Analysis Tools
mortality/aging
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• homozygous embryos die at midgestation similar to Krastm1Tyi
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Allele Symbol Allele Name Allele ID |
Krastm1Bbd targeted mutation 1, Mariano Barbacid MGI:3582830 |
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| Summary |
31 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• homozygous embryos die at midgestation similar to Krastm1Tyi
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 50% survival at 40 weeks of age following intratracheal instillation of Ad-Cre
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• following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre), 50% of mice die by 40 weeks
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre)
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre)
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| lung cancer | DOID:1324 |
OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210 |
J:172200 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• primary mouse embryonic fibroblasts exposed to 4OHT for 5 days to activate cre/ERT2 recombinase exhibit decreased proliferation that is similar to that in single Kras mutants without further additive effects
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre), mice show 50% survival at 63 weeks compared to 38 weeks in single Kras heterozygous controls, indicating an 83% increase in survival
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• tumor burden is reduced compared to single Kras heterozygotes; tumors that are found express Raf1
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• primary mouse embryonic fibroblasts exposed to 4OHT for 5 days to activate cre/ERT2 recombinase exhibit decreased proliferation compared to single Kras heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 50% mortality by 6 months of age
• 100% mortality by 1 year of age
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• all mice develop moderately to poorly differentiated pancreatic ductal adenocarcinomas, peritoneal explants, and perineural extensions
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• metastases develop affecting liver, diaphragm, lungs, lymph nodes, and spleen
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• all mice develop moderately to poorly differentiated pancreatic ductal adenocarcinomas, peritoneal explants, and perineural extensions
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:119988 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre), mice show 50% survival at 41.5 weeks compared to 40 weeks in single Kras heterozygous controls, indicating similar survival
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit decreased proliferation and early senescence of tumor cells compared with tamoxifen and infected with GFP-expressing adenovirus
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• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit reduced lesions compared to in mice treated with tamoxifen and infected with GFP-expressing adenovirus
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• in tamoxifen-treated mice as in similarly treated Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit early senescence of tumor cells compared with tamoxifen and infected with GFP-expressing adenovirus
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• tamoxifen-treated mice infected with a flp-expressing adenovirus exhibit decreased proliferation of tumor cells compared with tamoxifen and infected with GFP-expressing adenovirus
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the mean lifespan of mice treated tamoxifen is 34-42 weeks
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• in mice treated with tamoxifen at weaning
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• in mice treated with tamoxifen at weaning
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• in mice treated with tamoxifen at weaning
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| lung cancer | DOID:1324 |
OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210 |
J:161780 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 50% of tamoxifen-treated mice survive at 40 weeks
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• in mice treated with tamoxifen at weaning
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• in mice treated with tamoxifen at weaning
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• in mice treated with tamoxifen at weaning
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| lung cancer | DOID:1324 |
OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210 |
J:161780 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice treated tamoxifen at weaning exhibit an increase in lifespan of 8 weeks (42 weeks) compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd littermates (34 weeks)
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• tamoxifen-treated mice exhibit reduced tumor burden compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 50% survival at 34.9 weeks versus 31.2 weeks in single Kras mutants following intratracheal instillation of Ad-Cre, indicating a 16% increase in survival
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• primary mouse embryonic fibroblasts exposed to 4OHT for 5 days to activate cre/ERT2 recombinase exhibit decreased proliferation compared to single Kras heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre), mutants show 50% survival at 44 weeks compared to 37.5 weeks in single Kras heterozygous controls, indicating a slight 22% increase in survival
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice exhibit reduced tumor burden and tumor grade compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice exhibit an increase in lifespan compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd littermates
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• tamoxifen-treated mice exhibit reduced tumor burden and tumor grade compared with similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 50% survival for tamoxifen-treated mice is 25 weeks compared with 42 weeks for similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd littermates
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• lung tumors in tamoxifen-treated mice are more aggressive than in similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
• however, treatment with the Cdk4 inhibitor PD0332991 reduces tumor formation
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• in mice treated with tamoxifen
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• proliferation of lung cells in tamoxifen-treated mice exhibit 8- to 10-fold greater proliferation than in Cdk4tm2.1Bbd/Cdk4tm2.1Bbd Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• lung tumors in tamoxifen-treated mice are more aggressive than in similarly treated Krastm1Bbd/Kras+ Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
• however, treatment with the Cdk4 inhibitor PD0332991 reduces tumor formation
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• in mice treated with tamoxifen
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| lung cancer | DOID:1324 |
OMIM:211980 OMIM:608935 OMIM:612571 OMIM:612593 OMIM:614210 |
J:161780 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• lung cells in tamoxifen-treated mice exhibit 8- to 10-fold reduction in proliferation and early senescence compared to in similarly treated Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• tamoxifen-treated mice exhibit adenocarcinomas that are not as severe as in Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• proliferation of lung cells in tamoxifen-treated mice exhibit 8- to 10-fold less proliferation than in similarly treated Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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• tamoxifen-treated mice exhibit increased cell replicative senescence in the lungs compared to in similarly treated Krastm1Bbd/Krastm2Bbd Polr2atm1(cre/ERT2)Bbd/Polr2atm1(cre/ERT2)Bbd mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• latency to develop lung adenomas is significantly shorter compared to double mutants wild-type for Cdk4; however development of tumors characteristic of Cdk4tm1.1Bbd mutant mice is not accelerated
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• histiocytic sarcoma and other sarcomas are seen
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• anal papillomas are seen
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• focal metaplasia in the pancreatic ducts consisting of tall columnar cells with abundant apical mucin resembling gastric surface epithelial cells
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• focal metaplasia in the pancreatic ducts consisting of tall columnar cells with abundant apical mucin resembling gastric surface epithelial cells
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• latency to develop lung adenomas is significantly shorter compared to double mutants wild-type for Cdk4; however development of tumors characteristic of Cdk4tm1.1Bbd mutant mice is not accelerated
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• double mutants develop breathing difficulties after 7 - 8 months of age
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• frequent embryonic lethality; however, a significant number of double mutants survive
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• a large spectrum of multifocal lesions are seen in the lung including; small patches of bronchiolo-alveolar hyperplasias to large bronchiolo-alveolar adenomas that compress adjacent lung structures and appear to derive from type II pneumocytes
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• large bronchiolo-alveolar adenocarcinomas that compress adjacent lung structures and appear to derive from type II pneumocytes
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• histiocytic sarcoma and other sarcomas seen in 2 out of 20 and 3 out of 20 double mutants, respectively
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• anal papillomas seen in 3 out of 20 double mutants
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• MEFs expressing the oncogenic protein do not undergo proliferative senescence and proliferate continuously as immortal cells
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• a large spectrum of multifocal lesions are seen in the lung including; small patches of bronchiolo-alveolar hyperplasias to large bronchiolo-alveolar adenomas that compress adjacent lung structures and appear to derive from type II pneumocytes
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• large bronchiolo-alveolar adenocarcinomas that compress adjacent lung structures and appear to derive from type II pneumocytes
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• double mutants develop breathing difficulties after 7 - 8 months of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice live up to 40 weeks
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• by 24 weeks, mice develop tumors in the thymus
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• by 24 weeks, mice develop tumors in lungs
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• at 4 weeks after 5-hydroxytamoxifen treatment, a few small adenomas are observed in some animals
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• by 24 weeks, mice develop tumors in lungs
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• at 4 weeks after 5-hydroxytamoxifen treatment, a few small adenomas are observed in some animals
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die before week 32 due to increased lung cancer progression
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• 20 weeks after treatment, lungs are increased in size
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• 2 weeks after 5-hydroxytamoxifen treatment, small tumors are found in the lungs
• 20 weeks after treatment, lungs are oversized with 2-3 times as many tumors, many often >2mm in diameter, while lungs of Kras, Mapk14 heterozygotes have normal lungs with fewer, smaller tumors; tumors in Mapk14 homozygotes are more poorly differentiated and have higher mitotic indices
• at 26 weeks, total tumor number is slightly higher than in controls with much higher numbers of tumors larger than 2 mm in diameter and a higher ratio of lung mass to total mass
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• tumors are detected 2 weeks after 5-hydroxytamoxifen treatment and after 4 weeks, clear signs of adenomas are present in most lungs compared to only a few small adenomas in lungs of treated Kras, Mapk14tm2Nbr/+ control mice
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• adenocarcinomas are detected at 15 weeks but not in controls
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• lung differentiation is abnormal with increased SP-C-positive cells
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• mice also have tumors in the thymus and organs such as kidney and liver by 24 weeks after treatment whereas controls only have tumors in lungs and thymus
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• 2 weeks after 5-hydroxytamoxifen treatment, small tumors are found in the lungs
• 20 weeks after treatment, lungs are oversized with 2-3 times as many tumors, many often >2mm in diameter, while lungs of Kras, Mapk14 heterozygotes have normal lungs with fewer, smaller tumors; tumors in Mapk14 homozygotes are more poorly differentiated and have higher mitotic indices
• at 26 weeks, total tumor number is slightly higher than in controls with much higher numbers of tumors larger than 2 mm in diameter and a higher ratio of lung mass to total mass
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• tumors are detected 2 weeks after 5-hydroxytamoxifen treatment and after 4 weeks, clear signs of adenomas are present in most lungs compared to only a few small adenomas in lungs of treated Kras, Mapk14tm2Nbr/+ control mice
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• adenocarcinomas are detected at 15 weeks but not in controls
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• 20 weeks after treatment, lungs are increased in size
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after treatment with 4-hydroxy-tamoxifen for 24 weeks multiple lung adenomas develop by 7 months of age; however no difference in the latency, number, or size of tumors was seen compared to double mutants wild-type for Fntb
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• after treatment with 4-hydroxy-tamoxifen for 24 weeks multiple lung adenocarcinomas develop by 7 months of age; however no difference in the latency, number, or size of tumors was seen compared to double mutants wild-type for Fntb
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• after treatment with 4-hydroxy-tamoxifen for 24 weeks multiple lung adenomas develop by 7 months of age; however no difference in the latency, number, or size of tumors was seen compared to double mutants wild-type for Fntb
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• after treatment with 4-hydroxy-tamoxifen for 24 weeks multiple lung adenocarcinomas develop by 7 months of age; however no difference in the latency, number, or size of tumors was seen compared to double mutants wild-type for Fntb
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die prior to day 300
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• mice exhibit keratinized squamous metaplasia in the bulbourethral gland unlike wild-type mice
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• all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice
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• all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice
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• mice exhibit keratinized squamous metaplasia in the urethral gland unlike wild-type mice
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• mice exhibit keratinized squamous metaplasia in the bulbourethral gland unlike wild-type mice
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• mice exhibit keratinized squamous metaplasia in the urethral gland unlike wild-type mice
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• all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at 200 days, 100% of mice exhibit atypical hyperplasia unlike wild-type mice
• at 500 days, 93% of mice exhibit atypical hyperplasia unlike wild-type mice
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• in 7% of mice at 500 days
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• at 200 days, 67% of mice develop prostate intraepithelial neoplasia that display foci of small solid and cribiform intraluminal proliferation of atypical cells and nuclear atypia unlike wild-type mice
• at 500 days, 60% of mice exhibit prostate intraepithelial neoplasia unlike in wild-type mice
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• in 7% of mice at 500 days
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• at 200 days, 67% of mice develop prostate intraepithelial neoplasia that display foci of small solid and cribiform intraluminal proliferation of atypical cells and nuclear atypia unlike wild-type mice
• at 500 days, 60% of mice exhibit prostate intraepithelial neoplasia unlike in wild-type mice
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• at 200 days, 100% of mice exhibit atypical hyperplasia unlike wild-type mice
• at 500 days, 93% of mice exhibit atypical hyperplasia unlike wild-type mice
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• in 7% of mice at 500 days
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• at 200 days, 67% of mice develop prostate intraepithelial neoplasia that display foci of small solid and cribiform intraluminal proliferation of atypical cells and nuclear atypia unlike wild-type mice
• at 500 days, 60% of mice exhibit prostate intraepithelial neoplasia unlike in wild-type mice
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| prostate cancer | DOID:10283 |
OMIM:176807 OMIM:300147 OMIM:300704 OMIM:601518 OMIM:602759 OMIM:608656 OMIM:608658 OMIM:609299 OMIM:609558 OMIM:610321 OMIM:610997 OMIM:611100 OMIM:611868 OMIM:611928 OMIM:611955 OMIM:611958 OMIM:611959 |
J:143034 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• double mutants treated with 4-hydroxy-tamoxifen at 10 days of age develop breathing difficulties after 7 - 8 months of age
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• after treatment with 4-hydroxy-tamoxifen at 10 days of age, a large spectrum of multifocal lesions are seen in the lung at 7-8 months of age including; small patches of bronchiolo-alveolar hyperplasias to large bronchiolo-alveolar adenomas that compress adjacent lung structures and appear to derive from type II pneumocytes
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• after treatment with 4-hydroxy-tamoxifen at 10 days of age, at 7-8 months of age large bronchiolo-alveolar adenocarcinomas that compress adjacent lung structures and appear to derive from type II pneumocytes are seen
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• MEFs expressing the oncogenic protein do not undergo proliferative senescence and proliferate continuously as immortal cells
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• after treatment with 4-hydroxy-tamoxifen at 10 days of age, a large spectrum of multifocal lesions are seen in the lung at 7-8 months of age including; small patches of bronchiolo-alveolar hyperplasias to large bronchiolo-alveolar adenomas that compress adjacent lung structures and appear to derive from type II pneumocytes
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• after treatment with 4-hydroxy-tamoxifen at 10 days of age, at 7-8 months of age large bronchiolo-alveolar adenocarcinomas that compress adjacent lung structures and appear to derive from type II pneumocytes are seen
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• double mutants treated with 4-hydroxy-tamoxifen at 10 days of age develop breathing difficulties after 7 - 8 months of age
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• hyperplastic Harderian gland seen in double mutants treated with 4-hydroxy-tamoxifen at 10 days of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• properties are similar to those in human patients
• focal morphological lesions develop in acinar and centroacinar cells at 1-3 months
• acinar to ductal metaplasias develop
• some mice develop ductal adenocarcinomas by 12 months
• sometimes areas of non malignant hyperplasia develop
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• latency is increased if gene expression is delayed by maintaining exposure to doxycycline until 10 days of age
• if doxycycline exposure continues to 2 months of age, no pancreatic abnormalities develop
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• focal morphological lesions develop in acinar and centroacinar cells at 1-3 months
• acinar to ductal metaplasias develop
• some mice develop ductal adenocarcinomas by 12 months
• properties are similar to those in human patients
• sometimes areas of non malignant hyperplasia develop
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:119988 | |
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|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre), mutants show 50% survival at 63 weeks versus 48 weeks in single Kras mutants, a 40% increase in survival
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• 6 months following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre), only a few tumors are observed; tumors that are found express normal levels of Mapk1
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 50% survival at 46.3 weeks of age is seen following intratracheal instillation of Ad-Cre, a 20% increase in survival compared to single Kras mutants
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
|
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• Ad-Cre treated mice show 50% survival at 57 weeks of age compared to 33 weeks of age in single Kras heterozygous controls, indicating an almost 100% increase in survival
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• 6 months following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre), only a few tumors are observed; tumors that are present carry unrecombined Map2k1 alleles and express normal levels of Map2k1
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• Ad-Cre treated mutants show 50% survival at 52 weeks compared to 45 weeks in single Kras heterozygous controls, indicating a slight 19% increase in survival
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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• mice develop non-small cell lung carcinoma following intratracheal instillation of adenovirus expressing Cre-recombinase (Ad-Cre); tumor burden in similar to that seen in single Kras heterozygotes
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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 04/16/2024 MGI 6.23 |
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