Analysis Tools
mortality/aging
| N |
• mice live a full lifespan without development of tumorigenesis
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neoplasm
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Allele Symbol Allele Name Allele ID |
Csnk1a1tm1.1Ybn targeted mutation 1.1, Yinon Ben-Neriah MGI:5543667 |
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| Summary |
12 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice live a full lifespan without development of tumorigenesis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in the gut following tamoxifen treatment
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• in mouse embryonic fibroblasts following tamoxifen treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after 2 weeks of tamoxifen treatment
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• widespread high-grade dysplasia and numerous intramucosal carcinomas invading the lamina propria in most of the small-bowel crypts and villi within 2 weeks of tamoxifen treatment
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• increased proliferation after tamoxifen treatment throughout the crypt-villus axis
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• in the gut of tamoxifen treated mice but no more so than in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(Vil-cre/ERT2)23Syr mice
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• increased proliferation after tamoxifen treatment throughout the crypt-villus axis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• within 6 months, 7 of 9 tamoxifen-treated mice develop invasive carcinomas that permeates the bowel muscular wall into the subserosal fat with some involvement of the serosal surface (stage T4)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice exhibit severe dysplasia and intramucosal carcinomas throughout the small bowel
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• massive proliferation in the villi compartment in tamoxifen-treated mice
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• massive proliferation in the villi compartment in tamoxifen-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increased proliferation in the entire bowel
• distal gut dysplasia appears later than in mice with Trp53tm2.1Tyj (containing the R172H missense mutation)
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• jejunal and ileal organoids exhibit increased proliferation, decreased differentiation, and resemble highly dysplastic spheroids
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• high-grade dysplasia in the entire bowel
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• enlarged and dysplastic
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• enlarged and dysplastic
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• increased proliferation in the entire bowel
• distal gut dysplasia appears later than in mice with Trp53tm2.1Tyj (containing the R172H missense mutation)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Skin hyperpigmentation in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(KRT14-cre/ERT)20Efu/0 mice but not in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Trp53tm1Brn/Trp53tm1Brn Tg(KRT14-cre/ERT)20Efu/0 mice
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• after tamoxifen i.p. treatment, the epidermis becomes dysplastic with no melanin deposition
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• at day 28 after tamoxifen i.p. treatment, BrdU+ (proliferating) cells and beta-catenin nuclear staining are increased in the basal layer of the epidermis; however, most of the positive cells are multinucleated clumping cells indicating abnormal mitoses associated with epidermal dysplasia
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| N |
• mice do NOT develop skin hyperpigmentation after tamoxifen i.p. treatment
• melanin is mainly distributed in the dermis and less in the epidermis, similar to control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increased proliferation in the colon and ileum, but not the duodenum and jejunum
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• dysplastic in the colon and ileum, but not the duodenum and jejunum
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• increased proliferation in the colon and ileum, but not the duodenum and jejunum
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• jejunal and ileal organoids exhibit normal organoid differentiation and proliferation
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• increased proliferation in the colon and ileum, but not the duodenum and jejunum
• treatment of organoids with gallic acid a reversible increase in proliferation of enterocytes unlike in untreated cells that exhibit normal organoid differentiation and proliferation
• however, antibiotic treatment to eliminate gut bacteria rescues hyperproliferation proliferation defect
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• dysplastic in the colon and ileum, but not the duodenum and jejunum
• distal gut dysplasia appears earlier than in mice with null Trp53
• mice treated with gallic acid exhibit high-grade dysplastic foci unlike untreated mice\
• however, antibiotic treatment to eliminate gut bacteria results in shorter crypts and better organized villi
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• increased proliferation in the colon and ileum, but not the duodenum and jejunum
• treatment of organoids with gallic acid a reversible increase in proliferation of enterocytes unlike in untreated cells that exhibit normal organoid differentiation and proliferation
• however, antibiotic treatment to eliminate gut bacteria rescues hyperproliferation proliferation defect
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• hematopoietic stem and progenitor cells are more sensitive to lenalidomide in culture than cells from Csnk1a1tm1.1Ybn/+ Tg(Mx1-cre)1Cgn mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• enlarged and dysplastic
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• enlarged and dysplastic
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(KRT14-cre/ERT)20Efu/0 mice show skin hyperpigmentation of ears, paws, mouth, and trunk after tamoxifen treatment
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• increased melanin content in the ear epidermis at day 28 after topical 4-hydroxytamoxife (4HT) induction
• increased melanin content in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
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• a slow but significant increase of melanocyte numbers is noted in the tail epidermis during the first 14 days after topical 4HT induction, followed by a rapid increase thererafter; however, the number of dermal melanocytes is not significantly altered
• after topical 4HT induction, epidermal melanocytes become progressively larger and more dendritic, indicating melanocytic differentiation
• many dendritic melanocytes containing black melanin pigment are observed around p53+ keratinocytes at day 28 after tamoxifen i.p. treatment
• melanocyte number is increased in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
• treatment of 4HT-induced mice with oral imatinib (a Kit inhibitor) results in decreased melanocyte numbers in the epidermis at day P28 relative to vehicle-treated control mice
• intradermal injection of ACK2 (a Kit-neutralizing antibody) reduces the number of melanocytes in the epidermis at days 7 and 14 after 4HT induction relative to vehicle-treated control mice
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• a slow but significant increase of melanocyte numbers is noted in the tail epidermis during the first 14 days after topical 4HT induction, followed by a rapid increase thererafter
• melanocyte number is increased in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
• treatment of 4HT-induced mice with oral imatinib (a Kit inhibitor) results in decreased melanocyte numbers in the epidermis at day P28 relative to vehicle-treated control mice
• intradermal injection of ACK2 (a Kit-neutralizing antibody) reduces the number of melanocytes in the epidermis at days 7 and 14 after 4HT induction relative to vehicle-treated control mice
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• amount of eumelanin is significantly increased in the epidermis at day 28 after topical 4HT induction
• treatment of tamoxifen-injected mice with oral imatinib (a Kit inhibitor) results in severe reduction of eumelanin production relative to vehicle-treated control mice at day 28
• amount of pheomelanin remains unchanged during topical 4HT induction
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• at 1 month after tamoxifen i.p. treatment, mice show skin hyperpigmentation on the ears, paws, tail, mouth, and trunk relative to heterozygous control mice
• skin hyperpigmentation is accompanied by beta-catenin and p53 stabilization, preferential induction of p53 target genes, and p53-dependent up-regulation of Kit ligand
• treatment with ACK2 (a Kit-neutralizing antibody) or imatinib (a Kit inhibitor) abolishes the induction of hyperpigmentation, indicating that it requires the KitL/Kit pathway
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• hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
• topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction
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• hyperpigmentation of the paws at 1 month after tamoxifen i.p. treatment
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• hyperpigmentation of the tail at 1 month after tamoxifen i.p. treatment
• topical treatment with 4HT for 14 days induces skin hyperpigmentation on the tail, esp. at >3 weeks after induction
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• hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
• topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction
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• at day 28 after tamoxifen i.p. treatment, BrdU+ (proliferating) cells and beta-catenin nuclear staining are increased in the basal layer of the epidermis
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• after tamoxifen i.p. treatment, the epidermis becomes hyperplastic with increased melanin deposition
• treatment of tamoxifen-injected mice with oral imatinib (a Kit inhibitor) induces thinning of the epidermis with decreased melanin levels in the epidermis relative to vehicle-treated control mice
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• increased epidermal thickness in the ears 28 days after topical 4HT induction
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• increased melanin content in the ear epidermis at day 28 after topical 4-hydroxytamoxife (4HT) induction
• increased melanin content in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
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• a slow but significant increase of melanocyte numbers is noted in the tail epidermis during the first 14 days after topical 4HT induction, followed by a rapid increase thererafter; however, the number of dermal melanocytes is not significantly altered
• after topical 4HT induction, epidermal melanocytes become progressively larger and more dendritic, indicating melanocytic differentiation
• many dendritic melanocytes containing black melanin pigment are observed around p53+ keratinocytes at day 28 after tamoxifen i.p. treatment
• melanocyte number is increased in the dorsal epidermis at day 28 after tamoxifen i.p. treatment
• treatment of 4HT-induced mice with oral imatinib (a Kit inhibitor) results in decreased melanocyte numbers in the epidermis at day P28 relative to vehicle-treated control mice
• intradermal injection of ACK2 (a Kit-neutralizing antibody) reduces the number of melanocytes in the epidermis at days 7 and 14 after 4HT induction relative to vehicle-treated control mice
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• hyperpigmentation of the paws at 1 month after tamoxifen i.p. treatment
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• hyperpigmentation of the tail at 1 month after tamoxifen i.p. treatment
• topical treatment with 4HT for 14 days induces skin hyperpigmentation on the tail, esp. at >3 weeks after induction
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• tamoxifen-injected mice show induction of the DNA-damage response, as shown by increased gamma-H2AX staining in the epidermis
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• 24 h after exposure to a high, sunburn-inducing dose of UVB, hyperpigmented tails of tamoxifen-treated mice show absence of skin swelling and significantly fewer TUNEL+ apoptotic keratinocytes in the tail skin than similarly-treated control mice, indicating protection from UV (sunburn) damage
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• tamoxifen-injected mice show increased apoptosis in the epidermis, as shown by increased cleaved-caspase 3 expression
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| N |
• no skin tumor formation is observed for at least 9 months after tamoxifen i.p. treatment
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• hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
• topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction
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• hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
• topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction
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• hyperpigmentation of the ears at 1 month after tamoxifen i.p. treatment
• topical treatment with 4HT for 14 days induces skin hyperpigmentation on the ear, esp. at >3 weeks after induction
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• hyperpigmentation of the tail at 1 month after tamoxifen i.p. treatment
• topical treatment with 4HT for 14 days induces skin hyperpigmentation on the tail, esp. at >3 weeks after induction
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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 05/07/2024 MGI 6.23 |
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