Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppm1dtm1Lad mutation
(1 available);
any
Ppm1d mutation
(28 available)
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cellular
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• pancreatic islet proliferation is decreased in 4-6 month old mice, however, the phenotype is reversed in double mutant Ppm1dtm1Lad Mapk14tm1.1Dvb mice
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endocrine/exocrine glands
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• pancreatic islet proliferation is decreased in 4-6 month old mice, however, the phenotype is reversed in double mutant Ppm1dtm1Lad Mapk14tm1.1Dvb mice
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homeostasis/metabolism
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppm1dtm1Lad mutation
(1 available);
any
Ppm1d mutation
(28 available)
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mortality/aging
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• only 3 of 20 males survived to 2 years of age
• majority of female null littermates survived to this point, having a similar survival rate as wild-type controls
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• fewer than expected number of homozygous mutant pups at birth
• fewer male pups than female, indicating possible selection against male embryos during gestation
• analysis of midgestation embryos failed to show any obvious developmental abnormalities in null mice, authors suggest this may be the result of a portion of the males succumbing to early embryonic defects
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cellular
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• reduced numbers produced over time, authors suggest as a result of inability to maintain spermatogenesis
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• stimulation with LPS resulted in less robust response than wild-type controls
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• stimulation with either anti-CD3 and anti-CD28 or PHA resulted in reduced response compared to wild-type controls
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endocrine/exocrine glands
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• some older animals showed reduced thymus size and loss of normal architecture
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• extensive vacuolization, loss of normal cellular architecture, and sometimes, absence of mature spermatozoa
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growth/size/body
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• myeloid and plasmactyic hyperplasia
• hyperplasia was sometimes accompanied by loss of normal splenic architecture
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hematopoietic system
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• stimulation with LPS resulted in less robust response than wild-type controls
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• stimulation with either anti-CD3 and anti-CD28 or PHA resulted in reduced response compared to wild-type controls
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• some older animals showed reduced thymus size and loss of normal architecture
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• myeloid and plasmactyic hyperplasia
• hyperplasia was sometimes accompanied by loss of normal splenic architecture
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immune system
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• stimulation with LPS resulted in less robust response than wild-type controls
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• stimulation with either anti-CD3 and anti-CD28 or PHA resulted in reduced response compared to wild-type controls
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• some older animals showed reduced thymus size and loss of normal architecture
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• myeloid and plasmactyic hyperplasia
• hyperplasia was sometimes accompanied by loss of normal splenic architecture
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• lymph nodes hyperplastic, with infiltration by macrophages, neutrophils, and eosinophils
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• organs of older animals showed increased inflammation, particularly in those animals with skin lesions
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• increased mortality after infection with mouse-adapted pathogenic influenza virus
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reproductive system
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• reduced numbers produced over time, authors suggest as a result of inability to maintain spermatogenesis
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• extensive vacuolization, loss of normal cellular architecture, and sometimes, absence of mature spermatozoa
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• atrophic
• irregular tubules, with abnormal architecture
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• few males succeeded in producing offspring
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integument
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• 5% of animals showed ulcerated skin lesions
• 25% of older mice had fluid-filled neck abscesses
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mortality/aging
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• the median lifespan of 69 days
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neoplasm
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• based on median survival time, mice carrying double Atmtm1Awb allele were no more resistant to tumor formation induced by myc than mice with homozygous wild-type Ppm1d+ allele
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mortality/aging
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• the median lifespan of >130 days
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neoplasm
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• similar to mice carrying double Ppm1dtm1Lad allele without Cdkn2atm1Cjs allele, based on increased median survival time, mice carrying single Cdkn2atm1Cjs allele were considerably more resistant to tumor formation induced by myc than mice with homozygous wild-type Ppm1d+ allele
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mortality/aging
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• the median lifespan of 31 days
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neoplasm
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• based on median survival time, mice carrying single Trp53tm1Brd allele were no more resistant to tumor formation induced by myc than mice with homozygous wild-type Ppm1d+ allele
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cellular
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• double mutant Ppm1dtm1Lad Mapk14tm1.1Dvb mice exhibit pancreatic islet proliferation similar to wild-type, correcting the phenotype observed in Ppm1dtm1Lad mutant mice
• double mutant Ppm1dtm1Lad Mapk14tm1.1Dvb mice do not exhibit impaired glucose tolerance, correcting the phenotype observed in Ppm1dtm1Lad/ mutant mice
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppm1dtm1Lad mutation
(1 available);
any
Ppm1d mutation
(28 available)
Tg(IghMyc)22Bri mutation
(1 available)
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mortality/aging
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• the median lifespan of 138 days
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neoplasm
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• mice carrying double Ppm1dtm1Lad allele were considerably more resistant to tumor formation induced by myc than wild-type transgenic litter mates based on increased median survival time by about 60 days
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppm1dtm1Lad mutation
(1 available);
any
Ppm1d mutation
(28 available)
Tg(IghMyc)22Bri mutation
(1 available)
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mortality/aging
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• the median lifespan of 107 days
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neoplasm
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• mice carrying a single Ppm1dtm1Lad allele were considerably more resistant to tumor formation induced by myc than wild-type transgenic litter mates based on increased median survival time by about 30 days
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mortality/aging
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• the median lifespan of 130 days
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neoplasm
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• similar to mice carrying double Ppm1dtm1Lad allele without Mapk14tm1Dvb allele, based on increased median survival time, mice carrying single Mapk14tm1Dvb allele were considerably more resistant to tumor formation induced by myc than mice with homozygous wild-type Ppm1d+ allele
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Analysis Tools