Analysis Tools|
Allele Symbol Allele Name Allele ID |
Srftm1Zli targeted mutation 1, Zhenlin Li MGI:3046779 |
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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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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• all mice die 8 to 10 weeks after tamoxifen injection due to rapid progression to heart failure; mice appear sick and become inactive a few days before death
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• following tamoxifen treatment, hearts show an irregular alignment of cardiomyocytes, with frequent gaps between cells
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• amount of polymerized F-actin in cardiomyocytes progressively decreases after tamoxifen treatment
• myofibrils at the intercalated disks are often stretched and fragmented following tamoxifen treatment
• Z disks of cardiomyocytes are misaligned and myofibrils are split 60 days after tamoxifen treatment
• 60 days after tamoxifen treatment, cardiac tissue shows a lower density of myofibrils and a defect in demarcation of Z lines and M lines
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• 95% of intercalated disks of hearts are enlarged, irregularly shaped, and are thicker 60 days after tamoxifen treatment
• intercalated disks show extensive interdigitation and the presence of lacunae, a widened space at the site of myofibril attachment to the intercalated disks, following tamoxifen treatment
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• hearts show features of eccentric hypertrophy 2 months after tamoxifen treatment, with dilation of the ventricular chambers
• however, no concentric hypertrophy is seen
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• mild left ventricle enlargement is seen 1 month after tamoxifen treatment, without significant left atrium remodeling and moderately increased left ventricle mass index
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• dilation of the ventricular chambers is seen 2 months after tamoxifen treatment
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• mild fibrosis in subendocardial regions are seen 2 months after tamoxifen treatment
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• hearts are enlarged 2 months after tamoxifen treatment, with impaired contractility and relaxation
• however, thickening of the free wall is not seen
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• decrease in left ventricular contractility is seen 21 days after tamoxifen treatment, with a decrease in ejection fraction and mean shortening velocity of circumferential fibers
• contractility and relaxation are moderately altered at 1 month after tamoxifen treatment, however 2 months after tamoxifen treatment, a massive decrease in left ventricle contractility and relaxation are seen, with increased E/Ea ratio, indicating heart failure
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• contractility and relaxation are moderately altered at 1 month after tamoxifen treatment, however 2 months after tamoxifen treatment, a massive decrease in left ventricle contractility and relaxation are seen, with increased E/Ea ratio, indicating heart failure
|
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• heart failure is seen 8 to 10 weeks after tamoxifen treatment
|
|
• following tamoxifen treatment, hearts show an irregular alignment of cardiomyocytes, with frequent gaps between cells
|
|
• amount of polymerized F-actin in cardiomyocytes progressively decreases after tamoxifen treatment
• myofibrils at the intercalated disks are often stretched and fragmented following tamoxifen treatment
• Z disks of cardiomyocytes are misaligned and myofibrils are split 60 days after tamoxifen treatment
• 60 days after tamoxifen treatment, cardiac tissue shows a lower density of myofibrils and a defect in demarcation of Z lines and M lines
|
|
• 95% of intercalated disks of hearts are enlarged, irregularly shaped, and are thicker 60 days after tamoxifen treatment
• intercalated disks show extensive interdigitation and the presence of lacunae, a widened space at the site of myofibril attachment to the intercalated disks, following tamoxifen treatment
|
|
• hearts are enlarged 2 months after tamoxifen treatment, with impaired contractility and relaxation
• however, thickening of the free wall is not seen
|
|
• decrease in left ventricular contractility is seen 21 days after tamoxifen treatment, with a decrease in ejection fraction and mean shortening velocity of circumferential fibers
• contractility and relaxation are moderately altered at 1 month after tamoxifen treatment, however 2 months after tamoxifen treatment, a massive decrease in left ventricle contractility and relaxation are seen, with increased E/Ea ratio, indicating heart failure
|
|
• contractility and relaxation are moderately altered at 1 month after tamoxifen treatment, however 2 months after tamoxifen treatment, a massive decrease in left ventricle contractility and relaxation are seen, with increased E/Ea ratio, indicating heart failure
|
|
• Z disks of cardiomyocytes are misaligned 60 days after tamoxifen treatment
|
|
• hearts show features of eccentric hypertrophy 2 months after tamoxifen treatment, with dilation of the ventricular chambers
• however, no concentric hypertrophy is seen
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| dilated cardiomyopathy | DOID:12930 |
OMIM:PS115200 |
J:135043 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutant embryos begin to die around E10.5 however at E9.5 only 20% cre expressing homozygous embryos were found, rather than the expected 25%
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• the cytoplasmic volume of the cardiomyocytes is reduced
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• the trabeculae are thinner and less-abundant
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• at E11.5 the myocardial wall is severely disorganized
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• at E11.5 the myocardial wall is severely disorganized with varying degrees of ventricular atrophy, the thickness of the compact layer is significantly reduced, and the atrial wall thickness is severely reduced
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• the interventricular septum is thinner and disorganized
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• the lumens of the right and left atria are significantly enlarged
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• starting at E10.5 embryos develop severe hemorrages in and around the cardiac and ventral body wall regions
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• a dramatic increase in apoptotic cells is seen at E11.5 in the heart, limb buds, epidermis, and vessels
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• by E13.5 only growth-retarded or resorbed embryos are found
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• the cytoplasmic volume of the cardiomyocytes is reduced
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• the trabeculae are thinner and less-abundant
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• at E11.5 the myocardial wall is severely disorganized
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• at E11.5 the myocardial wall is severely disorganized with varying degrees of ventricular atrophy, the thickness of the compact layer is significantly reduced, and the atrial wall thickness is severely reduced
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• by E13.5 only growth-retarded or resorbed embryos are found
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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 12/17/2024 MGI 6.24 |
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