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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Apoetm1Bres
targeted mutation 1, Jan L Breslow
MGI:2137814
Summary 20 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Apoetm1Bres/Apoetm1Bres B6.129P2-Apoetm1Bres MGI:4437891
hm2
Apoetm1Bres/Apoetm1Bres either: (involves: 129P2/OlaHsd * BALB/c) or (involves: 129P2/OlaHsd * C57BL/6J) MGI:2174912
hm3
Apoetm1Bres/Apoetm1Bres involves: 129P2/OlaHsd * C57BL/6 MGI:3834756
hm4
Apoetm1Bres/Apoetm1Bres involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss MGI:3690368
ht5
Apoetm1Bres/Apoe+ either: (involves: 129P2/OlaHsd * BALB/c) or (involves: 129P2/OlaHsd * C57BL/6J) MGI:2174913
cn6
Apoetm1Bres/Apoetm1Bres
Bcl2tm1Irt/Bcl2tm1Irt
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * C57BL/6 MGI:3830965
cx7
Apoetm1Bres/Apoetm1Bres
Esr1tm1Ksk/Esr1tm1Ksk
B6.129P2-Apoetm1Bres Esr1tm1Ksk MGI:4437892
cx8
Apoetm1Bres/Apoetm1Bres
Cd59atm1Bpm/Cd59atm1Bpm
involves: 129 * 129P2/OlaHsd MGI:5298859
cx9
Apoetm1Bres/Apoetm1Bres
Plautm1Mlg/Plautm1Mlg
involves: 129 * C57BL/6 MGI:3527476
cx10
Apoetm1Bres/Apoetm1Bres
C6Q0/C6Q0
involves: 129P2/OlaHsd MGI:5298860
cx11
Apoetm1Bres/Apoetm1Bres
Mapk8tm1Flv/Mapk8tm1Flv
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 MGI:3691112
cx12
Apoetm1Bres/Apoetm1Bres
Mapk9tm1Flv/Mapk9tm1Flv
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3691097
cx13
Apoa2tm1Bres/Apoa2+
Apoetm1Bres/Apoetm1Bres
involves: 129P2/OlaHsd * 129S4/SvJae MGI:2655399
cx14
Apoa2tm1Bres/Apoa2tm1Bres
Apoetm1Bres/Apoetm1Bres
involves: 129P2/OlaHsd * 129S4/SvJae MGI:2655397
cx15
Apoetm1Bres/Apoetm1Bres
Cx3cr1tm1Ifc/Cx3cr1tm1Ifc
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:2450893
cx16
Apoetm1Bres/Apoetm1Bres
Ltb4r1tm1Adl/Ltb4r1tm1Adl
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3811013
cx17
Apoetm1Bres/Apoetm1Bres
Ifngr1tm1Agt/Ifngr1tm1Agt
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:4838232
cx18
Apoc1tm2Lmh/Apoc1tm2Lmh
Apoetm1Bres/Apoetm1Bres
involves: 129P2/OlaHsd * C57BL/6 MGI:3697329
cx19
Apoetm1Bres/Apoetm1Bres
Plgtm1Jld/Plgtm1Jld
involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss MGI:3690365
cx20
Apoetm1Bres/Apoetm1Bres
Fn1tm1Bwg/Fn1tm1Bwg
involves: 129S4/SvJae * C57BL/6 MGI:3046828


Genotype
MGI:4437891
hm1
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Genetic
Background
B6.129P2-Apoetm1Bres
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• treatment of ovariectomized females with estradiol inhibits lesion progression

homeostasis/metabolism
• in ovariectomized females exogenous estradiol treatment reduces fasting plasma cholesterol
• ovariectomized females not treated with estradiol display subcutaneous infiltration of lipid laden macrophages




Genotype
MGI:2174912
hm2
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Genetic
Background
either: (involves: 129P2/OlaHsd * BALB/c) or (involves: 129P2/OlaHsd * C57BL/6J)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• on a normal chow diet 3 out of 3 homozygotes developed lesions (mean area 3157 +/- 437 um2) compared to 0 out of 12 wild-type mice
• on a high fat high cholesterol diet all 9 homozygotes developed large lesions in the proximal aorta (mean area 9230 +/- 4700 um2) while no wild-type mice on the same diet developed lesions
• on a high fat high cholesterol diet lesions were found in the proximal aorta, and the coronary and pulmonary arteries

digestive/alimentary system
• in a vitamin A-fat tolerance test postprandial retinyl ester levels are very high by 4 hours and show no signs of decrease by 12 hours unlike in wild-type mice where retinyl ester levels return to baseline by 12 hours suggesting severely impaired clearance of dietary fat

homeostasis/metabolism
• much of the cholesterol increase is in the VLDL + IDL and LDL fractions
• the LDL fraction is increased to 100 +/- 22 mg/dl compared to 7 +/- 3 mg/dl in wild-type mice
• on a high fat high cholesterol diet the LDL fraction is increased to 143 +/- 65 mg/dl compared to 16 +/- 15 mg/dl in wild-type mice
• on a normal chow diet total plasma cholesterol is 494 +/- 95 mg/dl compared to 60 +/- 20 mg/dl in wild-type mice (J:2809)
• on a high fat high cholesterol diet total plasma cholesterol is 1821 +/- 395 mg/dl compared to 132 +/- 18 mg/dl in wild-type mice (J:2809)
• total plasma cholesterol is 501 +/- 40 compared to 98 +/- 5 mg/dl in wild-type mice (J:42426)
• however, total plasma cholesterol levels were not significantly elevated in heterozygous mice (101 +/- 10 mg/dl) (J:42426)
• much of the cholesterol increase is in the VLDL + IDL and LDL fractions
• the VLDL + IDL fraction is increased to 373 +/- 105 mg/dl compared to 21 +/- 6 mg/dl in wild-type mice
• on a high fat high cholesterol diet the VLDL + IDL fraction is increased to 1565 +/- 474 mg/dl compared to 50 +/- 14 mg/dl in wild-type mice
• triglyceride levels are increased compared to wild-type mice on either a normal or high fat high cholesterol diet

nervous system
• dendritic simplification is more prominent in the CA1-CA2 pyramidal cell layer and in the molecular layer
• at 4 months of age widespread vacuolization of apical dendrites and tortuous, dilated, and irregular dendrites are seen
• occasionally, the presynaptic terminals around the dendrites are distended
• this phenotype is mild at 4 months of age but becomes more severe with age
• malformations are more prominent in layers 2, 3, and 5 of the front-parietal region
• in 8 month old mutants a 30% loss of synapses is seen
• in 12 month old mutants, neurons in the fronto-parietal and hippocampal regions prominently display fragmentation and disruption of the neuritic processes
• neurons in the frontal cortex of 8 month old mutants have disarrayed microtubules, fragmented dendrites, and a distended and vacuolized endomembrane system and spinal apparatus




Genotype
MGI:3834756
hm3
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice fed a cholate-free diet containing 0.15% cholesterol for 6 months develop extensive lesions throughout the aorta; the extent of atherosclerosis in the entire aorta correlates with the size of lesions in the aortic origin
• a trend towards more lesions in males than females is observed
• on a high fat, high cholesterol diet, mutants exhibit moderate to severe aortic and carotid atherosclerosis

homeostasis/metabolism
• mice fed a cholate-free diet containing 0.15% cholesterol exhibit increased average total plasma cholesterol levels
• 4 of 4 aged mice (15-23 months) kept on a high fat, high cholesterol diet from 17 weeks of age develop cerebral xanthoma, consisting of crystalline cholesterol clefts, lipid globules and foam cells
• 2 of 9 mice on a normal diet develop small choroid plexus xanthomas




Genotype
MGI:3690368
hm4
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Gross appearance of aortic arches of Apoetm1Bres/Apoetm1Bres, Plgtm1Jld/Plgtm1Jld and Apoetm1Bres/Apoetm1Bres Plgtm1Jld/Plgtm1Jld mice

cardiovascular system
• 57 of 63 display aortic lesion at 18 to 25 weeks of age
• lesions contain fibrinogen deposits

homeostasis/metabolism
• small decrease in high density lipoprotein cholesterol




Genotype
MGI:2174913
ht5
Allelic
Composition
Apoetm1Bres/Apoe+
Genetic
Background
either: (involves: 129P2/OlaHsd * BALB/c) or (involves: 129P2/OlaHsd * C57BL/6J)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• a vitamin A-fat tolerance test suggests a mild defect in dietary fat clearance

homeostasis/metabolism
• total cholesterol is slightly but significantly elevated to 81 +/- 18 mg/dl compared to 60 +/- 20 mg/dl in wild-type mice
• on a high fat high cholesterol diet total cholesterol is not significantly different from wild-type mice




Genotype
MGI:3830965
cn6
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Bcl2tm1Irt/Bcl2tm1Irt
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Bcl2tm1Irt mutation (1 available); any Bcl2 mutation (41 available)
Lyz2tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• a higher level of intimal cell (macrophage) apoptosis is observed in atherosclerotic lesions relative to controls after receiving a Western diet for 10 weeks

cardiovascular system
N
• after 4 weeks on a Western diet, mice have similar lesion areas in proximal aortas and no or very rarely detected macrophage apoptosis in the lesions, very similar to pathology observed in controls
• 8 week-old mice fed a Western diet for 4 weeks display proximal aorta lesions similar to control animals
• necrotic areas observed in lesions are larger than observed in controls after receiving a Western diet for 10 weeks

homeostasis/metabolism
N
• mice show similar weights and levels of plasma lipoproteins to controls after 4 weeks on a Western diet

cellular
• a higher level of intimal cell (macrophage) apoptosis is observed in atherosclerotic lesions relative to controls after receiving a Western diet for 10 weeks

hematopoietic system
• a higher level of intimal cell (macrophage) apoptosis is observed in atherosclerotic lesions relative to controls after receiving a Western diet for 10 weeks




Genotype
MGI:4437892
cx7
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Esr1tm1Ksk/Esr1tm1Ksk
Genetic
Background
B6.129P2-Apoetm1Bres Esr1tm1Ksk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Esr1tm1Ksk mutation (2 available); any Esr1 mutation (67 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in ovariectomized females the ability of treatment with estradiol to inhibit lesion progression is impaired

homeostasis/metabolism
N
• unlike ovariectomized wild-type for Esr1, xanthoma formation is rarely seen
• in ovariectomized females exogenous estradiol treatment fails to reduce fasting plasma cholesterol

reproductive system
• in ovariectomized females implanted with estradiol




Genotype
MGI:5298859
cx8
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Cd59atm1Bpm/Cd59atm1Bpm
Genetic
Background
involves: 129 * 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Cd59atm1Bpm mutation (0 available); any Cd59a mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice fed a high-fat diet exhibit increased atherosclerotic plaque formation, decreased deposition of membrane attack complex, increased smooth muscle cells in early plaques, and decreased smooth muscle cells in advanced plaques compared with Apoetm1Bres homozygotes
• in advanced plaques of mice fed a high-fat diet
• in early plaques of mice fed a high-fat diet

muscle
• in advanced plaques of mice fed a high-fat diet
• in early plaques of mice fed a high-fat diet




Genotype
MGI:3527476
cx9
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Plautm1Mlg/Plautm1Mlg
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Plautm1Mlg mutation (3 available); any Plau mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• at >15 weeks of age, double homozygotes fed an atherogenic diet show only minimal destruction of the atherosclerotic aorta wall relative to Apoetm1Bres mice
• in double mutants, the media remain largely intact with continuous elastic membranes and multiple smooth-muscle cell layers; no infiltrating macrophages are detected, except at the base of the intimal plaque
• double mutants show no atherosclerotic aneurysmal dilation or rupture whereas Apoetm1Bres mice exhibit a >50% dilation in the diameter of the abdominal aorta
• at >15 weeks of age, double homozygotes fed an atherogenic diet display minimal fragmentation of the internal elastic membranes (EMs) in 10% of plaques; in contrast, Apoetm1Bres mice show fragmentation of EMs in 51% of plaques, and perforating transmedial ulceration in 21% of plaques




Genotype
MGI:5298860
cx10
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
C6Q0/C6Q0
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
C6Q0 mutation (1 available); any C6 mutation (56 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice fed a high-fat diet exhibit decreased atherosclerotic plaque formation and total vessel area affected compared with Apoetm1Bres homozygotes




Genotype
MGI:3691112
cx11
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Mapk8tm1Flv/Mapk8tm1Flv
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Mapk8tm1Flv mutation (3 available); any Mapk8 mutation (71 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• develop atherosclerosis similar to that seen in single Apoe homozygotes on a high-cholesterol diet for 14 weeks




Genotype
MGI:3691097
cx12
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Mapk9tm1Flv/Mapk9tm1Flv
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Mapk9tm1Flv mutation (2 available); any Mapk9 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• develop less atherosclerosis than single Apoe homozygotes when fed a high-cholesterol diet for 14 weeks

immune system
• isolated macrophages form filopodia-like projections in culture that are not observed in controls
• isolated peritoneal macrophages subjected to oxidized forms of low-density lipoproteins form only half as many foam cells as controls
• isolated peritoneal macrophages subjected to oxidized forms of low-density lipoproteins form only half as many foam cells as controls
• uptake and degradation of acetylated forms of low-density lipoproteins by macrophages is about one third that of controls
• cellular cholesterol efflux to apolipoprotein AI is increased in macrophages

hematopoietic system
• isolated macrophages form filopodia-like projections in culture that are not observed in controls
• isolated peritoneal macrophages subjected to oxidized forms of low-density lipoproteins form only half as many foam cells as controls
• isolated peritoneal macrophages subjected to oxidized forms of low-density lipoproteins form only half as many foam cells as controls
• uptake and degradation of acetylated forms of low-density lipoproteins by macrophages is about one third that of controls
• cellular cholesterol efflux to apolipoprotein AI is increased in macrophages

cellular
• isolated peritoneal macrophages subjected to oxidized forms of low-density lipoproteins form only half as many foam cells as controls




Genotype
MGI:2655399
cx13
Allelic
Composition
Apoa2tm1Bres/Apoa2+
Apoetm1Bres/Apoetm1Bres
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoa2tm1Bres mutation (1 available); any Apoa2 mutation (16 available)
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• 34% decrease in cholesterol levels compared to single Apoe homozygotes




Genotype
MGI:2655397
cx14
Allelic
Composition
Apoa2tm1Bres/Apoa2tm1Bres
Apoetm1Bres/Apoetm1Bres
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoa2tm1Bres mutation (1 available); any Apoa2 mutation (16 available)
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• 66% decrease in cholesterol levels compared to single Apoe homozygotes




Genotype
MGI:2450893
cx15
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Cx3cr1tm1Ifc/Cx3cr1tm1Ifc
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Cx3cr1tm1Ifc mutation (0 available); any Cx3cr1 mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• on a Western-type high-fat diet, double homozygotes show significant reductions in aortic atherosclerotic lesion area and thickness relative to single Apoe tm1Bres homozygotes (43%, 49%, and 36% at 5, 10, and 15 weeks, respectively)
• notably, double homozygotes exhibit retarded lesion development in both the aortic arch and thoracic/abdominal sections of the aorta; however, this difference is less pronounced in the arch

immune system
• after 10 weeks on a Western-type high-fat diet, double homozygotes exhibit a 40% reduction in macrophage infiltration of the aortic sinus relative to single Apoetm1Bres homozygotes

cellular
• after 10 weeks on a Western-type high-fat diet, double homozygotes exhibit a 40% reduction in macrophage infiltration of the aortic sinus relative to single Apoetm1Bres homozygotes

hematopoietic system
• after 10 weeks on a Western-type high-fat diet, double homozygotes exhibit a 40% reduction in macrophage infiltration of the aortic sinus relative to single Apoetm1Bres homozygotes




Genotype
MGI:3811013
cx16
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Ltb4r1tm1Adl/Ltb4r1tm1Adl
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Ltb4r1tm1Adl mutation (1 available); any Ltb4r1 mutation (20 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice exhibit a 55% reduced plaque burden compared to in Apoetm1Bres homozygotes
• when fed a Western diet, mice exhibit reduced plaque development, intimal area, and monocyte and T cell accumulation compared to in Apoetm1Bres homozygotes
• when fed a western diet, mice exhibit a 42.6% reduction in smooth muscle cells in the media and fibromuscular caps of lesions compared to in Apoetm1Bres homozygotes




Genotype
MGI:4838232
cx17
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Ifngr1tm1Agt/Ifngr1tm1Agt
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Ifngr1tm1Agt mutation (13 available); any Ifngr1 mutation (52 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• compared to in Apoetm1Bres homozygotes
• compared to in Apoetm1Bres homozygotes
• whether fed standard chow or a Western type diet, mice exhibit an increase in apoA-I levels compared to in wild-type mice

cardiovascular system
• with smaller lesions, reduced lesion lipid content, and decreased lesion cellularity compared to in Apoetm1Bres homozygotes




Genotype
MGI:3697329
cx18
Allelic
Composition
Apoc1tm2Lmh/Apoc1tm2Lmh
Apoetm1Bres/Apoetm1Bres
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoc1tm2Lmh mutation (0 available); any Apoc1 mutation (10 available)
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in controls, main cholesterol carrier is HDL and only ~10% is contained in the VLDL/LDL-sized fraction, while in mutants, most of the cholesterol (71%) is found in VLDL/LDL-sized fractions
• on a normal chow diet, mice are severely hypercholesterolemic compared to controls (12.5 mM vs 2.9 mM in controls)
• on mild high-fat/cholesterol (HFC) diet with 15% fat/0.25% cholesterol, serum cholesterol is increased 8-fold (to 31mM from 3.8 mM) with most of the increase found in VLDL/LDL-sized fractions




Genotype
MGI:3690365
cx19
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Plgtm1Jld/Plgtm1Jld
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Plgtm1Jld mutation (3 available); any Plg mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Gross appearance of aortic arches of Apoetm1Bres/Apoetm1Bres, Plgtm1Jld/Plgtm1Jld and Apoetm1Bres/Apoetm1Bres Plgtm1Jld/Plgtm1Jld mice

mortality/aging
• only about 50% survive beyond 20 weeks of age

growth/size/body
• exhibit a larger decrease in body weight after 2 months of age than single Plg homozygotes

cardiovascular system
• exhibit accelerated formation of and more extensive intimal lesions compared to single homozygous Apoe mutants
• lesions contain fibrinogen deposits

homeostasis/metabolism
• small reduction in HDL cholesterol




Genotype
MGI:3046828
cx20
Allelic
Composition
Apoetm1Bres/Apoetm1Bres
Fn1tm1Bwg/Fn1tm1Bwg
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Bres mutation (11 available); any Apoe mutation (145 available)
Fn1tm1Bwg mutation (1 available); any Fn1 mutation (129 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• on a high fat high cholesterol diet double homozygous mutants have reduced lesion area compared to Apoetm1Bres homozygotes

homeostasis/metabolism
• the cholesterol content of foam cells increases less in response to acetylated LDL compared to Apoetm1Bres homozygotes
• fasting VLDL cholesterol levels after maintenance on a high fat diet are decreased compared to Apoetm1Bres homozygotes





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