exhibit increased dp/dtmax-end-diastolic volume, the relationship between peak rate of pressure rise and EDV, which describes ventricular contractile performance
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• mice show an increase in diastolic myocardial stiffness
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• levels of manganese superoxide dismutase are reduced in scar-containing free-wall right ventricle, but not in non-scarred regions, suggesting impaired response to oxidative stress
• however, only very minor increases in reactive oxygen species are seen, indicating that cardiomyocyte degeneration most likely is not caused by increased oxidative stress
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• hypertrophic cardiomyocytes are seen in the right ventricle free wall as early as 15 days after birth
• however, aberrant proliferation of or apoptosis of cardiomyocytes is not seen and there is no evidence of increased DNA damage
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• lesions contain degenerating cardiomyocytes
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• mice exhibit increased dp/dtmax-end-diastolic volume, the relationship between peak rate of pressure rise and EDV, which describes ventricular contractile performance
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• cardiomyocyte sarcolemmal integrity is compromised in focal subepicardial areas between 15 and 25 days after birth
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• fewer IL9+ cells in IFN-alpha-treated mice following differentiation towards Th9 lineage
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• fewer IL9+ cells in IFN-alpha-treated mice following differentiation towards Th9 lineage
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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 04/30/2024 MGI 6.23 |
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