Analysis Tools|
Allele Symbol Allele Name Allele ID |
Gpx1tm1Kola targeted mutation 1, Ismail Kola MGI:2388705 |
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| Summary |
3 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• upon infection with P. berghei ANKA or P. berghei K173, homozygotes show no significant differences in malaria parasite burdens relative to wild-type mice, suggesting normal intraerythrocytic parasite progression and malarial immunity
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at 24 hrs after cold-induced brain injury, homozygotes exhibit an accelerated neuroinflammatory response, with a significant increase in Mac-1+ cells which rapidly declines by 96 hrs and reappears at 10 days post-injury, suggesting changes in response/activation/recruitment of macrophages and microglia to this type of injury
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• at 24 hrs after ischemia/reperfusion damage in the mid cerebral artery (MCA), homozygotes exhibit increased neuronal apoptosis, as shown by accelerated caspase-3 activation and increased TUNEL staining in post-ischemic mutant brains
(J:71798)
• at 24 and 96 hrs after cold-induced brain injury, homozygotes display significantly increased neuronal cell death in regions immediately proximal to the infarct core (penumbra)
(J:79183)
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• upon MCA stroke surgery, homozygotes display increased susceptibility to ischemia/reperfusion injury relative to wild-type mice
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• in response to ischemia/reperfusion damage in the MCA, homozygotes exhibit a a significantly increased infarct size (area in mm2) relative to wild-type mice
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• in response to ischemia/reperfusion damage in the MCA, homozygotes show an increased neurological deficit score (1.97 vs 0.9) and higher mortality rates (19% vs 7%) relative to wild-type mice, with most mutants dying from severe stroke rather than surgical complications
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• at 24 hrs after ischemia/reperfusion damage in the mid cerebral artery (MCA), homozygotes exhibit increased neuronal apoptosis, as shown by accelerated caspase-3 activation and increased TUNEL staining in post-ischemic mutant brains
(J:71798)
• at 24 and 96 hrs after cold-induced brain injury, homozygotes display significantly increased neuronal cell death in regions immediately proximal to the infarct core (penumbra)
(J:79183)
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• in response to ischemia/reperfusion injury, homozygotes exhibit a significant increase in lipid hydroperoxide levels after 24 hrs of reperfusion relative to wild-type mice
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• after cold-induced brain injury, homozygotes exhibit no significant differences in infarct size or blood-brain barrier integrity relative to similarly injured wild-type mice
• however, at 24 and 96 hrs after cold-induced brain injury, homozygotes exhibit a significant increase in the number of TUNEL-positive neurons with apoptotic nuclear morphology
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• upon MCA stroke surgery, homozygotes display increased susceptibility to ischemia/reperfusion injury relative to wild-type mice
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• in response to ischemia/reperfusion damage in the MCA, homozygotes exhibit a a significantly increased infarct size (area in mm2) relative to wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• homozygotes are obtained at the expected Mendelian ratios, and are fertile and healthy up to 12 months of age
• no histologic abnormalities are observed in brain, liver, kidney, lung, or heart at the age of 6 weeks
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• in culture, mutant mouse embryonic fibroblasts (MEFs) display senescence-like changes, including a 3.5-fold increase in adherent cell surface area, increased Cip1 expression levels, and a 3-fold elevation in NF-kappaB activation relative to wild-type MEFs
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• in culture, mutant MEFs exhibit significantly reduced [3H]-thymidine uptake, indicating reduced DNA synthesis and cellular growth relative to wild-type MEFs
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• homozygotes exhibit increased susceptibility to paraquat toxicity in a dose-dependent fashion; at 30 mg/kg body weight, 100% of homozygotes die within 5 hrs whereas wild-type mice remain unaffected even up to 10 days after i.p. injection
(J:49644)
• in culture, cortical neurons isolated from mutant mice show increased susceptibility to hydrogen peroxide-induced toxicity; at 65 M H2O2, 30% of mutant neurons die whereas all wild-type neurons remain viable
(J:49644)
• in culture, mutant MEFs exhibit a significant dose-dependent susceptibility to oxidative stress-mediated cell death
(J:87985)
• notably, in the annexin/PI assay, mutant MEFs show a small but significant increase in apoptosis in the absence of an added oxidant stress
(J:87985)
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• in culture, mutant MEFs exhibit a significant dose-dependent susceptibility to H2O2-mediated cell death
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• upon treatment with high concentrations of H2O2, mutant MEFs exhibit significantly increased cellular debris, indicating higher susceptibility to necrotic cell death
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• in culture, mutant MEFs exhibit significantly reduced cell population doubling rates relative to wild-type MEFs
• also, mutant MEFs show reduced responsiveness to the mitogenic properties of EGF and 10% FCS, indicating cell senescence
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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 10/29/2024 MGI 6.24 |
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