Analysis Tools|
Allele Symbol Allele Name Allele ID |
Vps35Gt(RRK261)Byg gene trap RRK261, BayGenomics MGI:4130266 |
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| Summary |
4 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• rearing frequency is decreased by 35.6% and 82.2% in 12- and 18- month old mice, respectively
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• in the open field, total distance and velocity of 12- and 18-month old mice is reduced
• however, performance in the rotarod and gait tests is normal
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• dopamine levels are reduced in the striatum and ventral midbrain at 6 month or older mutants
• ratios of 3,4-dihydroxyphenylacetic acid (DOPAC)/dopamine or 3,4-dihydroxyphenylacetic acid (HVA)/dopamine are much higher in 12 month old mutant striatum compared to controls
• however, 5-HT levels are normal
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• TH+ neurons exhibit disturbed and decreased fibers/processes in substantia nigra pars compacta of aged mice
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• decrease in the number of TH+ neurons in aged (12 months) mice, with an approximate 20% loss of TH+ somas in the substantia nigra pars compacta
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• mice show age-dependent accumulation of alpha-synuclein in in substantia nigra pars compacta-dopamine neurons
• both monomeric and oligomeric, or phosphorylated and unphosphorylated, species of alpha-synuclein are increased in mice older than 6 months, with an increase only in the ventral midbrain but not in the hippocampus
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• Lamp1-positive late endosomes/early lysosomes appear enlarged in dopamine neurons
• Lamp2-positive vesicles appear smaller in size in dopamine neurons
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Parkinson's disease 17 | DOID:0060897 |
OMIM:614203 |
J:225806 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after induced cortical ischemic stroke following tamoxifen-induced knockout
• decreased severity of motor function deficits after cortical ischemic stroke induced close to sensorimotor cortex following tamoxifen-induced knockout
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• increased number of macrophages in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• normal number of macrophages in contralateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• increased number of anti-inflammatory microglia in periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• increased number of microglia in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• normal number of microglia in contralateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• increased expression of TGFB in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• after induced cortical ischemic stroke following tamoxifen-induced knockout
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• increased number of macrophages in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• normal number of macrophages in contralateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• increased number of anti-inflammatory microglia in periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• increased number of microglia in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• normal number of microglia in contralateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• reduced expression of IL1B in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• increased expression of IL10 in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• increased expression of IL4 in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• reduced expression of IL6 in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• reduced expression of TNFA in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• decreased cortex infarction size after induced cortical ischemic stroke following tamoxifen-induced knockout
• decreased neuronal cell death after induced cortical ischemic stroke following tamoxifen-induced knockout
• decreased severity of motor function deficits after cortical ischemic stroke induced close to sensorimotor cortex following tamoxifen-induced knockout
• lower increase of astrocyte number (reduced astrocytosis) in periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• increased number of anti-inflammatory microglia in periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• reduced number of pro-inflammatory microglia in periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• after induced cortical ischemic stroke following tamoxifen-induced knockout
• decreased severity of motor function deficits after cortical ischemic stroke induced close to sensorimotor cortex following tamoxifen-induced knockout
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• increased number of anti-inflammatory microglia in periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• increased number of microglia in ipsilateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
• normal number of microglia in contralateral periinfarct area after induced cortical ischemic stroke following tamoxifen-induced knockout
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• after induced cortical ischemic stroke following tamoxifen-induced knockout
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Increase of amyloid beta deposits and amyloid beta 40 in the hippocampus and cortex of Vps35Gt(RRK261)Byg/Vps35+ Tg(APPSWE)2576Kha/0 mice
| N |
• mice exhibit normal paired-pulse facilitation and inhibitory synaptic transmission
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• in the hippocampus and cerebral cortex
• greater accumulation than in Tg(APPSWE)2576Kha mice
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• accelerated compared to in Tg(APPSWE)2576Kha mice
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• field excitatory postsynaptic potential slopes in the CA1 and dentate gyrus are reduced compared to in either single heterozygotes
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• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice
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• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice
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• in the CA1 at 2 months
• worsened at 4 months in the CA1
• however, long term potentiation in the dentate gyrus is normal
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• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice
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• at 4 months in the CA1
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• in a Morris water maze, mice exhibit increased latencies to finding the hidden platform and in pathway length compared with either single heterozygote
• deficits increase with age
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• in the hippocampus and cerebral cortex
• greater accumulation than in Tg(APPSWE)2576Kha mice
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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 12/10/2024 MGI 6.24 |
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