Analysis Tools
digestive/alimentary system
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• increase in proliferation of intestinal epithelial stem cells and the transit-amplifying cells following tamoxifen induction
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Allele Symbol Allele Name Allele ID |
Rab11atm1.1Ngao targeted mutation 1.1, Nan Gao MGI:5608786 |
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| Summary |
4 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increase in proliferation of intestinal epithelial stem cells and the transit-amplifying cells following tamoxifen induction
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• adult mice administered tamoxifen exhibit increased crypt cell proliferation
(J:215917)
• 2 days after tamoxifen administration, mice show a mild expansion of Olfm4+ crypt based columnar stem cells indicating entry of enterocytes into mitosis
(J:278932)
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• adult mice administered tamoxifen exhibit increased crypt cell proliferation
(J:215917)
• 2 days after tamoxifen administration, mice show a mild expansion of Olfm4+ crypt based columnar stem cells indicating entry of enterocytes into mitosis
(J:278932)
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• intestinal organoid cultures induced with tamoxifen produce a 2-fold increase in interleukin-6 secretion
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice show higher mortality rate 8 weeks after azoxymethane-dextran sulfate sodium (AOM-DSS) treatment
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• survivors show a higher mortality with aging
• germ-free mice show reduced mortality
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• about 40% mortality rate at weaning
• males show a higher mortality rate than females
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• mice exhibit a higher baseline level of inflammatory cytokines than wild-type mice
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• mice show increased susceptibility to AOM-DSS-induced tumorigenesis
• AOM-DSS-treated mice that survive post 8 weeks form 2 to 6 poorly differentiated c-Myc+ and BrdUrd+ tubular adenomas in the ileum that are not seen in wild-type mice; tumors show complex glandular (cribriforming) structures, marked nuclear pleiomorphism, necrosis, increased mitotic activities, and single infiltrating cells in mucosa, best classified as intramucosal carcinoma
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• mice develop tubular adenomas (low-grade epithelial dysplasia) at juvenile ages
• at 1 year, the distal intestines of approximately 30% of mice develop 2 to 3 well-demarcated tubular adenomas and high-grade dysplasia that exhibit complex glandular (cribriforming) structures, marked pleiomorphism, necrosis, and increased mitotic activities
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• mice show increased susceptibility to AOM-DSS-induced tumorigenesis
• AOM-DSS-treated mice that survive post 8 weeks form 2 to 6 poorly differentiated c-Myc+ and BrdUrd+ tubular adenomas in the ileum that are not seen in wild-type mice; tumors show complex glandular (cribriforming) structures, marked nuclear pleiomorphism, necrosis, increased mitotic activities, and single infiltrating cells in mucosa, best classified as intramucosal carcinoma
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• runting is seen at a young age
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• dilated intestinal lumen
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• reduction in goblet cells
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• epithelial hyperplasia and dysplasia continue to be present at 5 months of age
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• increase in numbers of cycling crypt cells at all postnatal stages indicating crypt hyperplasia
• enlarged crypt
• however, differentiation of enterocytes and intestinal secretory cell lineages is unaffected
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• shortened colon
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• in neonates, the intestinal villi frequently fuse and branch
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• intestines show blunted villi
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• mice develop tubular adenomas (low-grade epithelial dysplasia) at juvenile ages
• at 1 year, the distal intestines of approximately 30% of mice develop 2 to 3 well-demarcated tubular adenomas and high-grade dysplasia that exhibit complex glandular (cribriforming) structures, marked pleiomorphism, necrosis, and increased mitotic activities
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• mice show a stronger intestinal epithelial barrier function than wild-type mice
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• intestinal organoid cultures initiate bud outgrowths more rapidly and contain a larger population of proliferative cells than wild-type cultures
(J:215917)
• intestinal organoid cultures from germ-free mice show decreased proliferation
(J:215917)
• treatment of intestinal organoids with an NF-kappaB pathway inhibitor, BAY11-0782, results in reduction of cell proliferation
(J:215917)
• all mice exhibit irregular cribriform proliferation in villi at 150 days
(J:278932)
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• crypt hyperproliferation and low-grade dysplasia is seen throughout the small intestine from birth
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• increase in numbers of cycling crypt cells at all postnatal stages
• germ-free mice show an overall reduction of crypt cell proliferation compared to specific pathogen free conditions
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• macrophage infiltration into the intestinal submucosa
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• increase in numbers of cycling crypt cells at all postnatal stages indicating crypt hyperplasia
• enlarged crypt
• however, differentiation of enterocytes and intestinal secretory cell lineages is unaffected
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• macrophage infiltration into the intestinal submucosa
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• mice exhibit a higher baseline level of inflammatory cytokines than wild-type mice
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• intestinal organoid cultures produce higher levels of cytokines, including interleukin-6, interleukin-1 beta, and CXCL12
• luminal perfusion of TLR9 (endotoxin-free E.coli DNA) or TLR4 (LPS) agonists drastically activates cytokine responses in germ-free mutants compared to wild-type controls, indicating that intestinal epithelial cells show impaired tolerance to microbial TLR agonists
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• by intestinal organoid cultures
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• by intestinal organoid cultures
• intestinal organoid cultures from germ-free mice show reduced IL-6 secretion
• treatment of intestinal organoids with an NF-kappaB pathway inhibitor, BAY11-0782, results in a reduction of IL-6 production
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• reduction in goblet cells
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• increase in numbers of cycling crypt cells at all postnatal stages
• germ-free mice show an overall reduction of crypt cell proliferation compared to specific pathogen free conditions
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice show higher mortality due to increased tumor burden compared to single ApcMin mice
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• 2-month-old mice develop twice the number of adenomas that are 5 times larger and occupy larger epithelial fields as compared with tumor fields in single ApcMin mice
• mice show higher mortality due to increased tumor burden compared to single ApcMin mice
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• 2-month-old mice develop twice the number of adenomas that are 5 times larger and occupy larger epithelial fields as compared with tumor fields in single ApcMin mice
• mice show higher mortality due to increased tumor burden compared to single ApcMin mice
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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 06/12/2024 MGI 6.13 |
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