Analysis Tools
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• hematopoietic stem and progenitor cells (HSPCs) infected with MLL-AF9 and transplanted in lethally irradiated recipients treated with tamoxifen produce fewer white blood cells compared with control cells
• bone marrow HSPCs infected with MLL-AF9 or AML1-ETO and treated with tamoxifen exhibit reduced colony number and loss of blast colony morphology unlike control cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following treatment with tamoxifen
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• following treatment with tamoxifen, extramedullary hematopoiesis is observed in spleens
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• following treatment with tamoxifen, mice exhibit erythrocytosis
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• following treatment with tamoxifen, mice exhibit hematocrits close to 80%
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• following treatment with tamoxifen, mice exhibit increased serum erythropoietin levels
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• following treatment with tamoxifen
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• following treatment with tamoxifen
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• following treatment with tamoxifen
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• hematocrit level, erythropoietin level and spleen architecture and weight are similar to mice without cre/ESR1 allele
• the Epas1 allele functions to rescue the erythrocytosis phenotype
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• survival is improved relative to mice carrying the Egln1 null allele, but not to control levels
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following treatment with tamoxifen
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• following treatment with tamoxifen, extramedullary hematopoiesis is observed in spleens
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• following treatment with tamoxifen, mice exhibit hematocrits close to 80%
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• following treatment with tamoxifen, mice exhibit increased serum erythropoietin levels
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• following treatment with tamoxifen
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• following treatment with tamoxifen, however, survival is improved relative to tamoxifen treated Egln1tm2.1Fsl mice alone
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• following treatment with tamoxifen
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in the bronchioalveolar following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• in the bronchioalveolar following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• in restimulated cells from the parabronchial lymph node or splenocytes of tamoxifen-treated Dermatophagoides farinae-exposed mice
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• in restimulated cells from the parabronchial lymph node or splenocytes of tamoxifen-treated Dermatophagoides farinae-exposed mice
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• in restimulated cells from the parabronchial lymph node or splenocytes of tamoxifen-treated Dermatophagoides farinae-exposed mice
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• following exposure to Dermatophagoides farinae, tamoxifen-treated mice exhibit increased total cells in the bronchioalveolar fluid (5-fold increase in eosinophils and neutrophils), increased goblet cell metaplasia, and increased cytokine secretion (IL4, IL5, IL13, and IFN-gamma) compared with control mice
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• following exposure to Dermatophagoides farinae, tamoxifen-treated mice exhibit increased total cells in the bronchioalveolar fluid (5-fold increase in eosinophils and neutrophils), increased goblet cell metaplasia, and increased cytokine secretion (IL4, IL5, IL13, and IFN-gamma) compared with control mice
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• following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• in the bronchioalveolar following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• in the bronchioalveolar following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• bone marrow cells treated with tamoxifen exhibit normal reconstitution capacity hematopoiesis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• after tamoxifen treatment of adult mice
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• reduced response to Tnfsf13b in vitro 2 days, and in vivo 3 and 5 days after tamoxifen treatment
• lack of BrdU incorporation after Tnfsf13b induction in vivo 3 and 5 days after tamoxifen treatment
• proliferation in response to anti-Cd40 or anti-Ighm antibody induction
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• in mesenteric lymph nodes and Peyers patches reductions in total B cells occurred as early as days 512 post-tamoxifen treatment, with further reductions occurring through the last time point examined at day 30 post-tamoxifen
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• in mesenteric lymph nodes and Peyers patches
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• severe reduction
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• modest reduction
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• modest reduction
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• reduced response to Tnfsf13b in vitro 2 days, and in vivo 3 and 5 days after tamoxifen treatment
• lack of BrdU incorporation after Tnfsf13b induction in vivo 3 and 5 days after tamoxifen treatment
• proliferation in response to anti-Cd40 or anti-Ighm antibody induction
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• in mesenteric lymph nodes and Peyers patches reductions in total B cells occurred as early as days 512 post-tamoxifen treatment, with further reductions occurring through the last time point examined at day 30 post-tamoxifen
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• in mesenteric lymph nodes and Peyers patches
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• severe reduction
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• modest reduction
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• modest reduction
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• reduced response to Tnfsf13b in vitro 2 days, and in vivo 3 and 5 days after tamoxifen treatment
• lack of BrdU incorporation after Tnfsf13b induction in vivo 3 and 5 days after tamoxifen treatment
• proliferation in response to anti-Cd40 or anti-Ighm antibody induction
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• when bone marrow cells are used to reconstitute lethally irradiated mice, NP-KLH and tamoxifen treated chimeras exhibit a reduction in IgM+ plasma blasts cells compared to when wild-type bone marrow are used
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• following tamoxifen-treatment and immunization with NP-KLH
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• following tamoxifen-treatment and immunization with NP-KLH
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• greater than 5-fold following tamoxifen-treatment
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• when bone marrow cells are used to reconstitute lethally irradiated mice, NP-KLH and tamoxifen treated chimeras exhibit a reduction in IgM+ plasma blasts cells compared to when wild-type bone marrow are used
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• following tamoxifen-treatment and immunization with NP-KLH
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• following tamoxifen-treatment and immunization with NP-KLH
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• greater than 5-fold following tamoxifen-treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following tamoxifen-treatment and immunization with NP-KLH
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• following tamoxifen-treatment and immunization with NP-KLH
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• following tamoxifen-treatment and immunization with NP-KLH
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• following tamoxifen-treatment and immunization with NP-KLH
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in tamoxifen-treated mice
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• greater than 2-fold in tamoxifen-treated mice due to reduced intestinal absorption
• however, kidney function is normal
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• tamoxifen-treated mice fail to exhibit a change in phosphorus in response to nicotinamide unlike similarly treated control mice
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• after 10 week, tamoxifen-treated mice exhibit a 2-fold increase in focal phosphate content compared with similarly treated control mice
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• tamoxifen-treated mice exhibit reduced intestinal absorption of phosphorus compared with similarly treated control mice
• tamoxifen-treated mice fail to exhibit a change in phosphorus in response to nicotinamide unlike similarly treated control mice
• tamoxifen-treated mice exhibit reduced sodium dependent intestinal phosphate transport in the jejunum and ileum compared with similarly treated control mice
• however, tamoxifen-treated mice exhibit normal calcium and sodium-independent phosphate transport
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• in tamoxifen-treated mice
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• greater than 2-fold in tamoxifen-treated mice due to reduced intestinal absorption
• however, kidney function is normal
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• tamoxifen-treated mice develop calcification nodules in the lungs (pulmonary alveolar microlithiasis) unlike similarly treated control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the percentage of polyclonally stimulated apoptotic CD4+ T cells of the parabronchial lymph node from tamoxifen-treated is decreased compared to in control mice
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• the percentage of polyclonally stimulated proliferating CD4+ T cells of the parabronchial lymph node or spleen from tamoxifen-treated is increased compared to in control mice
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• in the bronchioalveolar following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• in the bronchioalveolar following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• the percentage of polyclonally stimulated apoptotic CD4+ T cells of the parabronchial lymph node from tamoxifen-treated is decreased compared to in control mice
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• the percentage of polyclonally stimulated proliferating CD4+ T cells of the parabronchial lymph node or spleen from tamoxifen-treated is increased compared to in control mice
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• in the bronchioalveolar following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• in the bronchioalveolar following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• in restimulated cells from the parabronchial lymph node or splenocytes of tamoxifen-treated Dermatophagoides farinae-exposed mice
• in CD3+/CD4+ T cells from tamoxifen-treated Dermatophagoides farinae-exposed mice
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• in restimulated cells from the parabronchial lymph node or splenocytes of tamoxifen-treated Dermatophagoides farinae-exposed mice
• in CD3+/CD4+ T cells from tamoxifen-treated Dermatophagoides farinae-exposed mice
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• in restimulated cells from the parabronchial lymph node or splenocytes of tamoxifen-treated Dermatophagoides farinae-exposed mice
• in CD3+/CD4+ T cells from tamoxifen-treated Dermatophagoides farinae-exposed mice
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• following exposure to Dermatophagoides farinae, tamoxifen-treated mice exhibit increased total cells in the bronchioalveolar fluid (5-fold increase in eosinophils and neutrophils), increased goblet cell metaplasia, and increased cytokine secretion (IL4, IL5, IL13, and IFN-gamma) compared with control mice
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• following exposure to Dermatophagoides farinae, tamoxifen-treated mice exhibit increased total cells in the bronchioalveolar fluid (5-fold increase in eosinophils and neutrophils), increased goblet cell metaplasia, and increased cytokine secretion (IL4, IL5, IL13, and IFN-gamma) compared with control mice
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• following exposure to Dermatophagoides farinae in tamoxifen-treated mice
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• the percentage of polyclonally stimulated apoptotic CD4+ T cells of the parabronchial lymph node from tamoxifen-treated is decreased compared to in control mice
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• the percentage of polyclonally stimulated proliferating CD4+ T cells of the parabronchial lymph node or spleen from tamoxifen-treated is increased compared to in control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• MigR1-MLL-AF9-transformed and tamoxifen-treated bone marrow cells exhibit impaired initiation and maintenance of leukemic transformation
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| N |
• tamoxifen-treated mice exhibit normal hematopoiesis, long-term hematopoietic stem cell maintenance, and stem and progenitor cell function
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• impaired cell cycle progression in tamoxifen-treated mouse embryonic cells with improper chromosome segregation
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• tamoxifen-treated mouse embryonic cells exhibit improper chromosome segregation
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• in tamoxifen-treated mouse embryonic cells stimulated with serum
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen treatment provokes infertility in females regardless of genotype
• after treatment is discontinued, control animals fully recover fertility, whereas mutant females remain infertile
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mouse embryonic fibroblasts exhibit diplo-chromosomes with unseparated arms unlike in control cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in the spleen of tamoxifen-treated mice
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• in tamoxifen-treated mice
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• tamoxifen-treated mice exhibit disturbed cell distribution with pronounced dysplasia and disrupted maturation in the erythroid, megakaryocytic and granulocytic lineages compared with control mice
• bone marrow from tamoxifen-treated mice exhibit reduced formation of colony forming units compared with control mice
• however, tamoxifen-treated mice exhibit normal numbers of hematopoietic stem cells
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• decreased granulocyte-macrophage progenitors and macrophage colony numbers from bone marrow of tamoxifen-treated mice
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• abnormal nuclear lobation and atypical mitosis in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• dysplastic granulocytes with nuclear hyposegmentation in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in the spleen of tamoxifen-treated mice
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• relative in tamoxifen-treated mice
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• impaired migration in hematopoietic stem and progenitor cells of tamoxifen-treated mice
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• increased chromosomal double-strand breaks and numerical and structural chromosomal aberrations 2 weeks after tamoxifen-treatment
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• anemic appearance of the bones in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• dysplastic granulocytes with nuclear hyposegmentation in tamoxifen-treated mice
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• in the spleen of tamoxifen-treated mice
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• relative in tamoxifen-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 N |
• tamoxifen-treated mice exhibit normal blood counts
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice survive 57 days unlike control mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• tamoxifen-treated mice develop T cell acute lymphoblastic leukemia unlike control mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• scruffy coat in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice survive 65 days compared with Pdk1tm1Dral Gt(ROSA)26Sortm9(cre/ESR1)Arte mice that survive 57
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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• in tamoxifen-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• B cells exhibit altered chromosome architecture genome wide in tamoxifen-treated mice
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• B cells in vitro stimulated with tamoxifen exhibit a defect in class-switch recombination
• tamoxifen-treated B cells show a reduction to class-switch recombination to IgG1
• tamoxifen-treated mice show an increase in microhomology-mediated DNA junctions in B cells
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• B cells exhibit altered chromosome architecture genome wide in tamoxifen-treated mice
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• B cells in vitro stimulated with tamoxifen exhibit a defect in class-switch recombination
• tamoxifen-treated B cells show a reduction to class-switch recombination to IgG1
• tamoxifen-treated mice show an increase in microhomology-mediated DNA junctions in B cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Microemboli and necrotic areas in Tnfaip3tm1Homy/Tnfaip3tm1Homy Gt(ROSA)26Sortm9(cre/ESR1)Arte/? liver
| N |
• no spontaneous development of abnormal phenotype
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• marked drop in hematopoietic cell after tamoxifen administration
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• die within several days of tamoxifen administration
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• microembolic and necrotic areas in the liver after tamoxifen administration
(J:212681)
• with white spots after tamoxifen administration
(J:212681)
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• massive apoptosis in major organs after tamoxifen administration
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• elevated levels of GM-CSF after tamoxifen administration
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• particularly elevated after tamoxifen administration
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• elevated after tamoxifen administration
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• particularly elevated after tamoxifen administration
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• particularly elevated TNF-alpha levels after tamoxifen administration
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• elevated levels of GM-CSF after tamoxifen administration
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• particularly elevated after tamoxifen administration
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• elevated after tamoxifen administration
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• particularly elevated after tamoxifen administration
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• particularly elevated TNF-alpha levels after tamoxifen administration
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• die within several days of tamoxifen administration
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• E11.5 neural precursor cells cultured for 9 days in the presence of S33Y beta-catenin and tamoxifen exhibit enhanced neuronal differentiation compared with similarly treated control Rnf2tm1Mvi cells
• E17.5 neural precursor cells cultured for 3 days in the presence of S33Y beta-catenin and tamoxifen exhibit enhanced neuronal differentiation compared with similarly treated control Rnf2tm1Mvi cells
• neuronal precursor cells treated with tamoxifen and subjected to growth factor deprivation at the late stage (12 days in culture) exhibit reduced astrocyte differentiation compared with similarly treated control Rnf2tm1Mvi cells
• at P2.5, tamoxifen-treated mice exhibit reduced astrocytic differentiation compared with similarly treated control Rnf2tm1Mvi cells
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• E11.5 neural precursor cells cultured for 9 days in the presence of S33Y beta-catenin and tamoxifen exhibit enhanced neuronal differentiation compared with similarly treated control Rnf2tm1Mvi cells
• E17.5 neural precursor cells cultured for 3 days in the presence of S33Y beta-catenin and tamoxifen exhibit enhanced neuronal differentiation compared with similarly treated control Rnf2tm1Mvi cells
• neuronal precursor cells treated with tamoxifen and subjected to growth factor deprivation at the late stage (12 days in culture) exhibit reduced astrocyte differentiation compared with similarly treated control Rnf2tm1Mvi cells
• at P2.5, tamoxifen-treated mice exhibit reduced astrocytic differentiation compared with similarly treated control Rnf2tm1Mvi cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen treated mice develop kindey cysts
• however, treatment with Genz-123346 inhibits cystogenesis
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• tamoxifen-treated mice exhibit progressive renal function decline over 4 to 5 weeks
• however, treament with Genz-123346 improves kidney fucntion
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• tamoxifen treated mice develop kindey cysts
• however, treatment with Genz-123346 inhibits cystogenesis
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| polycystic kidney disease 1 | DOID:0110858 |
OMIM:173900 |
J:162080 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following tamoxifen-treatment, mouse embryonic fibroblasts (MEFs) exhibit random migration in response to an HMGB1 gradient unlike wild-type cells
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• 180 minutes after exposure to HMGB1, tamoxifen-treated MEFs exhibit reduced migration velocity compared with wild-type mice
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• following tamoxifen-treatment, MEFs exhibit impaired chemotaxis in response to HMGB1 compared with wild-type cells that is not rescued by Nfkb2
• however, chemotaxis in response to PDGF is normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• a decrease in the CD71- Ter119+ population, an intermediate erythroid progenitor stage in the bone marrow
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• 50 days after tamoxifen induction with a subcutaneous pellet
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• 50 days after tamoxifen induction with a subcutaneous pellet
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• 50 days after tamoxifen induction with a subcutaneous pellet
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• almost entire structure is affected by 3 weeks following tamoxifen treatment
• instead of normal granulosa cells, cells with morphological characteristics of Sertoli cells (prominent basal lamina, tripartite nuclei, numerous veil-like cytoplasmic extensions pointing toward lumen) are observed 3 weeks following tamoxifen treatment; Leydig cell markers are also detected in mutant gonads
• one week after start of tamoxifen treatment, many granulosa cells start to transdifferentiate into Sertoli-like cells; unlike normal granulosa cells, these abnormal cells do not undergo apoptosis at end of a follicle life cycle and are still present after 6 months
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• 3 weeks following tamoxifen treatment, typical follicular structure of ovary resembles seminiferous tubules of testis
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• 8-week-old female mice treated for 5 days with tamoxifen and analysed 3 weeks later exhibit gonadal sex reversal
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• almost entire structure is affected by 3 weeks following tamoxifen treatment
• instead of normal granulosa cells, cells with morphological characteristics of Sertoli cells (prominent basal lamina, tripartite nuclei, numerous veil-like cytoplasmic extensions pointing toward lumen) are observed 3 weeks following tamoxifen treatment; Leydig cell markers are also detected in mutant gonads
• one week after start of tamoxifen treatment, many granulosa cells start to transdifferentiate into Sertoli-like cells; unlike normal granulosa cells, these abnormal cells do not undergo apoptosis at end of a follicle life cycle and are still present after 6 months
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• 3 weeks following tamoxifen treatment, typical follicular structure of ovary resembles seminiferous tubules of testis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following exposure to tamoxifen, neuronal differentiation in culture induced by FGF2 deprivation or S33Y beta-catenin expression is enhanced compared to in similarly treated control mice
• following exposure to tamoxifen, the reduction in Ngn1+ cells in the late neurogenic phase (E17.5) is suppressed compared to in similarly treated control mice
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• following exposure to tamoxifen, neuronal differentiation in culture induced by FGF2 deprivation or S33Y beta-catenin expression is enhanced compared to in similarly treated control mice
• following exposure to tamoxifen, the reduction in Ngn1+ cells in the late neurogenic phase (E17.5) is suppressed compared to in similarly treated control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increased under Th1-, Th17- and induced regulatory T cell-skewing conditions following tamoxifen-treatment
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• reduced under Th17-skewing conditions following tamoxifen-treatment
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• reduced regulatory T cell differentiation under induced regulatory T cell-skewing conditions following tamoxifen-treatment
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• increased under Th1-, Th17- and induced regulatory T cell-skewing conditions following tamoxifen-treatment
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• reduced under Th17-skewing conditions following tamoxifen-treatment
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• reduced regulatory T cell differentiation under induced regulatory T cell-skewing conditions following tamoxifen-treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• changes in leukocyte numbers are consistent with a chronic myelomonocytic leukemia (CMML)-like disease
• transplantation of bone marrow cells into lethally irradiated congenic wild-type mice followed by tamoxifen treatment also results in a CMML-like disease
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• seen in all mice 4 weeks after the last tamoxifen injection
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• at 4 weeks after the last tamoxifen injection peripheral blood shows cytological features consistent with myelodysplasia
• increase in the number of lineage-negative ScaI? c-Kit+ myeloid progenitor cells in the spleen and bone marrow as early as 2 weeks after the last tamoxifen treatment
• atypical immature cells with myelomonocytic features detected after tamoxifen treatment
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• expansion of the myeloid lineage in the spleen, lymph nodes and bone marrow at 4 weeks after the last tamoxifen injection
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• 4 weeks after the last tamoxifen injection
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• signs of erythroid dysplasia after tamoxifen treatment
• prominent basophilic stippling after tamoxifen treatment
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• at 4 weeks after the last tamoxifen injection peripheral blood shows cytological features consistent with ineffective erythropoiesis
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• after tamoxifen treatment
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• after tamoxifen treatment
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• bilobed granulocytes after tamoxifen treatment
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• hypersegmented and hyposegmented neutrophils after tamoxifen treatment
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• 4 weeks after the last tamoxifen injection
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• detected as early as 1 week after the last tamoxifen treatment
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• giant platelets detected after tamoxifen treatment
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• elevated total leukocyte numbers at 4 weeks after the last tamoxifen injection
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• 4 weeks after the last tamoxifen injection
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• in the spleen and bone marrow as early as 2 weeks after the last tamoxifen treatment
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• cells taken from tamoxifen treated mice fail to reconstitute the bone marrow of lethally irradiated congenic wild-type mice
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• cultured cells collected 1 month after the last tamoxifen treatment produce fewer colonies and replated cells do not produce well formed colonies
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• neutrophilic inflammation and infiltration of myeloblastic cells after tamoxifen treatment
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• seen in all mice 4 weeks after the last tamoxifen injection
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• at 4 weeks after the last tamoxifen injection peripheral blood shows cytological features consistent with myelodysplasia
• increase in the number of lineage-negative ScaI? c-Kit+ myeloid progenitor cells in the spleen and bone marrow as early as 2 weeks after the last tamoxifen treatment
• atypical immature cells with myelomonocytic features detected after tamoxifen treatment
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• expansion of the myeloid lineage in the spleen, lymph nodes and bone marrow at 4 weeks after the last tamoxifen injection
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• bilobed granulocytes after tamoxifen treatment
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• hypersegmented and hyposegmented neutrophils after tamoxifen treatment
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• 4 weeks after the last tamoxifen injection
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• elevated total leukocyte numbers at 4 weeks after the last tamoxifen injection
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• 4 weeks after the last tamoxifen injection
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• microthrombi in the heart after tamoxifen treatment
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• multifocal necrosis after tamoxifen treatment
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• multifocal necrosis after tamoxifen treatment
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• neutrophilic inflammation and infiltration of myeloblastic cells after tamoxifen treatment
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• seen in all mice 4 weeks after the last tamoxifen injection
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| myelodysplastic syndrome | DOID:0050908 |
OMIM:614286 |
J:187380 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen treatment induces mild but progressive hematological defects
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|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
N |
• tamoxifen-treated mice exhibit functionally active NK T cells
|
|
|
• following exposure to NP-KLH with alpha-GalCer, germinal center B cells from tamoxifen-treated mice fail to exhibit an increase in numbers unlike in wild-type mice
|
|
|
• tamoxifen-treated mice exhibit reduced late primary antibody response on transfer of OT-II CD4+ T cells compared with wild-type
|
|
|
• following immunization with NP-KLH and alpha-GalCer, tamoxifen-treated mice exhibit reduced NP-specific IgG that is more severe than in Sh2d1atm1Cpt homozygotes
|
|
|
• following exposure to NP-KLH with alpha-GalCer, tamoxifen treated mice produce less anti-NP-IgM compared with wild-type mice
|
|
|
• following exposure to NP-KLH with alpha-GalCer, germinal center B cells from tamoxifen-treated mice fail to exhibit an increase in numbers unlike in wild-type mice
|
|
|
• following immunization with NP-KLH and alpha-GalCer, tamoxifen-treated mice exhibit reduced NP-specific IgG that is more severe than in Sh2d1atm1Cpt homozygotes
|
|
|
• following exposure to NP-KLH with alpha-GalCer, tamoxifen treated mice produce less anti-NP-IgM compared with wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
N |
• tamoxifen-treated mice exhibit functionally active NK T cells
|
|
|
• following exposure to NP-KLH with alpha-GalCer, germinal center B cells from tamoxifen-treated mice fail to exhibit an increase in numbers unlike in wild-type mice
|
|
|
• tamoxifen-treated mice exhibit reduced late primary antibody response on transfer of OT-II CD4+ T cells compared with wild-type
|
|
|
• following immunization with NP-KLH and alpha-GalCer, tamoxifen-treated mice exhibit reduced NP-specific IgG that is more severe than in Sh2d1atm1Cpt homozygotes
|
|
|
• following exposure to NP-KLH with alpha-GalCer, tamoxifen treated mice produce less anti-NP-IgM compared with wild-type mice
|
|
|
• following exposure to NP-KLH with alpha-GalCer, germinal center B cells from tamoxifen-treated mice fail to exhibit an increase in numbers unlike in wild-type mice
|
|
|
• following immunization with NP-KLH and alpha-GalCer, tamoxifen-treated mice exhibit reduced NP-specific IgG that is more severe than in Sh2d1atm1Cpt homozygotes
|
|
|
• following exposure to NP-KLH with alpha-GalCer, tamoxifen treated mice produce less anti-NP-IgM compared with wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• after 1 week, tamoxifen-treated mice exhibit decreased regulatory T cell number compared with control mice that is thymus independent and associated with reduced cell proliferation
|
|
• regulatory T cells from tamoxifen-treated mice exhibit reduced suppression function and a 2-fold reduction in proliferation compared with wild-type cells
|
|
• after 1 week, tamoxifen-treated mice exhibit decreased regulatory T cell number compared with control mice that is thymus independent and associated with reduced cell proliferation
|
|
• regulatory T cells from tamoxifen-treated mice exhibit reduced suppression function and a 2-fold reduction in proliferation compared with wild-type cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
• following tamoxifen treatment at E10.5 expression analysis indicates a delay in germ cell differentiation at E14.5 that is no longer detectable by E16.5
|
|
|
• following tamoxifen treatment at E10.5 expression analysis indicates a delay in germ cell differentiation at E14.5 that is no longer detectable by E16.5
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• leukemia-initiating cells plated in methylcellulose cultures in the presence of tamoxifen exhibit decreased blast colony number and loss of blast colony formation due to increased apoptosis compared with control cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Testicular degeneration in Nabp2tm1.1Kkha/Nabp2tm1.1Kkha Gt(ROSA)26Sortm9(cre/ESR1)Arte/Gt(ROSA)26Sor+ mice
|
• in tamoxifen-treated mice
|
|
N |
• tamoxifen-treated female mice exhibit normal fertility
|
|
|
• premature sloughing from the supporting Sertoli cells in tamoxifen-treated mice
|
|
|
• due to apoptosis and premature sloughing from the supporting Sertoli cells in tamoxifen-treated mice
• decreased elongated spermatids
|
|
|
• in tamoxifen-treated mice
|
|
|
• in tamoxifen-treated mice
|
|
|
• in tamoxifen-treated mice
|
|
|
• bilateral degeneration; tubules showed degenerate, sometimes vacuolated, or
necrotic spermatogenic cells, the latter with pyknotic nuclei and
hypereosinophilic cytoplasm, or apoptotic body formation in tamoxifen-treated mice
|
|
|
• from tamoxifen-treated mice with longer intervals between litters
|
|
|
• in tamoxifen-treated mice
|
|
• splenic and metastatic B lymphomas, T cell lymphoma in thymus, hepatocellular carcinoma and B or T lymphoblastic leukemia in 11 of 35 of tamoxifen-treated mice
|
|
• in thymus of some tamoxifen-treated mice
|
|
• in some tamoxifen-treated mice
|
|
• B or T lymphoblastic leukemia in some tamoxifen-treated mice
|
|
• splenic and metastatic B lymphomas in some tamoxifen-treated mice
|
|
|
• premature sloughing from the supporting Sertoli cells in tamoxifen-treated mice
|
|
|
• due to apoptosis and premature sloughing from the supporting Sertoli cells in tamoxifen-treated mice
• decreased elongated spermatids
|
|
• tamoxifen-treated mice exposed to ionizing radiation exhibit distended crypt lumina lined by attenuated enterocytes, desquamated necrotic cellular debris and a small increase of cells near deep crypts with apoptotic bodies
• however, blood counts are normal in irradiated tamoxifen-treated mice
|
|
• in irradiated tamoxifen-treated mice
|
|
|
• in tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
• at E14.5 and E18.5
|
|
• tamoxifen-treated mice exposed to ionizing radiation exhibit distended crypt lumina lined by attenuated enterocytes, desquamated necrotic cellular debris and a small increase of cells near deep crypts with apoptotic bodies
|
|
• in irradiated tamoxifen-treated mice
|
|
• in thymus of some tamoxifen-treated mice
|
|
• in irradiated tamoxifen-treated mice
|
|
• in thymus of some tamoxifen-treated mice
|
|
|
• in tamoxifen-treated mice
|
|
|
• in tamoxifen-treated mice
|
|
|
• bilateral degeneration; tubules showed degenerate, sometimes vacuolated, or
necrotic spermatogenic cells, the latter with pyknotic nuclei and
hypereosinophilic cytoplasm, or apoptotic body formation in tamoxifen-treated mice
|
| N |
• blood counts are normal in irradiated tamoxifen-treated mice
|
|
• in irradiated tamoxifen-treated mice
|
|
• in thymus of some tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
• in some tamoxifen-treated mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 48 hours after tamoxifen treatment, mice exhibit slight lymphoid necrosis in the cortex of the thymus compared with control mice
• 72 hours after tamoxifen treatment, mice exhibit lymphoid necrosis in the thymus, predominantly in the periarterial lymphoid sheaths, with lymphoid depletion compared with control mice
|
|
• 48 and 72 hours after tamoxifen treatment
|
|
• slight in tamoxifen treated mice at 48 hours of both erythroid and myeloid cells
• further decrease after 72 hours in tamoxifen-treated mice
|
|
• 72 hours after tamoxifen treatment
|
|
• 72 hours after tamoxifen treatment
|
|
• 72 hours after tamoxifen treatment
|
|
• 72 hours after tamoxifen treatment
|
|
• 48 and 72, but not 24, hours after tamoxifen treatment
|
|
• 48 and 72, but not 24, hours after tamoxifen treatment
|
|
• 72 hours after tamoxifen treatment, mice exhibit lymphoid necrosis in the spleen, predominantly in the periarterial lymphoid sheaths, with lymphoid depletion compared with control mice
|
|
• 72 hours after tamoxifen treatment
|
|
• decreased at 72 hours in tamoxifen-treated mice
|
|
• 72 hours after tamoxifen treatment, mice exhibit atrophy of the small and large intestine mucosa with sloughing of mucosal epithelial cells and/or necrotic decries in the crypts compared with control mice
|
|
• 24 and 48 hours after tamoxifen treatment, mice exhibit several single cell necroses in the epithelia of small and large intestine crypts unlike control mice
|
|
• 24 and 48 hours after tamoxifen treatment, mice exhibit several single cell necroses in the epithelia of small and large intestine crypts unlike control mice
|
|
• 48 hours after tamoxifen treatment, mice exhibit increased single cell necroses at the base of villi in the small intestine compared with control mice
|
|
• 72 hours after tamoxifen treatment, mice exhibit atrophy of the stomach mucosa predominantly in the pyloric region and characterized by exfoliation of necrotic epithelial cells into the gastric lumen and thinning of the gastric epithelial cells, especially the gastric gland epithelium, compared with control mice
|
|
• in tamoxifen-treated mice
|
|
• increased total protein in tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
• total and albumin to globulin ratio in tamoxifen-treated mice
|
|
• 24 and 48 hours after tamoxifen treatment, mice exhibit several single cell necroses in the epithelia of small and large intestine crypts unlike control mice
• 48 hours after tamoxifen treatment, mice exhibit increased single cell necroses at the base of villi in the small intestine compared with control mice
• 48 hours after tamoxifen treatment, mice exhibit slight lymphoid necrosis in the cortex of the thymus compared with wild-type mice
• 72 hours after tamoxifen treatment, mice exhibit lymphoid necrosis in the thymus and spleen, predominantly in the periarterial lymphoid sheaths, with lymphoid depletion compared with control mice
|
|
• slight at 72 hours in tamoxifen-treated mice
|
|
• decreased at 72 hours in tamoxifen-treated mice
|
|
• 24 and 48 hours after tamoxifen treatment, mice exhibit several single cell necroses in the epithelia of small and large intestine crypts unlike control mice
|
|
• 24 and 48 hours after tamoxifen treatment, mice exhibit several single cell necroses in the epithelia of small and large intestine crypts unlike control mice
|
|
• increased adrenal gland weight at 72 hours after tamoxifen treatment
|
|
• 48 hours after tamoxifen treatment, mice exhibit slight lymphoid necrosis in the cortex of the thymus compared with control mice
• 72 hours after tamoxifen treatment, mice exhibit lymphoid necrosis in the thymus, predominantly in the periarterial lymphoid sheaths, with lymphoid depletion compared with control mice
|
|
• 48 and 72 hours after tamoxifen treatment
|
|
• slight at 72 hours in tamoxifen-treated mice
|
|
• 48 hours after tamoxifen treatment, mice exhibit slight lymphoid necrosis in the cortex of the thymus compared with control mice
• 72 hours after tamoxifen treatment, mice exhibit lymphoid necrosis in the thymus, predominantly in the periarterial lymphoid sheaths, with lymphoid depletion compared with control mice
|
|
• 48 and 72 hours after tamoxifen treatment
|
|
• 72 hours after tamoxifen treatment
|
|
• 48 and 72, but not 24, hours after tamoxifen treatment
|
|
• 72 hours after tamoxifen treatment, mice exhibit lymphoid necrosis in the spleen, predominantly in the periarterial lymphoid sheaths, with lymphoid depletion compared with control mice
|
|
• 72 hours after tamoxifen treatment
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• reduction in the number of mature resting plasma cells in the bone marrow following immunization with TNP-KLH and treatment with tamoxifen
|
|
• the number of P3-plasma cells in the blood in elevated in TNP-KLH immunized and boosted mice treated with tamoxifen
|
|
• the number of P1-plasmablasts is diminished in the spleen in TNP-KLH immunized and boosted mice treated with tamoxifen
|
|
• reduction in EdU+ mature P3-plasma cells in the bone marrow of TNP-KLH immunized and tamoxifen treated mice indicating reduced mature plasma turnover
• however, the EdU+ P2-plasma cell subset is unchanged
|
|
• reduction in the number of mature resting plasma cells in the bone marrow following immunization with TNP-KLH and treatment with tamoxifen
|
|
• the number of P3-plasma cells in the blood in elevated in TNP-KLH immunized and boosted mice treated with tamoxifen
|
|
• the number of P1-plasmablasts is diminished in the spleen in TNP-KLH immunized and boosted mice treated with tamoxifen
|
|
• reduction in EdU+ mature P3-plasma cells in the bone marrow of TNP-KLH immunized and tamoxifen treated mice indicating reduced mature plasma turnover
• however, the EdU+ P2-plasma cell subset is unchanged
|
|
• mice immunized and boosted with TNP-KLH and treated with tamoxifen exhibit a reduction in the CD138/Taci+ plasmablast/plasma cell population, notably the CD19-negative mature resting P3-plasma cells in the spleen and bone marrow
• mice immunized and boosted with TNP-KLH and treated with tamoxifen show a decrease in total number of antibody secreting cells in the bone marrow
• however, the numbers of NTP-specific antibody secreting in the spleen and bone marrow remain unchanged after tamoxifen treatment
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in tamoxifen-treated mice
|
|
• beyond the pachytene stage in tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
• one third normal in tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
• beyond the pachytene stage in tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
• one third normal in tamoxifen-treated mice
|
|
• in tamoxifen-treated mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• reduced in CD19+ B cells isolated from tamoxifen-treated mice and treated with IL4 and LPS, LPS, or IL4 and alphaCD40
|
|
• in CD19+ B cells isolated from tamoxifen-treated mice and treated with IL4 and LPS, LPS, or IL4 and alphaCD40
|
|
• reduced in CD19+ B cells isolated from tamoxifen-treated mice and treated with IL4 and LPS, LPS, or IL4 and alphaCD40
|
|
• in CD19+ B cells isolated from tamoxifen-treated mice and treated with IL4 and LPS, LPS, or IL4 and alphaCD40
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• neural progenitor cells treated with tamoxifen exhibit increased binucleated and pyknotic cells compared with controls
• slightly increase in the number of binucleated mouse embryonic fibroblasts treated with tamoxifen
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• hematopoietic cells from tamoxifen-treated mice are more sensitive to gamma-irradiation compared with control cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• following tamoxifen treatment
|
|
• tamoxifen treatment at E7.5 results in axial turning defects in most mice at E9.5
|
|
• tamoxifen treatment at E6.5 reproduces the gross phenotypes seen in germline null mice
|
|
• loss of branchial arches following tamoxifen treatment
|
|
• decrease in cephalic mesoderm at E10 in embryos treated with tamoxifen at E8.0
|
|
• tamoxifen treatment at E6.5 results in collapse of the mesenchyme
|
|
• vascular disintegration following tamoxifen treatment
|
|
• at E10 in embryos treated with tamoxifen at E8.0
|
|
• in MEFs tamoxifen treatment results in an accumulation of cells in G1/G0 and loss of S-phase and mitotic cells
|
|
• in pharyngeal mesodermal cells at E10, 48h past tamoxifen treatment
• however mitotic indices in branchial arch, neural tube, and heart cells are similar to controls
|
|
• following tamoxifen treatment
|
|
• reduced MEF cell growth following tamoxifen treatment
• however, tamoxifen treatment of embryonic stem cells does not alter cell growth
|
|
• loss of branchial arches following tamoxifen treatment
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• within days of tamoxifen-induction
|
|
• following tamoxifen-induction, mucosal epithelial cells of the mucosae of the stomach and the small and large intestines exhibit widespread degeneration and necrosis compared with control mice
|
|
• distended and filled with yellowish clear fluid following tamoxifen-induction
|
|
• following tamoxifen-induction, mice exhibit mucosal epithelial degeneration of cecal mucosa compared with control mice
|
|
• following tamoxifen-induction, mice exhibit mucosal epithelial degeneration of duodenal mucosa compared with control mice
|
|
• following tamoxifen-induction, mice exhibit ulceration of nonglandular mucosa and parietal cell degeneration of glandular mucosa compared with control mice
|
|
• parietal cell degeneration of glandular mucosa following tamoxifen-induction
|
|
• distended and filled with food following tamoxifen-induction
|
|
• parietal cell degeneration of glandular mucosa following tamoxifen-induction
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
• 12 days following tamoxifen-treatment in male mice
• however, female mice remain normal
|
|
|
• following tamoxifen-treatment, male mice exhibit similar observations as in homozygous conditional knock-ins but with lower severity
|
|
|
• following tamoxifen-treatment in male mice
• however, female mice remain normal
|
|
|
• following tamoxifen-treatment in male mice
• however, female mice remain normal
|
|
|
• following tamoxifen-treatment, one female mouse exhibited a black focal mild discoloration of the spleen
|
|
|
• poor coat condition following tamoxifen-treatment in male mice
• however, female mice remain normal
|
|
|
• following tamoxifen-treatment, one female mouse exhibited a black focal mild discoloration of the spleen
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• within 10 to 11 days of tamoxifen-induction
|
|
• following tamoxifen-induction, mice exhibit widespread mucosal epithelial degeneration more so in the small and large intestines and less in the stomach compared with control mice
• however, mice do not exhibit a distended intestine morphology
|
|
• focal atypical hyperplasia of mucosal crypts with small clusters of enlarged atypical crypts lined by tall dysplastic basophilic epithelial cells in the small intestine following tamoxifen-induction
|
|
• following tamoxifen-induction, mice exhibit swollen and basophilic surface epithelial cells in the large intestine compared with control mice
|
|
• loss of mucosal crypts in some areas of the large intestine following tamoxifen-induction
|
|
• following tamoxifen-induction, mice exhibit swollen villous epithelial cells with excessive vacuoles in the small intestine compared with control mice
|
|
• following tamoxifen-induction, mice exhibit loose or discolored intestine content
|
|
• thin following tamoxifen-treatment
|
|
• in moribund mice following tamoxifen-induction
|
|
• following tamoxifen-treatment
|
|
• poor coat condition following tamoxifen-treatment
|
|
• loss of mucosal crypts in some areas of the large intestine following tamoxifen-induction
|
|
• focal atypical hyperplasia of mucosal crypts with small clusters of enlarged atypical crypts lined by tall dysplastic basophilic epithelial cells in the small intestine following tamoxifen-induction
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice treated with tamoxifen exhibit degeneration of intestinal crypts
|
|
• mice treated with tamoxifen exhibit villous blunting
|
|
• mice treated with tamoxifen exhibit villous fusion
|
|
• mice treated with tamoxifen exhibit segmental, submucosal edema in the large intestine
|
|
• mice treated with tamoxifen exhibit increased apoptosis in the small intestine
|
|
• mice treated with tamoxifen exhibit mild enteritis
|
|
• mice treated with tamoxifen exhibit degeneration of intestinal crypts
|
|
• mice treated with tamoxifen show thymic atrophy
|
|
• mice treated with tamoxifen lose between 13 and 28% of their body weight after 6 to 7 days
|
|
• mice treated with tamoxifen show thymic atrophy
|
|
• mice treated with tamoxifen exhibit pyknotic and karyorrhectic lymphocytes in secondary lymphoid organs
|
|
• mice treated with tamoxifen exhibit segmental, submucosal edema in the large intestine
|
|
• mice treated with tamoxifen exhibit mild enteritis
|
|
• mice treated with tamoxifen show thymic atrophy
|
|
• mice treated with tamoxifen exhibit pyknotic and karyorrhectic lymphocytes in secondary lymphoid organs
|
| N |
• mice treated with tamoxifen do not show signs of morbidity after 5 days
|
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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