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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Apoetm2(APOE*3)Mae
targeted mutation 2, Nobuyo Maeda
MGI:2157240
Summary 6 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae B6.129P2-Apoetm2(APOE*3)Mae MGI:4355223
hm2
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae involves: 129P2/OlaHsd * C57BL/6 MGI:5142242
hm3
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae involves: 129P2/OlaHsd * C57BL/6J MGI:3695698
cx4
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Ldlrtm1(LDLR)Mae/Ldlr+
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4355226
cx5
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Tg(Thy1-APPSwDutIowa)BWevn/?
involves: 129P2/OlaHsd * C57BL/6 MGI:4355225
cx6
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Tg(APPSWE)2576Kha/?
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:4355224


Genotype
MGI:4355223
hm1
Allelic
Composition
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Genetic
Background
B6.129P2-Apoetm2(APOE*3)Mae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm2(APOE*3)Mae mutation (2 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice travel more in an open field during the habituation and acquisition phase than do Apoetm3(APOE*4)Mae mice
• particularly females
• females become slightly less active in testing phase
• no longer significantly more active in the retention phase and females clearly less active




Genotype
MGI:5142242
hm2
Allelic
Composition
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm2(APOE*3)Mae mutation (2 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• aged (65-127 weeks) mutants fed a high-fat diet exhibit minor retinal pigment epithelium (RPE) changes such as RPE vacuolization

vision/eye
• aged (65-127 weeks) mutants fed a high-fat diet exhibit minor retinal pigment epithelium (RPE) changes such as RPE vacuolization




Genotype
MGI:3695698
hm3
Allelic
Composition
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm2(APOE*3)Mae mutation (2 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• lesion size half that in Apoetm3(APOE*4)Mae after 3 months on an atherogenic diet
• small plaques, typically an accumulation of several foam cells are seen in 4 of 11 females aged 10-12 months; considerably less severe than seen in Apoetm1(APOE)Mae homozygotes
• after 12 weeks on a high fat/high cholesterol diet, develop significantly larger atherosclerotic plaques in the aortic sinus area than wild-type, indicating increased susceptibility to dietary-induced atherosclerosis

homeostasis/metabolism
• normal total cholesterol and triglyceride levels in fasted plasma when maintained on normal low fat chow diet, however show a difference in the distribution of plasma lipoproteins and apolipoprotein E
• beta-migrating lipoproteins (LDL) and plasma apoB100 levels are decreased and the apoE distribution is shifted from high density lipoproteins to larger lipoprotein particles
• the fractional catabolic rate of exogenously administered remnant particles in the beta-VLDL range without apoE is 6-fold slower than in wild-type
• fasted mutants show an increase in pre-beta-migrating lipoproteins (VLDL) and absence of beta-migrating particles (LDL)
• seen in fasted mice on a normal low fat chow diet
• relative to Apoetm3(APOE*4)Mae regardless of diet
• decreased cholesterol/fatty acid ratio on a normal diet relative to Apoetm3(APOE*4)Mae
• decreased diameter of VLDL particles relative to Apoetm3(APOE*4)Mae
• increased clearance of Apoe deficient VLDL relative to Apoetm3(APOE*4)Mae
• on a high fat/high cholesterol diet, show a 5-fold increase in total cholesterol compared to a 1.5-fold increase in wild-type, indicating increased susceptibility to dietary-induced hypercholesterolemia
• relative to Apoetm3(APOE*4)Mae regardless of diet
• on a high fat/high cholesterol diet, triglyceride levels are reduced to a smaller extent (18% vs. 50% in wild-type) than in wild-type
• relative to Apoetm3(APOE*4)Mae regardless of diet
• in the HDL fraction relative to Apoetm3(APOE*4)Mae regardless of diet

immune system
• in response to lipopolysaccharide injection with a minimum after 3 hours
• in response to lipopolysaccharide injection with a minimum after 1 hour




Genotype
MGI:4355226
cx4
Allelic
Composition
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)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:
Apoetm2(APOE*3)Mae mutation (2 available); any Apoe mutation (145 available)
Ldlrtm1(LDLR)Mae mutation (2 available); any Ldlr mutation (76 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• very little plaque development
• significantly lower lipid levels on a normal fat diet

nervous system
• very little plaque development




Genotype
MGI:4355225
cx5
Allelic
Composition
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Tg(Thy1-APPSwDutIowa)BWevn/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm2(APOE*3)Mae mutation (2 available); any Apoe mutation (145 available)
Tg(Thy1-APPSwDutIowa)BWevn mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• increased number of neuroreactive microglia in cortex
• decreased number of neuroreactive microglia in thalamic region
• plaque deposition in cortical parenchyma increased 20%
• reduced deposition in cerebral microvasculature
• microglia are tightly associated with parenchymal plaque amyloid
• increased number of neuroreactive astrocytes in cortex
• decreased number of neuroreactive astrocytes in thalamic region

hematopoietic system
• increased number of neuroreactive microglia in cortex
• decreased number of neuroreactive microglia in thalamic region

immune system
• increased number of neuroreactive microglia in cortex
• decreased number of neuroreactive microglia in thalamic region

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




Genotype
MGI:4355224
cx6
Allelic
Composition
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Tg(APPSWE)2576Kha/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm2(APOE*3)Mae mutation (2 available); any Apoe mutation (145 available)
Tg(APPSWE)2576Kha mutation (5 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
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age
• deposition delayed until after 12 months of age
• less plaque development than in Tg(APPSWE)2576Kha, Apoetm3(APOE*4Mae mice
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age

homeostasis/metabolism
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age
• deposition delayed until after 12 months of age
• less plaque development than in Tg(APPSWE)2576Kha, Apoetm3(APOE*4Mae mice
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory