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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gpx1tm1Kola
targeted mutation 1, Ismail Kola
MGI:2388705
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Gpx1tm1Kola/Gpx1tm1Kola B6.129S2(CF1)-Gpx1tm1Kola MGI:3606933
hm2
Gpx1tm1Kola/Gpx1tm1Kola involves: 129S2/SvPas * BALB/c * CF-1 MGI:2450520
hm3
Gpx1tm1Kola/Gpx1tm1Kola involves: 129S2/SvPas * CF-1 MGI:3606742


Genotype
MGI:3606933
hm1
Allelic
Composition
Gpx1tm1Kola/Gpx1tm1Kola
Genetic
Background
B6.129S2(CF1)-Gpx1tm1Kola
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gpx1tm1Kola mutation (2 available); any Gpx1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
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




Genotype
MGI:2450520
hm2
Allelic
Composition
Gpx1tm1Kola/Gpx1tm1Kola
Genetic
Background
involves: 129S2/SvPas * BALB/c * CF-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gpx1tm1Kola mutation (2 available); any Gpx1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• 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

nervous system
• 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)
• upon MCA stroke surgery, homozygotes display increased susceptibility to ischemia/reperfusion injury relative to wild-type mice
• 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
• 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

cellular
• 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)
• 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

homeostasis/metabolism
• 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
• upon MCA stroke surgery, homozygotes display increased susceptibility to ischemia/reperfusion injury relative to wild-type mice
• 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




Genotype
MGI:3606742
hm3
Allelic
Composition
Gpx1tm1Kola/Gpx1tm1Kola
Genetic
Background
involves: 129S2/SvPas * CF-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gpx1tm1Kola mutation (2 available); any Gpx1 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
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

cellular
• 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
• in culture, mutant MEFs exhibit significantly reduced [3H]-thymidine uptake, indicating reduced DNA synthesis and cellular growth relative to wild-type MEFs
• 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)
• in culture, mutant MEFs exhibit a significant dose-dependent susceptibility to H2O2-mediated cell death
• upon treatment with high concentrations of H2O2, mutant MEFs exhibit significantly increased cellular debris, indicating higher susceptibility to necrotic cell death
• 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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last database update
11/19/2024
MGI 6.24
The Jackson Laboratory