normal phenotype
• viable and fertile with no gross abnormalities
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Allele Symbol Allele Name Allele ID |
Epn2tm1Ocr targeted mutation 1, Ottavio Cremona MGI:4356016 |
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Summary |
7 genotypes
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• viable and fertile with no gross abnormalities
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
Reduced tumor growth in Epn1tm1.1Wami/Epn1tm1.1Wami Epn2tm1Ocr/Epn2tm1Ocr Tg(Cdh5-cre/ERT2)CIVE23Mlia/0 Tg(TRAMP)8247Ng/0 mice
• tamoxifen-treated mice exhibit decreased mortality compared with Tg(TRAMP)8247Ng control mice
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• tamoxifen-treated mice develop smaller tumors compared with Tg(TRAMP)8247Ng control mice
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
Disrupted endothelial junctions in tumor vessels of Epn1tm1.1Wami/Epn1tm1.1Wami Epn2tm1Ocr/Epn2tm1Ocr Tg(Cdh5-cre/ERT2)CIVE23Mlia/0 mice
• tamoxifen-treated mice transplanted with GL261glioma cells survive longer than with control mice
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• tamoxifen-treated mice transplanted with Lewis Lung carcinoma (LLC) cells exhibit disorganized, fragile, immature, enlarged and leaky tumor vessels compared with control mice
• however, treatment with a VEGFR2 kinase inhibitor restored tumor vasculature
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• tamoxifen-treated mice subjected to AOM/DSS exhibit reduced tumor incidence and decreased tumor growth compared with control mice
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• tamoxifen-treated mice transplanted with Lewis Lung carcinoma (LLC) cells develop fewer, smaller tumors that grow at a slower rate compared with control mice
• tamoxifen-treated mice transplanted with GL261glioma cells develop smaller tumors compared with control mice
• tamoxifen-treated mice subjected to AOM/DSS exhibit reduced tumor incidence and decreased tumor growth compared with control mice
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• tamoxifen-treated mice transplanted with Lewis Lung carcinoma (LLC) cells exhibit disorganized, fragile, immature, enlarged and leaky tumor vessels compared with control mice
• however, treatment with a VEGFR2 kinase inhibitor restored tumor vasculature
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• endothelial cells treated with tamoxifen exhibit enhanced VEGF-stimulated migration compared with control cells
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• endothelial cells treated with tamoxifen exhibit disrupted endothelial junctions compared with control cells
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• endothelial cells treated with tamoxifen exhibit enhanced VEGF-stimulated proliferation compared with control cells
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• of tumor vasculature in tamoxifen-treated mice transplanted with Lewis Lung carcinoma (LLC) cells
• however, vascular permeability of blood vessels in major organs is normal
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• endothelial cells treated with tamoxifen exhibit enhanced VEGF-stimulated migration compared with control cells
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• endothelial cells treated with tamoxifen exhibit enhanced VEGF-stimulated proliferation compared with control cells
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• tamoxifen-treated mice subjected to AOM/DSS exhibit reduced tumor incidence and decreased tumor growth compared with control mice
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
Reduced tumor growth in Epn1tm1.1Wami/Epn1tm1.1Wami Epn2tm1Ocr/Epn2tm1Ocr Tg(Cdh5-cre/ERT2)CIVE23Mlia/0 and Epn1tm1.1Wami/Epn1tm1.1Wami Epn2tm1Ocr/Epn2tm1Ocr Tg(Cdh5-cre)7Mlia/0 mice
• mice transplanted with Lewis Lung carcinoma (LLC) cells develop fewer tumors that grow at a slower rate compared with control mice
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• not as severe as in mice heterozygous for the Epn2 mutation and homozygous for the Epn1 mutation
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• not as severe as in mice heterozygous for the Epn2 mutation and homozygous for the Epn1 mutation
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• not as severe as in mice heterozygous for the Epn2 mutation and homozygous for the Epn1 mutation
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• percentage of mice surviving to 10 months of age is reduced
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• die between E9.5 and E11.5
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• fail to undergo axial rotation in the sagital plane
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• arrest by E9.5
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• at E9.0
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• at E9.0 picnotic cells are seen in the neural tube
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• at E9.0
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• somites that do form are irregular in size and shape
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• somites that do form are irregular in size and shape
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• severely impaired somitogenesis resulting in a reduction in the number of somites formed by E9.5
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• at E9.0
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• lack large vitelline vessels and the sinusoids are larger and dilated at E9.0 indicating failure to remodel the vascular plexus
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• at E9.0, vessels in the telencephalic region fail to form finely branched trees, instead a coarse network of uniformly sized vessels is present
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• at E9.0 picnotic cells are seen in the neural tube
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• at E9.0
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• at E9.0 in the intersomitic region, vessels are only present in areas where somites develop and these vessels are disorganized compared to controls
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• at E9.0, vessels in the telencephalic region fail to form finely branched trees, instead a coarse network of uniformly sized vessels is present
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• defects in angiogenic vascular remodeling
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• atrophic ventricular wall seen at E9.5
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N |
• no defects in proliferation or clathrin mediated endocytosis are detected in MEFs in contrast results from previous experiments using Epn1 knockdown cells
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• at E9.0
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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 12/10/2024 MGI 6.24 |
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