immune system
• mice fail to develop viral deja vu disease unlike wild-type mice
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Allele Symbol Allele Name Allele ID |
Tg(Thy1-cre)1Vln transgene insertion 1, Fred Van Leuven MGI:2684620 |
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Summary |
6 genotypes
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mice fail to develop viral deja vu disease unlike wild-type mice
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• following ischemia/reperfusion injury
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• following ischemia/reperfusion injury
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• following ischemia/reperfusion injury, retina exhibit reduced retinal ganglion cell (RGC) loss and increased RGC and neuronal survival with less apoptosis compared with wild-type mice
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• following ischemia/reperfusion injury
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• following ischemia/reperfusion injury
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• aggregation of recombined retinal ganglion cells
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• aggregation of recombined retinal ganglion cells
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• hindlimb clasping is observed in 18 month old mice
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• less time spent on rotating rods as compared to controls at 12 months of age
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• reduced rearing is observed by 18 months of age
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• increased cell death in neurons after treatment with 10um glutamate
• increase in total and cell surface levels of glutamate receptors
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• increase in autophagosome/lysosome proteins in spinal motor neuron axons of 9 month old mice
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• increased astrogliosis and microgliosis is observed in the spinal cord of 18 month old mice
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• increased cell death in neurons after treatment with 10um glutamate
• increase in total and cell surface levels of glutamate receptors
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• increased astrogliosis and microgliosis is observed in the spinal cord of 18 month old mice
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• decrease in gastrocnemius muscle weight in 24 month old males
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• myofiber de/regeneration, decrease in size of muscle fiber, and inflammatory cell infiltration of gastrocnemius muscle in 24 month old males
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• increased cell death in neurons after treatment with 10um glutamate
• increase in total and cell surface levels of glutamate receptors
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• increased astrogliosis and microgliosis is observed in the spinal cord of 18 month old mice
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• increased astrogliosis and microgliosis is observed in the spinal cord of 18 month old mice
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• accumulation of acetylated alpha-tubulin in spinal motor neuron axons of 9 month old mice
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• decrease in numbers of spinal motor neurons in lumbar spinal cord in 18 month, but not 9 month old mice
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• neuromuscular junctions (NMJ) in 18 month old mice are partially or fully fragmented
• severe denervation in NMJ of 18 month old mice
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• decrease in gastrocnemius muscle weight in 24 month old males
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• retention of object recognition is normal at 1 hr after training but testing of animals 3 hours after familiarization with an object reveals significant impairment relative to controls
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N |
• no thioflavin-S-reactive amyloid plaques or diffuse amyloid deposits are detected in mice up to 18 months of age
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• with tetanic stimulation of hippocampal slices, after an initial slight decrease, the slope of the fEPSP approached control levels; LTP in transgenic brain slices is comparable to controls
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• mice do not display any behavioral or cognitive deficits
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N |
• brains of 6 month-old mice do not show any morphological abnormalities like cerebral hemorrhages, cavities or tumors; no defects are observed up to 2 years of age
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• levels of amyloid beta-40 and -42 (Abeta40, Abeta42) are reduced relative to controls; C-terminal fragments of APP accumulate in brains
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• initial phase of the slope of fEPSP is lower (168% vs 221% in controls) 15 minutes after tetanic stimulation; slope of fEPSP progressively increases to approach control levels 2 hours following stimulation
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• levels of amyloid beta-40 and -42 (Abeta40, Abeta42) are reduced relative to controls; C-terminal fragments of APP accumulate in brains
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
Alzheimer's disease | DOID:10652 | J:87229 | ||
Alzheimer's disease 3 | DOID:0110042 |
OMIM:607822 |
J:87229 |
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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