homeostasis/metabolism
N |
• mice do not develop hyperglycemia even at 14 weeks of age
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Allele Symbol Allele Name Allele ID |
Tg(Tagln-cre)1Jjl transgene insertion 1, John J Lepore MGI:3577106 |
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Summary |
8 genotypes
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice do not develop hyperglycemia even at 14 weeks of age
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
Klf15tm2Jain/Klf15tm2Jain Tg(Tagln-cre)1Jjl/0 Apoetm1Unc/Apoetm1Unc aortas develop more atherosclerotic lesions after a high fat diet challenge
N |
• mice fed a high fat diet exhibit the same circulating levels of cholesterol and triglycerides as in Apoetm1Unc homozygotes
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• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes
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• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes
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• in mice fed a high fat diet compared with Apoetm1Unc homozygotes
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• decreased vascular smooth muscle cells in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes
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• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes
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• decreased vascular smooth muscle cells in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes
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• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• all die between E18.5 and P2
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• 6 of 11 embryos show a retroesophageal right subclavian artery
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• 7 of 11 embryos exhibit a hypoplastic aortic arch
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• 7 of 11 embryos have an interrupted aortic arch
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• seen in 1/11 mutant mice
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• seen in 7 of 11 embryos
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• seen in 4 of 11 embryos
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• all embryos exhibit a membranous ventricular septal defect
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• cardiopulmonary development is not disrupted
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• in survivors
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• alveolar enlargement in survivors
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• in survivors
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• in survivors
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• keratin cyst formation is observed
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• generalized growth retardation is observed compared to controls
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• mice develop spontaneous cutaneous SCC lesions, as well as dysplastic precursor lesions
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• with aging, hyperkeratinization of tail is seen
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• aberrant hair follicle cycling occurs
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• starting at 2-3 weeks, mice display hair and whisker loss; diffuse alopecia is observed
• at 10 months of age, alopecia has progressed almost to completion
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• hypoplastic dermis with increased cellularity is observed
• by 6 months of age, most mice develop hyperkeratotic cutaneous nodules, with all mutants exhibiting multiple lesions by 10 months of age
• examination of some nodules reveals papillomas or inflamed infundibular cyts
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• keratin cyst formation is observed
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• cutaneous nodules show hyperproliferative keratinocytic lesions exhibiting cellular atypia and an invasive growth pattern
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice are viable and born in expected Mendelian ratios
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• no vasculature defects are observed during development
• homozygote mice are born at the expected ratios
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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 11/12/2024 MGI 6.24 |
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