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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Apoetm3(APOE*4)Mae
targeted mutation 3, Nobuyo Maeda
MGI:2158398
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae B6.129P2-Apoetm3(APOE*4)Mae MGI:4355228
hm2
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae involves: 129P2/OlaHsd * C57BL/6 MGI:4355227
cx3
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Ldlrtm1(LDLR)Mae/Ldlr+
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4355231
cx4
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Tg(Thy1-APPSwDutIowa)BWevn/?
involves: 129P2/OlaHsd * C57BL/6 MGI:4355230
cx5
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Tg(APPSWE)2576Kha/?
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:4355229


Genotype
MGI:4355228
hm1
Allelic
Composition
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Genetic
Background
B6.129P2-Apoetm3(APOE*4)Mae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm3(APOE*4)Mae mutation (3 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• low retention in water maze tests (J:97643)
• performance improves more with training than for Apoetm2(APOE*3)Mae mice (J:97643)
• performance in "delayed matching to place" does not improve (J:97643)
• low retention in water maze tests (J:97643)
• performance improves more with training than for Apoetm2(APOE*3)Mae mice (J:97643)
• performance in "delayed matching to place" does not improve (J:97643)
• females are deficient in their ability to recognize spatial changes in object configuration in open field tests (J:97643)
• females are deficient in their ability to recognize spatial changes in object configuration in open field tests (J:97643)




Genotype
MGI:4355227
hm2
Allelic
Composition
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm3(APOE*4)Mae mutation (3 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• weight gain slows down after 4 weeks on high fat diets relative to Apoetm2(APOE*3)Mae (J:151284)
• weight gain slows down after 4 weeks on high fat diets relative to Apoetm2(APOE*3)Mae (J:151284)

homeostasis/metabolism
• reduced insulin stimulated glucose uptake by epididymal fat (J:151284)
• reduced insulin stimulated glucose uptake by epididymal fat (J:151284)
• after 2 months on a high fat diet (J:151284)
• after 2 months on a high fat diet (J:151284)
• slower clearance of lipid from the blood after ingestion (J:151284)
• slower clearance of lipid from the blood after ingestion (J:151284)
• relative to Apoetm2(APOE*3)Mae regardless of diet (J:74417)
• relative to Apoetm2(APOE*3)Mae regardless of diet (J:74417)
• relative to Apoetm2(APOE*3)Mae regardless of diet (J:74417)
• increased cholesterol/fatty acid ratio on a normal diet relative to Apoetm2(APOE*3)Mae (J:74417)
• increased diameter of VLDL particles relative to Apoetm2(APOE*3)Mae (J:74417)
• reduced clearance of Apoe deficient VLDL relative to Apoetm2(APOE*3)Mae (J:74417)
• relative to Apoetm2(APOE*3)Mae regardless of diet (J:74417)
• increased cholesterol/fatty acid ratio on a normal diet relative to Apoetm2(APOE*3)Mae (J:74417)
• increased diameter of VLDL particles relative to Apoetm2(APOE*3)Mae (J:74417)
• reduced clearance of Apoe deficient VLDL relative to Apoetm2(APOE*3)Mae (J:74417)
• in the HDL fraction relative to ApoeApoetm2(APOE*3)Mae regardless of diet (J:74417)
• in the HDL fraction relative to ApoeApoetm2(APOE*3)Mae regardless of diet (J:74417)
• relative to Apoetm2(APOE*3)Mae regardless of diet (J:74417)
• relative to Apoetm2(APOE*3)Mae regardless of diet (J:74417)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit perivascular amyloid beta immunoreactivity in the eyes indicating amyloid beta deposits (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit perivascular amyloid beta immunoreactivity in the eyes indicating amyloid beta deposits (J:101147)

cardiovascular system
• lesion size twice that in Apoetm2(APOE*3)Mae mice after 3 months on an atherogenic diet (J:74417)
• lesion size twice that in Apoetm2(APOE*3)Mae mice after 3 months on an atherogenic diet (J:74417)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit neovascularization, ranging from mild neovascularization confined to an area adjacent to the RPE and Bruch's membrane to more extensive neovascularization that extends through the RPE and subretinal space and into the neural retina (J:101147)
• some aged miced fed a high-fat diet exhibit extensive neovascular lesions that involve the outer retinal vasculature (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit neovascularization, ranging from mild neovascularization confined to an area adjacent to the RPE and Bruch's membrane to more extensive neovascularization that extends through the RPE and subretinal space and into the neural retina (J:101147)
• some aged miced fed a high-fat diet exhibit extensive neovascular lesions that involve the outer retinal vasculature (J:101147)

adipose tissue
• fewer small adipocytes (J:151284)
• fewer small adipocytes (J:151284)
• less epididymal fat than in Apoetm2(APOE*3)Mae mice (J:151284)
• less epididymal fat than in Apoetm2(APOE*3)Mae mice (J:151284)

immune system
• in response to lipopolysaccharide injection, peaking after 3 hours (J:86768)
• in response to lipopolysaccharide injection, peaking after 3 hours (J:86768)
• in response to lipopolysaccharide injection, peaking after 1 hour (J:86768)
• in response to lipopolysaccharide injection, peaking after 1 hour (J:86768)
• higher level of HSV-1 shedding 6 days after ocular infection (J:138241)
• higher numbers of virus in the trigeminal nerve than in controls (J:138241)
• higher level of HSV-1 shedding 6 days after ocular infection (J:138241)
• higher numbers of virus in the trigeminal nerve than in controls (J:138241)

vision/eye
• aged (65-127 weeks) mutants fed a high-fat diet exhibit neovascularization, ranging from mild neovascularization confined to an area adjacent to the RPE and Bruch's membrane to more extensive neovascularization that extends through the RPE and subretinal space and into the neural retina (J:101147)
• some aged miced fed a high-fat diet exhibit extensive neovascular lesions that involve the outer retinal vasculature (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit neovascularization, ranging from mild neovascularization confined to an area adjacent to the RPE and Bruch's membrane to more extensive neovascularization that extends through the RPE and subretinal space and into the neural retina (J:101147)
• some aged miced fed a high-fat diet exhibit extensive neovascular lesions that involve the outer retinal vasculature (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit severe retinal pigment epithelium (RPE) changes, including RPE hyperpigmentation, hypopigmentation and atrophy resulting in a thinner RPE cell layer, thick sub-RPE basal deposits and soft drusenoid deposits rich in neutral lipids (J:101147)
• RPE migration and proliferation are seen in areas of vascular invasion of the retina in aged mutants fed a high-fat diet (J:101147)
• aged mutants fed a high-fat diet exhibit disorganized or absent RPE basal infoldings and accumulation of deposits between the RPE and Bruch's membrane of varying thickness (J:101147)
• mutants that develop neovascularization show capillaries present on the RPE (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit severe retinal pigment epithelium (RPE) changes, including RPE hyperpigmentation, hypopigmentation and atrophy resulting in a thinner RPE cell layer, thick sub-RPE basal deposits and soft drusenoid deposits rich in neutral lipids (J:101147)
• RPE migration and proliferation are seen in areas of vascular invasion of the retina in aged mutants fed a high-fat diet (J:101147)
• aged mutants fed a high-fat diet exhibit disorganized or absent RPE basal infoldings and accumulation of deposits between the RPE and Bruch's membrane of varying thickness (J:101147)
• mutants that develop neovascularization show capillaries present on the RPE (J:101147)
• atrophy of the retinal pigment epithelium is seen in aged mutants fed a high-fat diet (J:101147)
• atrophy of the retinal pigment epithelium is seen in aged mutants fed a high-fat diet (J:101147)
• corneal hazing 9 days after ocular infection with HSV-1 (J:138241)
• stromal opacity in 70% of mice by day 11 (J:138241)
• corneal hazing 9 days after ocular infection with HSV-1 (J:138241)
• stromal opacity in 70% of mice by day 11 (J:138241)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit thinning of the outer nuclear layer (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit thinning of the outer nuclear layer (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit Bruch's membrane thickening (J:101147)
• mutants that develop neovascularization show regions of thinning or loss of Bruch's membrane and capillaries present on choroidal sides of Bruch's membrane (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit Bruch's membrane thickening (J:101147)
• mutants that develop neovascularization show regions of thinning or loss of Bruch's membrane and capillaries present on choroidal sides of Bruch's membrane (J:101147)

nervous system
• aged (65-127 weeks) mutants fed a high-fat diet exhibit perivascular amyloid beta immunoreactivity in the eyes indicating amyloid beta deposits (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit perivascular amyloid beta immunoreactivity in the eyes indicating amyloid beta deposits (J:101147)

pigmentation
• aged (65-127 weeks) mutants fed a high-fat diet exhibit severe retinal pigment epithelium (RPE) changes, including RPE hyperpigmentation, hypopigmentation and atrophy resulting in a thinner RPE cell layer, thick sub-RPE basal deposits and soft drusenoid deposits rich in neutral lipids (J:101147)
• RPE migration and proliferation are seen in areas of vascular invasion of the retina in aged mutants fed a high-fat diet (J:101147)
• aged mutants fed a high-fat diet exhibit disorganized or absent RPE basal infoldings and accumulation of deposits between the RPE and Bruch's membrane of varying thickness (J:101147)
• mutants that develop neovascularization show capillaries present on the RPE (J:101147)
• aged (65-127 weeks) mutants fed a high-fat diet exhibit severe retinal pigment epithelium (RPE) changes, including RPE hyperpigmentation, hypopigmentation and atrophy resulting in a thinner RPE cell layer, thick sub-RPE basal deposits and soft drusenoid deposits rich in neutral lipids (J:101147)
• RPE migration and proliferation are seen in areas of vascular invasion of the retina in aged mutants fed a high-fat diet (J:101147)
• aged mutants fed a high-fat diet exhibit disorganized or absent RPE basal infoldings and accumulation of deposits between the RPE and Bruch's membrane of varying thickness (J:101147)
• mutants that develop neovascularization show capillaries present on the RPE (J:101147)
• atrophy of the retinal pigment epithelium is seen in aged mutants fed a high-fat diet (J:101147)
• atrophy of the retinal pigment epithelium is seen in aged mutants fed a high-fat diet (J:101147)

Mouse Models of Human Disease
OMIM ID Ref(s)
Macular Degeneration, Age-Related, 1; ARMD1 603075 J:101147




Genotype
MGI:4355231
cx3
Allelic
Composition
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Ldlrtm1(LDLR)Mae/Ldlr+
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm3(APOE*4)Mae mutation (3 available); any Apoe mutation (64 available)
Ldlrtm1(LDLR)Mae mutation (2 available); any Ldlr mutation (46 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• significantly lower lipid levels on a normal fat diet (J:146721)
• significantly lower lipid levels on a normal fat diet (J:146721)
• greater increase in total cholesterol when fed a high fat diet than seen in Apoetm2(APOE*3)Mae mice (J:146721)
• very high total cholesterol to triglyceride ratio on a high fat diet (J:146721)
• increased number of non-HDL particles (J:146721)
• plasma cholesterol decrease over time relative to mice lacking Ldlrtm1(LDLR)Mae (J:146721)
• greater increase in total cholesterol when fed a high fat diet than seen in Apoetm2(APOE*3)Mae mice (J:146721)
• very high total cholesterol to triglyceride ratio on a high fat diet (J:146721)
• increased number of non-HDL particles (J:146721)
• plasma cholesterol decrease over time relative to mice lacking Ldlrtm1(LDLR)Mae (J:146721)
• higher triglyceride levels in females on a normal fat diet (J:146721)
• higher triglyceride levels in females on a normal fat diet (J:146721)
• significant plaque development on a high fat diet relative to Apoetm2(APOE*3)Mae mice who show very little plaque development (J:146721)
• significant plaque development on a high fat diet relative to Apoetm2(APOE*3)Mae mice who show very little plaque development (J:146721)

nervous system
• significant plaque development on a high fat diet relative to Apoetm2(APOE*3)Mae mice who show very little plaque development (J:146721)
• significant plaque development on a high fat diet relative to Apoetm2(APOE*3)Mae mice who show very little plaque development (J:146721)




Genotype
MGI:4355230
cx4
Allelic
Composition
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Tg(Thy1-APPSwDutIowa)BWevn/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm3(APOE*4)Mae mutation (3 available); any Apoe mutation (64 available)
Tg(Thy1-APPSwDutIowa)BWevn mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• increased number of neuroreactive microglia in cortex (J:136318)
• decreased number of neuroreactive microglia in thalamic region (J:136318)
• increased number of neuroreactive microglia in cortex (J:136318)
• decreased number of neuroreactive microglia in thalamic region (J:136318)
• plaque deposition in cortical parenchyma increased 20% (J:136318)
• reduced deposition in cerebral microvasculature (J:136318)
• microglia are tightly associated with parenchymal plaque amyloid (J:136318)
• plaque deposition in cortical parenchyma increased 20% (J:136318)
• reduced deposition in cerebral microvasculature (J:136318)
• microglia are tightly associated with parenchymal plaque amyloid (J:136318)
• increased number of neuroreactive astrocytes in cortex (J:136318)
• decreased number of neuroreactive astrocytes in thalamic region (J:136318)
• increased number of neuroreactive astrocytes in cortex (J:136318)
• decreased number of neuroreactive astrocytes in thalamic region (J:136318)

hematopoietic system
• increased number of neuroreactive microglia in cortex (J:136318)
• decreased number of neuroreactive microglia in thalamic region (J:136318)
• increased number of neuroreactive microglia in cortex (J:136318)
• decreased number of neuroreactive microglia in thalamic region (J:136318)

immune system
• increased number of neuroreactive microglia in cortex (J:136318)
• decreased number of neuroreactive microglia in thalamic region (J:136318)
• increased number of neuroreactive microglia in cortex (J:136318)
• decreased number of neuroreactive microglia in thalamic region (J:136318)

homeostasis/metabolism
• plaque deposition in cortical parenchyma increased 20% (J:136318)
• reduced deposition in cerebral microvasculature (J:136318)
• microglia are tightly associated with parenchymal plaque amyloid (J:136318)
• plaque deposition in cortical parenchyma increased 20% (J:136318)
• reduced deposition in cerebral microvasculature (J:136318)
• microglia are tightly associated with parenchymal plaque amyloid (J:136318)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:136318




Genotype
MGI:4355229
cx5
Allelic
Composition
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Tg(APPSWE)2576Kha/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm3(APOE*4)Mae mutation (3 available); any Apoe mutation (64 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels with very few parenchymal plaques at 15 months (J:98636)
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels with very few parenchymal plaques at 15 months (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels (J:98636)

homeostasis/metabolism
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels with very few parenchymal plaques at 15 months (J:98636)
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels with very few parenchymal plaques at 15 months (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels (J:98636)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:98636





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last database update
02/02/2016
MGI 6.02
The Jackson Laboratory