Analysis Tools|
Allele Symbol Allele Name Allele ID |
Tg(Myh6-Ppp3ca)37Eno transgene insertion 37, Eric N Olson MGI:3056186 |
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| Summary |
14 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at 3 weeks of age, transgenic mice display a ~2-fold increase in heart weight to tibia length ratio compared to non transgenic mice
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• at 3 weeks of age, transgenic mice display a ~2-fold increase in heart weight to tibia length ratio compared to non transgenic mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• Dscr1-deficiency induces a greater increase in cardiac hypertrophy in combination with Tg(Myh6-Ppp3ca)37Eno expression than in wild-type or Dscr1l1-deficiency with transgene expression
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• Dscr1-deficiency induces a greater increase in cardiac hypertrophy in combination with Tg(Myh6-Ppp3ca)37Eno expression than in wild-type or Dscr1l1-deficiency with transgene expression
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• died by 20-28 days of age
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• 110% increase in myocyte size compared to a 34% increase in mice expressing only the transgene
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• showed massive cardiac enlargement that exceeded the hypertrophy induced by the transgene alone
• at 3 weeks of age, 244% increase in heart weight/body weight ratio compared to a 149% increase in mice expressing only the transgene
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• 110% increase in myocyte size compared to a 34% increase in mice expressing only the transgene
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• showed massive cardiac enlargement that exceeded the hypertrophy induced by the transgene alone
• at 3 weeks of age, 244% increase in heart weight/body weight ratio compared to a 149% increase in mice expressing only the transgene
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• cardiac hypertrophy due to hypertrophy of individual cardiomyocytes
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• cardiac mass increases by 220% as opposed to 110% for controls
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• cardiac hypertrophy due to hypertrophy of individual cardiomyocytes
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• cardiac mass increases by 220% as opposed to 110% for controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• transgenic mice are highly susceptible to sudden death from heart failure with none surviving beyond 8 weeks of age
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• by 4 weeks of age mutant hearts are 3-fold larger than wild-type due to hypertrophy
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• by 4 weeks of age mutant hearts are 3-fold larger than wild-type due to hypertrophy
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• hypertrophy induced by the transgene was reduced
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• hypertrophy induced by the transgene was reduced
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• myofibrillar hypertrophy
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• identical to control mice with the transgene alone
• three fold increase in heart/body weight ratio
• wall thickening
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• myofibrillar hypertrophy
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• identical to control mice with the transgene alone
• three fold increase in heart/body weight ratio
• wall thickening
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• dramatic cardiac hypertrophy as indicated by an increase in heart weight to body weight ratio at 1 month of age that is similar to single Tg(Myh6-Ppp3ca)37Eno mice
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• thickening of the left ventricle free wall and septum are decreased compared to single Tg(Myh6-Ppp3ca)37Eno mice
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• mice show an increase in cardiac fibrosis compared to single Tg(Myh6-Ppp3ca)37Eno mice
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• dramatic cardiac hypertrophy as indicated by an increase in heart weight to body weight ratio at 1 month of age that is similar to single Tg(Myh6-Ppp3ca)37Eno mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• half die by 10 weeks of age and all die by 18 weeks of age
• die earlier than mice carrying Tg(Myh6-Ppp3ca)37Eno alone
• appear to die from heart failure
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• decrease in left ventricular wall thickness
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• increase in left ventricular dimension and decrease in wall thickness
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• fractional shortening is around 10%
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• fractional shortening is around 10%
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• null mice expressing the transgene do not show cardiomyocyte hypertrophy or fibrosis in with expression of this transgene, in contrast to wild-type transgenic mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice show large atrial clots
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• cardiac hypertrophy is not enhanced above that observed in Tg(Myh6-Mef2c)2Jmol single transgenic animals
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• degree of functional decompensation is not enhanced compared to Tg(Myh6-Mef2c)2Jmol single transgenic mice
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• degree of functional decompensation is not enhanced compared to Tg(Myh6-Mef2c)2Jmol single transgenic mice
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• cardiac hypertrophy is not enhanced above that observed in Tg(Myh6-Mef2c)2Jmol single transgenic animals
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• cardiac hypertrophy is not enhanced above that observed in Tg(Myh6-MEF2A)1Jmol single transgenic animals
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• cardiac hypertrophy is not enhanced above that observed in Tg(Myh6-MEF2A)1Jmol single transgenic animals
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• about 50% survive to 20 weeks of age
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• hypertrophy is attenuated in mice treated with an adeno-virus expressing Mlip as neonates
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• hypertrophy is attenuated in mice treated with an adeno-virus expressing Mlip as neonates
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• transgenic mice are highly susceptible to sudden death from heart failure
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• at 3 weeks of age, transgenic mice display a ~2-fold increase in heart weight to tibia length ratio
(J:109586)
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• the heart to body weight ratio is increased 2-3 fold as early as P18 with concentric hypertrophy seen, both ventricles and atria are affected
(J:93176)
• cyclosporin A treatment prevented hypertrophy and fibrosis
(J:93176)
• at 3 weeks of age, showed a 149% increase in heart weight/body weight ratio compared to wild-type
(J:94665)
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• 34% increase in myocyte area compared to wild-type
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• the ventricular cardiomyocytes are disorganized, hypertrophic and display enlarged nuclei
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• at 3 weeks of age, transgenic mice display a ~2-fold increase in heart weight to tibia length ratio
(J:109586)
|
|
• the heart to body weight ratio is increased 2-3 fold as early as P18 with concentric hypertrophy seen, both ventricles and atria are affected
(J:93176)
• cyclosporin A treatment prevented hypertrophy and fibrosis
(J:93176)
• at 3 weeks of age, showed a 149% increase in heart weight/body weight ratio compared to wild-type
(J:94665)
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• dilation of the ventricles is seen in older transgenic mice
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• dilation of the ventricles is seen in older transgenic mice
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• extensive, primarily interstitial fibrosis is seen in the ventricular walls sometimes associated with myofiber degeneration
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• perivascular edema in the lungs is seen in transgenic mice that die suddenly
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• perivascular edema in the lungs is seen in transgenic mice that die suddenly
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• 34% increase in myocyte area compared to wild-type
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• the ventricular cardiomyocytes are disorganized, hypertrophic and display enlarged nuclei
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• extensive, primarily interstitial fibrosis is seen in the ventricular walls sometimes associated with myofiber degeneration
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| dilated cardiomyopathy | DOID:12930 |
OMIM:PS115200 |
J:93176 | |
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 11/05/2024 MGI 6.24 |
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