Analysis Tools
nervous system
| N |
• astrocytes secrete a normal composition of lipid particles
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Allele Symbol Allele Name Allele ID |
Clutm1Jakh targeted mutation 1, Judith A K Harmony MGI:2181011 |
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| Summary |
5 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• astrocytes secrete a normal composition of lipid particles
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit no evidence of tubulointerstitial disease, vascular lesions, inflammatory infiltrates, necrosis, or amyloid deposits, regardless of the extent of glomerulopathy
• glomerular basement membranes are normal and lack discernible deposits
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• collapse of capillary lumens at 21 months of age
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• up to 75% of glomeruli exhibit moderate to severe mesangial lesions at 21 months of age
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• mesangial hypercellularity noted in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
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• electron-dense tubulo-fibrillar structures arranged in parallel arrays are detected in the mesangial matrix at 21 months, consistent with immune complex deposits
• more electron-dense deposits found in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
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• variable mesangial expansion observed at 21 months, but not at 6 months, of age
• more severe mesangial expansion noted in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
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• at 21 months of age, mice display progressive mesangial expansion, collapse of capillary lumens, and deposition of collagen and immune complexes, unlike wild-type and heterozygous controls
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• immune complexes of IgG, IgM, IgA, and in some cases C1q, C3, and C9 are detected in the mesangium at 21 months of age
• increased deposition of C1q and C3 in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
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• immune complexes of IgG, IgM and IgA are noted as early as 4 weeks of age
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• accumulation of collagen deposits in the glomeruli
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| N |
• mice display no signs of proteinuria or any alterations in serum and urine proteins relative to controls
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• collapse of capillary lumens at 21 months of age
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• mesangial hypercellularity noted in 6-mo-old mice that have undergone unilateral nephrectomy at 3 months and are then fed a high-protein diet
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after immunization with cardiac myosin, mutant hearts become pale and enlarged, mutants exhibit 3-fold greater heart tissue injury than wild-type
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• 21 days after myocarditis initiation, mice show significant cardiac tissue injury than wild-type mice
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• after immunization, myocyte necrosis is observed in some animals
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• 7 weeks following myocarditis, widespread loss of myocardial fibers is found in mutant hearts, whereas none is seen in wild-type controls
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• ventricular damage in females is 6-fold greater than in wild-type females; males do not show as severe cardiac damage
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• postmyocarditis heart function is impaired with decreased shortening fraction measured in mutants;
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• severe, diffuse inflammation with large inflammatory aggregates occurs after immunization with cardiac myosin
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• severe myocarditis after immunization with cardiac myosin, more severe than in wild-type
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• 21 days after myocarditis initiation, mice show significant cardiac tissue injury than wild-type mice
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• after immunization, myocyte necrosis is observed in some animals
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• 7 weeks following myocarditis, widespread loss of myocardial fibers is found in mutant hearts, whereas none is seen in wild-type controls
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• postmyocarditis heart function is impaired with decreased shortening fraction measured in mutants;
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• severe, diffuse inflammation with large inflammatory aggregates occurs after immunization with cardiac myosin
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• severe myocarditis after immunization with cardiac myosin, more severe than in wild-type
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• immunized mice show cardiac edema
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits
• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes
• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed
• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu
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• at 3 months, cerebrospinal fluid levels of Abeta40 are elevated; Abeta40 increase is greater than in transgenic, single Apoe-null mice
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• at 3 months, cerebrospinal fluid levels of Abeta42 are elevated
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• mice have significant amyloid burden, greater than shown by other genotypes
• at 12 months, mice have highest tissue levels of soluble Abeta40 and Abeta42, with high levels of insoluble Abeta42
• at 3 months, mice have higher levels of carbonate soluble Abeta40 and Abeta42 compared to other genotypes
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• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits
• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes
• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed
• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu
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• at 3 months, cerebrospinal fluid levels of Abeta40 are elevated; Abeta40 increase is greater than in transgenic, single Apoe-null mice
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• at 3 months, cerebrospinal fluid levels of Abeta42 are elevated
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Alzheimer's disease | DOID:10652 | J:107702 | ||
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition
(J:78357)
• decreased percentage of Abeta-immunoreactive deposits that are thioflavine-S-positive (2.46 vs 19.4% thioflavine load/Abeta load) compared to Clu-sufficient mice
(J:78357)
• many Abeta deposits have few or no detectable dystrophic neurites around them
(J:78357)
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex
(J:107702)
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• a 10-fold reduction in dystrophic neurites in hippocampi at 12 months compared to Clu-sufficient transgenic mice and a 5-fold reduction in number of dystrophic neurites per amyloid deposit
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• only 20% of mice have thioflavine-S-positive (fibrillar Abeta or amyloid) deposits in the cortex at 12 months
• mice have lower hippocampal amyloid burden (0.89%) at 12 months than Clu-sufficient transgenic mice; amyloid load increases to 2.25% by 15 months
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• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition
(J:78357)
• decreased percentage of Abeta-immunoreactive deposits that are thioflavine-S-positive (2.46 vs 19.4% thioflavine load/Abeta load) compared to Clu-sufficient mice
(J:78357)
• many Abeta deposits have few or no detectable dystrophic neurites around them
(J:78357)
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex
(J:107702)
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Alzheimer's disease | DOID:10652 | J:78357 | ||
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 04/16/2024 MGI 6.23 |
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