normal phenotype
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• mice are indistinguishable from wild-type
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Analysis Tools|
Allele Symbol Allele Name Allele ID |
Fen1+ wild type MGI:2432996 |
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| Summary |
6 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are indistinguishable from wild-type
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• average % of near-tetraploid aneuploidy in heterozygous mutant MEFs cells is 9.6% relative to 6.6% for wild-type MEFs
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• under normal culture conditions, heterozygous mutant MEFs show mild-to-moderate defects in cell growth relative to wild-type MEFs
• upon treatment with camptothecin (CPT), the number of heterozygous mutant live cells is increased by only 1.7% per day, whereas the number of wild-type cells is increased by 10% per day
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• heterozygous mutant MEFs exhibit significantly more spontaneous chromosome breaks (1.0%) than wild-type MEFs (0.6%)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• heterozygotes are generally viable and fertile with a normal life span
• a small number show thymic atropy and become moribund at 5 or 11 months of age
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• some mice found with non-Hodgkin's lymphoma of B cells
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• one example found of Paneth cell hyperplasia in the small intestine
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• heterozygotes are generally viable and fertile with a normal life span
• a small number show thymic atropy and become moribund at 5 or 11 months of age
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• one example found of Paneth cell hyperplasia in the small intestine
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• heterozygotes are generally viable and fertile with a normal life span
• a small number show thymic atropy and become moribund at 5 or 11 months of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• heterozygotes are viable, fertile and morphologically normal in terms of size and growth, with no detectable histological abnormalities at 12-15 months of age relative to wild-type littermates
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• primary MEFs exhibit significantly decreased cell survival following exposure to mitomycin C
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• primary MEFs exhibit significantly decreased cell survival following exposure to methylmethanesulfonate
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• primary MEFs show ~12-fold higher spontaneous mutation rate than wild-type MEFs, as determined by an Hprt mutant assay
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• mice develop significant extrameduallry hematopoiesis
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• in 35% cases, large cluster or sheet-like plasma cells are seen in the interfollicular region
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• in 35% cases, large cluster or sheet-like plasma cells are seen in the interfollicular region
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• mice develop a lymphoproliferative phenotype, characterized by marked follicular and interfollicular hyperplasia
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• mice develop autoimmunity and a lymphoproliferative disorder by 9-12 months of age
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• at 9-12 months of age, the serum anti-nuclear antigen antibody levels are 1.12 +/- 0.8 unit/ul relative to 0.35 +/- 0.3 unit/ul in wild-type mice
• CLIFT analysis revealed that antibodies to nuclear antigens present in sera are against dsDNA
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• at 9-12 months of age, the serum levels of anti-double stranded DNA antibodies are significantly higher than in wild-type controls
• DNA-IgG complex abundance is 2-3-fold higher than that in wild-type sera
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• at 9-12 months of age, 43% of mice develop chronic lung inflammation relative to 19% of age-matched wild-type mice
• at >6 months of age, a significant number of mice develop chronic subcutaneous inflammation around the external urogenital area
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• mice show deposition of IgG-C3 immune complexes onto the glomeruli and capillary walls of the kidneys
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• at 9-12 months of age, 43% of mice develop chronic lung inflammation relative to 19% of age-matched wild-type mice
• deposition of IgG-C3 immune complex onto cells in the lungs
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• mice develop pulmonary interstitial inflammation characterized by pneumonocyte hyperplasia and accumulation of inflammatory cells, including significant lymphoplasmacytic infiltrate
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• at 14-20 months of age, 36.7% of mice developed lung adenoma relative to 17.6% of age-matched wild-type mice
• all mice had only one tumor, similar to affected wild-type mice
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• mice show deposition of IgG-C3 immune complexes onto the glomeruli and capillary walls of the kidneys
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• at 9-12 months of age, 43% of mice develop chronic lung inflammation relative to 19% of age-matched wild-type mice
• deposition of IgG-C3 immune complex onto cells in the lungs
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• mice develop pulmonary interstitial inflammation characterized by pneumonocyte hyperplasia and accumulation of inflammatory cells, including significant lymphoplasmacytic infiltrate
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• at 14-20 months of age, 36.7% of mice developed lung adenoma relative to 17.6% of age-matched wild-type mice
• all mice had only one tumor, similar to affected wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• median survival of 9 months as compared to 13 months for Apctm1Rak single heterozygotes
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• 100% develop gastrointestinal tumors by 1 year of age
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• incidence of malignant tumors is higher than in Apctm1Rak single heterozygotes
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• extensive microsatellite instability in tumor DNA
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• 100% develop gastrointestinal tumors by 1 year of age
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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 12/30/2025 MGI 6.24 |
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