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Phenotypes Associated with This Genotype
Genotype
MGI:3618376
Allelic
Composition
Mapk8ip1tm1Rjd/Mapk8ip1tm1Rjd
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk8ip1tm1Rjd mutation (2 available); any Mapk8ip1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in vitro, mutant hippocampal neurons exhibit reduced stress-induced apoptosis following exposure to the excitotoxin kainate
• mutant neurons are also resistant to the apoptotic effects of anoxic stress induced by oxygen-glucose deprivation, as shown by reduced labeling in TUNEL assays and increased cell survival
• following exposure to kainite-induced excitotoxic stress, mutant hippocampal neurons display attenuated JNK activation despite a normal level of Jun protein expression
• in vivo, homozygotes show a severe reduction in the extent of kainate-induced lesions in the CA3 subfield of the hippocampus, with a reduced distribution of TUNEL-positive and GFAP-positive astroglial fibers relative to wild-type mice
• no differences in JNK activation is observed following exposure to ultraviolet radiation or treatment with the drug anisomycin
• NMDA-mediated current amplitude is decreased relative to in wild-type mice

homeostasis/metabolism
N
• contrary to expectations, homozygotes display normal islet morphology, normal expression of insulin and glucagon, as well as normal blood glucose levels and performance in glucose tolerance tests relative to wild-type mice
• in vitro, mutant hippocampal neurons exhibit reduced stress-induced apoptosis following exposure to the excitotoxin kainate
• mutant neurons are also resistant to the apoptotic effects of anoxic stress induced by oxygen-glucose deprivation, as shown by reduced labeling in TUNEL assays and increased cell survival
• following exposure to kainite-induced excitotoxic stress, mutant hippocampal neurons display attenuated JNK activation despite a normal level of Jun protein expression
• in vivo, homozygotes show a severe reduction in the extent of kainate-induced lesions in the CA3 subfield of the hippocampus, with a reduced distribution of TUNEL-positive and GFAP-positive astroglial fibers relative to wild-type mice
• no differences in JNK activation is observed following exposure to ultraviolet radiation or treatment with the drug anisomycin

cellular
• in vitro, mutant hippocampal neurons exhibit reduced stress-induced apoptosis following exposure to the excitotoxin kainate
• mutant neurons are also resistant to the apoptotic effects of anoxic stress induced by oxygen-glucose deprivation, as shown by reduced labeling in TUNEL assays and increased cell survival
• following exposure to kainite-induced excitotoxic stress, mutant hippocampal neurons display attenuated JNK activation despite a normal level of Jun protein expression
• in vivo, homozygotes show a severe reduction in the extent of kainate-induced lesions in the CA3 subfield of the hippocampus, with a reduced distribution of TUNEL-positive and GFAP-positive astroglial fibers relative to wild-type mice
• no differences in JNK activation is observed following exposure to ultraviolet radiation or treatment with the drug anisomycin


Contributing Projects:
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
04/30/2024
MGI 6.23
The Jackson Laboratory