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Mice homozygous for the Apoetm1Unc mutation on the DBA/2J background may be useful in studies of diet-induced obesity without diabetes, Alzheimer's Disease, neurodegeneration, atherosclerosis and hypercholesterolemia.


The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Congenic; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BL/6
Donor Strain 129P2 via E14TG2a ES cell line
Generation Definitions
Donating Investigator IMR Colony,   The Jackson Laboratory

Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged APOE deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

The Apoetm1Unc mutant strain was developed in the laboratory of Dr. Nobuyo Maeda at The University of North Carolina at Chapel Hill. The 129-derived E14Tg2a ES cell line was used. The plasmid used is designated as pNMC109 and the founder line is T-89 in the primary reference. The mice were backcrossed to C57BL/6J for 10 generation and then backcrossed to DBA/2J for 5 generations (using a speed congenic protocol) before being made homozygous.

Control Information

   Wild-type from the colony
   000671 DBA/2J
  Considerations for Choosing Controls

Related Strains

Alzheimer's Disease Models
005987   129-Achetm1Loc/J
006409   129S1.129(Cg)-Tg(APPSw)40Btla/Mmjax
008077   129S1/Sv-Bchetm1Loc/J
016198   129S6.Cg-Tg(Camk2a-tTA)1Mmay/JlwsJ
014556   129S6/SvEv-Apoetm4Mae/J
006555   A.129(B6)-Tg(APPSw)40Btla/Mmjax
005708   B6.129-Apbb1tm1Quhu/J
004714   B6.129-Bace1tm1Pcw/J
004098   B6.129-Klc1tm1Gsn/J
004193   B6.129-Psen1tm1Mpm/J
003615   B6.129-Psen1tm1Shn/J
005300   B6.129-Tg(APPSw)40Btla/Mmjax
005617   B6.129P-Psen2tm1Bdes/J
002609   B6.129P2-Nos2tm1Lau/J
007685   B6.129P2-Psen1tm1Vln/J
007999   B6.129P2-Sorl1Gt(Ex255)Byg/J
008087   B6.129S1-Bchetm1Loc/J
002509   B6.129S2-Plautm1Mlg/J
005301   B6.129S2-Tg(APP)8.9Btla/J
004163   B6.129S4-Cdk5r1tm1Lht/J
010959   B6.129S4-Grk5tm1Rjl/J
010960   B6.129S4-Grk5tm2Rjl/J
002213   B6.129S4-Ngfrtm1Jae/J
006406   B6.129S4-Tg(APPSwLon)96Btla/Mmjax
006469   B6.129S4-Tg(PSEN1H163R)G9Btla/J
012564   B6.129S5-Dhcr24tm1Lex/SbpaJ
004142   B6.129S7-Aplp2tm1Dbo/J
004133   B6.129S7-Apptm1Dbo/J
007251   B6.129X1-Mapttm1Hnd/J
013040   B6.Cg-Apoetm1Unc Ins2Akita/J
005642   B6.Cg-Clutm1Jakh/J
005491   B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
009126   B6.Cg-Nos2tm1Lau Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
005866   B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/Mmjax
008730   B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
005864   B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
007575   B6.Cg-Tg(CAG-Ngb,-EGFP)1Dgrn/J
016197   B6.Cg-Tg(CAG-OTC/CAT)4033Prab/J
005855   B6.Cg-Tg(Camk2a-Prkaca)426Tabe/J
007004   B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ
004996   B6.Cg-Tg(DBH-Gal)1923Stei/J
007673   B6.Cg-Tg(Gad1-EGFP)3Gfng/J
004662   B6.Cg-Tg(PDGFB-APP)5Lms/J
006293   B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2Mmjax
006006   B6.Cg-Tg(Prnp-APP)A-2Dbo/J
008596   B6.Cg-Tg(Prnp-Abca1)EHol/J
006005   B6.Cg-Tg(Prnp-App/APPswe)E1-2Dbo/Mmjax
007180   B6.Cg-Tg(Prnp-ITM2B/APP695*40)1Emcg/J
007182   B6.Cg-Tg(Prnp-ITM2B/APP695*42)A12Emcg/J
005999   B6.Cg-Tg(SBE/TK-luc)7Twc/J
012597   B6.Cg-Tg(Thy1-COL25A1)861Yfu/J
007051   B6.Cg-Tg(tetO-APPSwInd)102Dbo/Mmjax
007052   B6.Cg-Tg(tetO-APPSwInd)107Dbo/Mmjax
007049   B6.Cg-Tg(tetO-APPSwInd)885Dbo/Mmjax
009337   B6.FVB-Tg(Prnp-RTN3)2Yanr/J
006394   B6;129-Apba2tm1Sud Apba3tm1Sud Apba1tm1Sud/J
008364   B6;129-Chattm1(cre/ERT)Nat/J
008476   B6;129-Ncstntm1Sud/J
004807   B6;129-Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Mmjax
007605   B6;129P-Psen1tm1Vln/J
005618   B6;129P2-Bace2tm1Bdes/J
008333   B6;129P2-Dldtm1Ptl/J
002596   B6;129P2-Nos2tm1Lau/J
003822   B6;129S-Psen1tm1Shn/J
012639   B6;129S4-Mapttm3(HDAC2)Jae/J
012869   B6;129S6-Apbb2tm1Her/J
006410   B6;129S6-Chattm2(cre)Lowl/J
005993   B6;129S6-Pcsk9tm1Jdh/J
008636   B6;C-Tg(Prnp-APP695*/EYFP)49Gsn/J
007002   B6;C3-Tg(Prnp-ITM2B/APP695*42)A12Emcg/Mmjax
008169   B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J
000231   B6;C3Fe a/a-Csf1op/J
008850   B6;SJL-Tg(Mt1-LDLR)93-4Reh/AgnJ
003378   B6C3-Tg(APP695)3Dbo Tg(PSEN1)5Dbo/J
004462   B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
003741   B6D2-Tg(Prnp-MAPT)43Vle/J
016556   B6N.129-Ptpn5tm1Pjlo/J
018957   B6N.129S6(B6)-Chattm2(cre)Lowl/J
024841   B6N.Cg-Tg(Prnp-MAPT*P301S)PS19Vle/J
006554   B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
012621   C.129S(B6)-Chrna3tm1.1Hwrt/J
002328   C.129S2-Plautm1Mlg/J
003375   C3B6-Tg(APP695)3Dbo/Mmjax
005087   C57BL/6-Tg(Camk2a-IDE)1Selk/J
005086   C57BL/6-Tg(Camk2a-MME)3Selk/J
008833   C57BL/6-Tg(Camk2a-UBB)3413-1Fwvl/J
007027   C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
010800   C57BL/6-Tg(Thy1-PTGS2)300Kand/J
010703   C57BL/6-Tg(Thy1-PTGS2)303Kand/J
005706   C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J
006618   C57BL/6-Tg(tetO-COX8A/EYFP)1Ksn/J
007677   CB6-Tg(Gad1-EGFP)G42Zjh/J
007072   CByJ.129P2(B6)-Nos2tm1Lau/J
006472   D2.129(B6)-Tg(APPSw)40Btla/Mmjax
013719   D2.Cg-Apoetm1Unc Ins2Akita/J
003718   FVB-Tg(GadGFP)45704Swn/J
013732   FVB-Tg(NPEPPS)1Skar/J
013156   FVB-Tg(tetO-CDK5R1*)1Vln/J
015815   FVB-Tg(tetO-MAPT*P301L)#Kha/JlwsJ
002329   FVB.129S2-Plautm1Mlg/J
025105   FVB.Cg-Tg(Camk2a-tTA)1Mmay/DboJ
003753   FVB/N-Tg(Eno2CDK5R1)1Jdm/J
006143   FVB/N-Tg(Thy1-cre)1Vln/J
025104   FVB/N-Tg(tetO/Prnp-MAPT*P301L,-luc)Y74Dbo/J
008051   NOD.129P2(B6)-Ctsbtm1Jde/RclJ
008390   STOCK Apptm1Sud/J
012640   STOCK Hdac2tm1.2Rdp/J
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
004779   STOCK Mapttm1(EGFP)Klt/J
014092   STOCK Tg(ACTB-tTA2,-MAPT/lacZ)1Luo/J
014544   STOCK Tg(tetO-ABL1*P242E*P249E)CPdav/J
View Alzheimer's Disease Models     (111 strains)

View Strains carrying   Apoetm1Unc     (15 strains)

View Strains carrying other alleles of Apoe     (5 strains)

Additional Web Information

Visit the Alzheimer's Disease Mouse Model Resource site for helpful information on Alzheimer's Disease and research resources.


Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Apolipoprotein E; APOE
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Alzheimer Disease 2   (APOE)
Alzheimer Disease 4   (APOE)
Lipoprotein Glomerulopathy; LPG   (APOE)
Macular Degeneration, Age-Related, 1; ARMD1   (APOE)
Sea-Blue Histiocyte Disease   (APOE)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.


        involves: 129P2/OlaHsd * C57BL/6
  • homeostasis/metabolism phenotype
  • increased circulating triglyceride level
    • circulating triglyceride levels are 39% higher than in wild-type controls   (MGI Ref ID J:16573)


  • mortality/aging
  • premature death
    • 35% dead by 18 months   (MGI Ref ID J:73202)
  • cardiovascular system phenotype
  • abnormal aorta wall morphology
    • endothelial nitric oxide synthase (eNOS) in mutant aortic wall is distinctly reduced   (MGI Ref ID J:101576)
    • Cx43 distribution at cell-cell junction shows significant disruption   (MGI Ref ID J:142083)
  • abnormal blood flow velocity
    • anesthetized homozygotes show significantly increased transaortic blood velocities relative to wild-type mice with peak aortic velocity at 133.4 7.8 cm/s vs 89.2 5.8 cm/s, and mean aortic velocity at 35.9 2.7 vs 22.0 1.6 cm/s, respectively   (MGI Ref ID J:108154)
    • in addition, anesthetized homozygotes show significantly increased transmitral blood velocities relative to wild-type mice with peak mitral velocities at 92 7.2 cm/s vs 47.2 5.3 cm/s, and mean mitral velocities at 20.6 1.7 vs 11.4 1.3 cm/s, respectively   (MGI Ref ID J:108154)
    • no significant differences in heart rate, peak aortic acceleration or ejection time are observed in the conscious or anesthetized state, when normalized to body weight   (MGI Ref ID J:108154)
    • however, homozygotes show alterations in aortic arch acceleration suggestive of increased peripheral wave reflections   (MGI Ref ID J:108154)
  • abnormal blood vessel physiology
    • pulse wave velocity is insignificantly elevated at 4 months   (MGI Ref ID J:60364)
    • pulse wave velocity significantly elevated at 13 months   (MGI Ref ID J:60364)
    • abnormal blood-brain barrier function
      • impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex   (MGI Ref ID J:69455)
    • decreased vasodilation
      • homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice   (MGI Ref ID J:101576)
    • vascular inflammation
      • aortae show macrophage and T cell extravasation within atherosclerotic lesions   (MGI Ref ID J:91058)
  • abnormal kidney arterial blood vessel morphology
    • arterioles of the vascular pole show a "foamy" degeneration of smooth muscle cells   (MGI Ref ID J:125978)
  • abnormal spiral modiolar artery morphology
    • homozygotes fed an atherosclerotic diet develop atherosclerotic alterations in the spiral modiolar artery (SMA)   (MGI Ref ID J:101576)
    • in contrast, no such changes are detected in the SMA of homozygotes fed a normal diet   (MGI Ref ID J:101576)
    • spiral modiolar artery stenosis
      • lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal diet   (MGI Ref ID J:101576)
  • arteriosclerosis
    • homozygotes exhibit a 13% increase in aortic pulse-wave velocity (PWV) relative to wild-type mice (428 14.5 cm/s vs 379 10.1 cm/s), indicating increased arterial stiffness and reduced vascular elasticity   (MGI Ref ID J:108154)
    • atherosclerotic lesions   (MGI Ref ID J:133606)
      • advanced atherosclerotic lesions; massive atheromas with abundant cholesterol crystals, neutral lipids, and diminished extracellular matrix in arotic roots and coronary arteries   (MGI Ref ID J:73202)
      • at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation   (MGI Ref ID J:108154)
      • lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions   (MGI Ref ID J:108154)
      • regular exercise does not reduce atherosclerotic lesion formation in homozygotes, as shown by a comparable % oil red-O staining of whole aortas from sedentary and exercised mutant mice   (MGI Ref ID J:97385)
      • at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta   (MGI Ref ID J:101576)
      • the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet   (MGI Ref ID J:101576)
      • plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes   (MGI Ref ID J:101576)
      • 23% of luminal surface in the aortic arch and thoracic aorta is covered by plaques at 4 months of age   (MGI Ref ID J:60364)
      • 61% covered by plaques at 13 months of age   (MGI Ref ID J:60364)
      • thickened intima, foam cell accumulation and thin collagen cap   (MGI Ref ID J:60364)
      • focal fragmentation of elastic laminae   (MGI Ref ID J:60364)
      • intimal lesions are observed in atherosclerotic aortas in mutants   (MGI Ref ID J:105736)
      • major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch   (MGI Ref ID J:142083)
      • lesions comprise around 14-16% of total aortic arch area in male and female mutants   (MGI Ref ID J:142083)
      • aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area   (MGI Ref ID J:142083)
      • increased susceptibility to atherosclerosis
        • severity of atherosclerosis is 2-fold and 99-fold higher in atherosclerotic diet homozygotes than in normal diet homozygotes and C57BL/6J control mice, respectively   (MGI Ref ID J:101576)
        • on a high fat, high cholesterol diet, mutants exhibit moderate to severe aortic and carotid atherosclerosis   (MGI Ref ID J:43846)
  • cardiac hypertrophy
    • at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild-type mice   (MGI Ref ID J:108154)
  • decreased systemic vascular resistance
    • under anesthesia, homozygotes appear to exhibit significantly reduced peripheral vascular resistance and compliance in the presence of normal blood pressures   (MGI Ref ID J:108154)
  • dilated glomerular capillary
    • at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries   (MGI Ref ID J:125978)
  • glomerular capillary thrombosis
    • lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice   (MGI Ref ID J:125978)
    • such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium   (MGI Ref ID J:125978)
  • increased cardiac output
    • under anesthesia, homozygotes exhibit elevated flow velocities suggesting elevated cardiac output   (MGI Ref ID J:108154)
  • increased cardiac stroke volume
    • under anesthesia, homozygotes appear to exhibit significantly increased stroke volume   (MGI Ref ID J:108154)
  • increased heart weight
    • at 13 months, homozygotes show a 23% increase in heart weight relative to wild-type mice (186 7.1 vs. 151 2.5 mg)   (MGI Ref ID J:108154)
  • kidney microaneurysm
    • at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries   (MGI Ref ID J:125978)
  • vascular stenosis
    • vascular stenosis is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet   (MGI Ref ID J:101576)
    • spiral modiolar artery stenosis
      • lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal diet   (MGI Ref ID J:101576)
  • muscle phenotype
  • decreased vasodilation
    • homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice   (MGI Ref ID J:101576)
  • impaired muscle relaxation
    • relaxation response to acetylcholine in blood vessels is significantly attenuated at 13 months of age   (MGI Ref ID J:60364)
    • maximal response to acetylcholine is considerably reduced   (MGI Ref ID J:60364)
  • homeostasis/metabolism phenotype
  • abnormal circulating cholesterol level
    • decreased HDL/total cholesterol ratio   (MGI Ref ID J:73202)
    • decreased HDL/LDL ratio   (MGI Ref ID J:73202)
    • decreased circulating HDL cholesterol level   (MGI Ref ID J:91058)
    • increased circulating cholesterol level   (MGI Ref ID J:91058)
      • increasing with age; 4-fold increase in plasma total cholesterol levels in 10-12 week old mutants and 13-fold increase at 29 weeks   (MGI Ref ID J:73202)
      • exercise (15 or 60 min/day swim) causes no significant changes in total cholesterol levels among homozygotes or wild-type mice relative to sedentary, genotype-matched controls   (MGI Ref ID J:97385)
      • on a normal diet, homozygotes display significantly increased plasma total cholesterol (TC) levels relative to C57BL/6J control mice   (MGI Ref ID J:101576)
      • on an atherosclerotic diet, homozygotes show a further significant increase in plasma TC levels relative to homozygotes on a normal diet   (MGI Ref ID J:101576)
      • 5 fold increase in total cholesterol at 24 and 36 weeks   (MGI Ref ID J:125978)
      • total serum cholesterol 70 fold higher than controls on a normal diet   (MGI Ref ID J:104609)
      • total serum cholesterol 20 fold higher than controls on high fat diet where controls show 4 fold increase over normal diet   (MGI Ref ID J:104609)
      • significantly increased relative to wild-type controls at 24 weeks of age; levels in mutants after induction of chronic graft versus host disease (cGVH) to induce systemic lupus erythematosus (SLE) are equivalent to the Apoe-null mice   (MGI Ref ID J:133606)
      • increased circulating LDL cholesterol level   (MGI Ref ID J:91058)
        • on a normal diet, homozygotes display significantly increased plasma LDL cholesterol levels relative to C57BL/6J control mice   (MGI Ref ID J:101576)
        • on an atherosclerotic diet, homozygotes show a further significant increase in plasma LDL levels relative to homozygotes on a normal diet   (MGI Ref ID J:101576)
      • increased circulating VLDL cholesterol level   (MGI Ref ID J:91058)
        • on a normal diet, homozygotes display significantly increased plasma VLDL cholesterol levels relative to C57BL/6J control mice   (MGI Ref ID J:101576)
        • on an atherosclerotic diet, homozygotes show a further significant increase in plasma VLDL cholesterol levels relative to homozygotes on a normal diet   (MGI Ref ID J:101576)
  • abnormal circulating homocysteine level
    • decrease in plasma total homocysteine levels   (MGI Ref ID J:73202)
  • abnormal enzyme/coenzyme activity
    • activity of cholesterol synthesis enzyme HMG-CoA reductase is reduced up to 60% in aging mice compared to 30% in wild-type aging mice   (MGI Ref ID J:73202)
  • decreased circulating glucose level   (MGI Ref ID J:73202)
  • decreased circulating triglyceride level   (MGI Ref ID J:93987)
  • glomerular capillary thrombosis
    • lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice   (MGI Ref ID J:125978)
    • such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium   (MGI Ref ID J:125978)
  • hyperlipidemia
    • homozygotes develop hyperlipidemia; however, HDL cholesterol levels, body weight and blood glucose remain unchanged relative to C57BL/6J control mice on a normal diet, with no further differences noted on an atheroscletoric diet   (MGI Ref ID J:101576)
  • increased circulating triglyceride level   (MGI Ref ID J:91058)
    • 2-fold increase in plasma triglyceride levels in 10-12 week old mutants   (MGI Ref ID J:73202)
    • on a normal diet, homozygotes display significantly increased plasma triglyceride levels relative to C57BL/6J control mice   (MGI Ref ID J:101576)
    • on an atherosclerotic diet, homozygotes show a further significant increase in plasma triglyceride levels relative to homozygotes on a normal diet   (MGI Ref ID J:101576)
  • xanthoma
    • 1 of 11 aged mice on a normal diet develops cerebral xanthoma   (MGI Ref ID J:43846)
    • eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components   (MGI Ref ID J:73202)
  • growth/size/body region phenotype
  • decreased body length
    • nose to rump length less than controls at both 1 and 3 months   (MGI Ref ID J:136630)
  • decreased body weight   (MGI Ref ID J:60364)
    • at 13 months, homozygotes show a 22% reduction in body weight relative to wild-type mice (34.5 0.9 vs. 44.5 1.1 g)   (MGI Ref ID J:108154)
  • increased susceptibility to weight gain
    • body weight was less than controls at 3 months but identical at 8 months   (MGI Ref ID J:136630)
  • hematopoietic system phenotype
  • abnormal B cell activation
    • spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23   (MGI Ref ID J:133606)
  • abnormal T cell number
    • increased numbers of cytokine producing T cells   (MGI Ref ID J:47027)
    • abnormal CD4-positive, alpha beta T cell number   (MGI Ref ID J:108154)
      • clusters of CD4+ cells found in fatty streak lesions   (MGI Ref ID J:47027)
      • ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet   (MGI Ref ID J:47027)
      • increased T-helper 2 cell number   (MGI Ref ID J:47027)
  • decreased follicular B cell number
    • decreased relative to controls   (MGI Ref ID J:133606)
  • decreased hematocrit
    • at 13 months, awake, unanesthetized homozygotes display slightly but significantly reduced hematocrits ( 11%) relative to wild-type mice at 41.7 1.1% vs 46.6 0.4%; in contrast, systolic blood pressures remain unaffected (140 7.6 mmHg vs 136 7.4 mmHg)   (MGI Ref ID J:108154)
  • decreased marginal zone B cell number
    • with induction of SLE by cGVH, levels are slightly decreased compared to wild-type   (MGI Ref ID J:133606)
  • increased B cell number
    • newly formed B cells are significantly increased compared to wild-type   (MGI Ref ID J:133606)
    • increased marginal zone B cell number
      • increased 2-fold compared to wild-type   (MGI Ref ID J:133606)
  • increased immunoglobulin level
    • mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants   (MGI Ref ID J:133606)
    • increased IgM level
      • IgM response to tetanus toxoid is significantly increased as compared to controls   (MGI Ref ID J:61564)
  • increased spleen weight
    • increased spleen weight while the thymus weight remains normal   (MGI Ref ID J:61564)
  • cellular phenotype
  • oxidative stress
    • regular exercise fails to reduce endogenous oxidant load and mitochondrial damage in hypercholesterolemic mutant mice   (MGI Ref ID J:97385)
    • in contrast, regular exercise results in reduced mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities in normocholesterolemic control mice   (MGI Ref ID J:97385)
  • hearing/vestibular/ear phenotype
  • abnormal cochlea morphology
    • endothelial nitric oxide synthase (eNOS) in mutant cochlea is distinctly reduced   (MGI Ref ID J:101576)
    • abnormal basilar membrane morphology
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic basilar membrane   (MGI Ref ID J:101576)
    • abnormal stria vascularis morphology
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic stria vascularis   (MGI Ref ID J:101576)
    • abnormal tectorial membrane morphology
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic tectorial membrane   (MGI Ref ID J:101576)
    • cochlear inner hair cell degeneration
      • at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn   (MGI Ref ID J:101576)
      • IHC loss at the base turn is exacerbated by an atherosclerotic diet   (MGI Ref ID J:101576)
    • cochlear outer hair cell degeneration
      • at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn   (MGI Ref ID J:101576)
      • OHC loss at the base turn is exacerbated by an atherosclerotic diet   (MGI Ref ID J:101576)
    • organ of Corti degeneration
      • at 24 weeks, homozygotes fed a normal diet show significant degeneration of the organ of Corti in the basal turn while the middle turn is relatively normal   (MGI Ref ID J:101576)
      • degeneration of the organ of Corti is excerbated by an atherosclerotic diet, with complete loss noted in the basal turn in some animals   (MGI Ref ID J:101576)
  • deafness
    • homozygotes fed a normal diet display hearing loss esp. at high frequencies as compared with C57BL/6J control mice   (MGI Ref ID J:101576)
    • a high positive correlation between ABR thresholds at 16 and 8 kHz, or click and atherosclerotic lesions, and atherosclerotic plaque area of the aorta, and plasma total choelsterol levels is observed in both normal diet and high-fat diet homozygotes   (MGI Ref ID J:101576)
  • increased or absent threshold for auditory brainstem response
    • at 10 weeks, homozygotes fed a normal diet display higher ABR thresholds than C57BL/6J control mice at all test frequencies, with more hearing loss noted at 32 kHz; by 24 weeks, further hearing loss is detected at all test stimuli levels   (MGI Ref ID J:101576)
    • homozygotes fed an atherosclerotic diet show higher ABR thresholds than homozygotes fed a normal diet   (MGI Ref ID J:101576)
  • nervous system phenotype
  • abnormal blood-brain barrier function
    • impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex   (MGI Ref ID J:69455)
  • cochlear ganglion degeneration
    • at 24 weeks, homozygotes fed a normal diet show a reduced number of spiral ganglion cells in the basal turn of the cochlea   (MGI Ref ID J:101576)
    • loss of ganglion cells is excerbated by an atherosclerotic diet   (MGI Ref ID J:101576)
  • cochlear inner hair cell degeneration
    • at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn   (MGI Ref ID J:101576)
    • IHC loss at the base turn is exacerbated by an atherosclerotic diet   (MGI Ref ID J:101576)
  • cochlear outer hair cell degeneration
    • at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn   (MGI Ref ID J:101576)
    • OHC loss at the base turn is exacerbated by an atherosclerotic diet   (MGI Ref ID J:101576)
  • immune system phenotype
  • abnormal immune system morphology   (MGI Ref ID J:47027)
    • abnormal T cell number
      • increased numbers of cytokine producing T cells   (MGI Ref ID J:47027)
      • abnormal CD4-positive, alpha beta T cell number   (MGI Ref ID J:108154)
        • clusters of CD4+ cells found in fatty streak lesions   (MGI Ref ID J:47027)
        • ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet   (MGI Ref ID J:47027)
        • increased T-helper 2 cell number   (MGI Ref ID J:47027)
    • decreased follicular B cell number
      • decreased relative to controls   (MGI Ref ID J:133606)
    • decreased marginal zone B cell number
      • with induction of SLE by cGVH, levels are slightly decreased compared to wild-type   (MGI Ref ID J:133606)
    • increased B cell number
      • newly formed B cells are significantly increased compared to wild-type   (MGI Ref ID J:133606)
      • increased marginal zone B cell number
        • increased 2-fold compared to wild-type   (MGI Ref ID J:133606)
    • increased spleen weight
      • increased spleen weight while the thymus weight remains normal   (MGI Ref ID J:61564)
  • abnormal immune system physiology   (MGI Ref ID J:61564)
    • abnormal B cell activation
      • spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23   (MGI Ref ID J:133606)
    • abnormal immune serum protein physiology   (MGI Ref ID J:61564)
      • decreased interferon-gamma secretion
        • production is reduced when fed a high cholesterol diet   (MGI Ref ID J:47027)
      • increased immunoglobulin level
        • mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants   (MGI Ref ID J:133606)
        • increased IgM level
          • IgM response to tetanus toxoid is significantly increased as compared to controls   (MGI Ref ID J:61564)
    • decreased susceptibility to type IV hypersensitivity reaction
      • decreased antigen specific delayed hypersensitivity response   (MGI Ref ID J:61564)
    • increased autoantibody level
      • after induction of cGVH-SLE, IgG and IgM anti-oxidized LDL and anti-cardiolipin antibodies are increased compared to wild-type or Apoe-null controls   (MGI Ref ID J:133606)
      • increased anti-nuclear antigen antibody level
        • after induction of cGVH-SLE, mice display greatly increased levels of anti-chromatin antibodies compared to wild-type controls or non-cGVH mutants   (MGI Ref ID J:133606)
        • increased anti-double stranded DNA antibody level
          • after induction of cGVH-SLE, mice display greatly increased levels compared to wild-type controls or non-cGVH-SLE mutants   (MGI Ref ID J:133606)
    • increased susceptibility to systemic lupus erythematosus   (MGI Ref ID J:133606)
    • vascular inflammation
      • aortae show macrophage and T cell extravasation within atherosclerotic lesions   (MGI Ref ID J:91058)
  • behavior/neurological phenotype
  • abnormal spatial learning
    • longer latency to find the platform in Morris maze tests   (MGI Ref ID J:120203)
    • slow to acquire a preference for the target quadrant and the magnitude of the preference is always less than controls   (MGI Ref ID J:120203)
  • increased thigmotaxis
    • elevated thigmotaxis in Morris maze tests   (MGI Ref ID J:120203)
  • renal/urinary system phenotype
  • abnormal kidney arterial blood vessel morphology
    • arterioles of the vascular pole show a "foamy" degeneration of smooth muscle cells   (MGI Ref ID J:125978)
  • abnormal renal glomerulus morphology
    • increased glomerular tuft area   (MGI Ref ID J:125978)
    • glomerular cell numbers are increased   (MGI Ref ID J:125978)
    • dilated glomerular capillary
      • at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries   (MGI Ref ID J:125978)
    • expanded mesangial matrix
      • progressive increase in glomerular matrix, already evident at 24 weeks, associated with accumulation of laminin and collagen IV   (MGI Ref ID J:125978)
    • glomerular capillary thrombosis
      • lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice   (MGI Ref ID J:125978)
      • such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium   (MGI Ref ID J:125978)
    • mesangiolysis
      • loss of mesangial matrix sometimes at 36 weeks but never at 24 weeks or in controls   (MGI Ref ID J:125978)
    • renal glomerulus lipidosis
      • glomerular foam cells in the mesangium, capillary lumina and within the glomerular stalk close to the vascular pole   (MGI Ref ID J:125978)
      • lipid deposits in arteriolar walls in the vascular poles   (MGI Ref ID J:125978)
      • lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice   (MGI Ref ID J:125978)
  • kidney microaneurysm
    • at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries   (MGI Ref ID J:125978)
  • liver/biliary system phenotype
  • abnormal liver physiology
    • no significant change in serum alanine transaminase with high fat diet as is seen in controls (marker for liver damage)   (MGI Ref ID J:104609)
    • hepatic uptake of LDL is increased two fold   (MGI Ref ID J:104609)
  • vision/eye phenotype
  • abnormal eye electrophysiology   (MGI Ref ID J:84688)
    • implicit times increased for a and b waves of dark adapted electroretinogram   (MGI Ref ID J:70245)
    • wave amplitudes attenuated for a and b waves of dark adapted electroretinogram   (MGI Ref ID J:70245)
  • abnormal retinal inner nuclear layer morphology
    • perinuclear vacuolation on a high cholesterol diet   (MGI Ref ID J:70245)
    • thin retinal inner nuclear layer
      • cell numbers reduced   (MGI Ref ID J:70245)
  • thin retinal outer nuclear layer
    • cell numbers reduced   (MGI Ref ID J:70245)
  • taste/olfaction phenotype
  • impaired olfaction
    • preference for plain water over 0.1% iso-amyl alcohol moderate compared to the strong preference shown by controls   (MGI Ref ID J:89344)
    • slower than control to find buried food pellet although found pellets visually more rapidly   (MGI Ref ID J:89344)
    • latency to taste vanillin-cued quinine significantly increased only at day 5   (MGI Ref ID J:89344)
  • skeleton phenotype
  • abnormal bone structure   (MGI Ref ID J:111209)
    • increased bone mineral density
      • higher bone mineralization density in vertebral bodies   (MGI Ref ID J:111209)
      • increased bone volume to tissue volume ratio   (MGI Ref ID J:111209)
    • increased bone trabecula number
      • increased number of trabeculae   (MGI Ref ID J:111209)
    • increased compact bone thickness
      • in vertebral bodies and tibia   (MGI Ref ID J:111209)
  • abnormal skeleton physiology   (MGI Ref ID J:111209)
    • abnormal osteoblast physiology
      • increased rate of bone formation   (MGI Ref ID J:111209)
  • respiratory system phenotype
  • abnormal lung hysteresivity
    • percent increase in hysteresivity with age greater than in controls   (MGI Ref ID J:136630)
  • abnormal lung volume
    • lung volume similar to controls at 3 months but 2.5 fold greater at 8 months of age   (MGI Ref ID J:136630)
  • abnormal pulmonary alveolus morphology
    • fewer but larger alveoli at 3 months of age   (MGI Ref ID J:136630)
    • less surface area to volume   (MGI Ref ID J:136630)
  • increased airway resistance
    • resistance to airflow greater than controls at 3 months but not at 8 months of age   (MGI Ref ID J:136630)
  • increased lung compliance
    • dynamic and static compliance greater than controls at 8 months of age   (MGI Ref ID J:136630)
  • integument phenotype
  • skin lesions
    • progressive skin lesions, mainly seen as eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components   (MGI Ref ID J:73202)


        involves: 129P2/OlaHsd * C57BL/6
  • cardiovascular system phenotype
  • atherosclerotic lesions
    • greater than in wild-type   (MGI Ref ID J:80689)
    • fatty streaks with foam cells are found in the proximal aorta of 3-8 month old mice fed normal chow   (MGI Ref ID J:16573)
    • the foam cells are often adjacent to valve attachment sites and can form multi-layers   (MGI Ref ID J:16573)
    • lesions get bigger with age and near total occlusion at the entrance of a coronary artery can be observed at 8 months of age   (MGI Ref ID J:16573)
    • 75% of mice develop lesions in the aortic arch with most females and some males having calcification within the lesions   (MGI Ref ID J:40136)
    • aortic cartilaginous metaplasia is noted in the most severely affected mice   (MGI Ref ID J:40136)
  • homeostasis/metabolism phenotype
  • decreased circulating HDL cholesterol level
    • mean HDL levels (33 mg/dl) are 45% of that found in controls   (MGI Ref ID J:16573)
  • hyperlipidemia
    • relative to wild-type   (MGI Ref ID J:80689)
  • increased circulating cholesterol level
    • relative to wild-type   (MGI Ref ID J:80689)
    • mean total cholesterol levels are elevated about 5-fold over wild-type to 434 mg/dl   (MGI Ref ID J:16573)
    • total cholesterol levels are about 4-fold higher than controls with a mean of 379 mg/dl   (MGI Ref ID J:40136)
    • increased circulating LDL cholesterol level
      • mice have elevated levels of LDL in the blood   (MGI Ref ID J:16573)
    • increased circulating VLDL cholesterol level
      • the majority of lipoprotein particles in the blood are in the VLDL size range   (MGI Ref ID J:16573)
  • increased circulating triglyceride level
    • relative to wild-type   (MGI Ref ID J:80689)
    • circulating triglyceride levels are 123 mg/dl compared to 73 mg/dl in controls   (MGI Ref ID J:16573)
  • increased prostaglandin level
    • amount of PGE2 in aortas is 4X higher than in controls   (MGI Ref ID J:125376)
    • PGE2 level doubles on a high fat diet   (MGI Ref ID J:125376)
  • nervous system phenotype
  • abnormal astrocyte physiology
    • astrocytes secrete less phospholipids or free cholesterol compared to wild-type astrocytes   (MGI Ref ID J:58019)
  • abnormal synapse morphology
    • elevated cholesterol in the exofacial leaflet of the synaptic plasma membrane but not so high as for Ldlr deficient mice   (MGI Ref ID J:43043)
    • cholesterol levels in the cytofacial leaflet are reduced   (MGI Ref ID J:43043)
  • immune system phenotype
  • lung inflammation
    • isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding   (MGI Ref ID J:83615)
  • respiratory system phenotype
  • lung inflammation
    • isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding   (MGI Ref ID J:83615)


        either: B6.129P2-Apoetm1Unc/J or (involves: 129P2/OlaHsd * C57BL/6J * ICR)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • no alterations in passive avoidance learning are observed; coordination levels measured in rotorod tests are similar to wild-type   (MGI Ref ID J:100975)
    • abnormal spatial learning
      • 6-month old female mice show subtle learning impairment in water maze task compared to transgenic mutants; 6-month old males show significantly decreased learning ability in the Morris water maze test   (MGI Ref ID J:100975)
    • decreased vertical activity
      • mice have fewer rearing events and shorter rearing times than wild-type controls   (MGI Ref ID J:100975)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • mice exhibit age-dependent loss of synaptophysin-reactive terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus mice exhibit age-dependent loss of synaptophysin-reactive terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus, similar to wild-type   (MGI Ref ID J:100975)
    • upon 18 mg/kg kainic acid injection, significant loss of neocortical synaptophysin-positive presynaptic terminals and disruption of hippocampal axons are observed, similar to wild-type   (MGI Ref ID J:55835)
    • mice show significant loss of synaptophysin-positive presynaptic terminals and neuronal dendrites of the neocortex and hippocampus with age (7-9 months compared to 3-4 months) mice show significant loss of synaptophysin-positive presynaptic terminals and neuronal dendrites of the neocortex and hippocampus with age (7-9 months compared to 3-4 months), similar to wild-type   (MGI Ref ID J:55835)


        involves: 129P2/OlaHsd
  • behavior/neurological phenotype
  • increased anxiety-related response
    • in the elevated-plus maze, mice show increased anxiety with reduced time and distance moved in the open arms; mice have significantly lower number of open-arm entries than wild-type   (MGI Ref ID J:101973)
    • effect is age-dependent; phenotype is present in older mice, but not in young 2-4 month-old mice   (MGI Ref ID J:101973)
  • increased startle reflex
    • response is higher in mice at 6 months of age compared to wild-type   (MGI Ref ID J:101973)
  • homeostasis/metabolism phenotype
  • abnormal circulating cholesterol level
    • circulating VLDL/LDL cholesterol levels are increased compared to in Apobec1tm1Chan homozygotes and wild-type mice   (MGI Ref ID J:48202)
    • increased circulating cholesterol level
      • when fed a chow or Western-type diet for 2 weeks, mice exhibit increased serum cholesterol compared with Apobec1tm1Chan homozygotes and wild-type mice   (MGI Ref ID J:48202)
  • decreased cerebral infarction size
    • compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice   (MGI Ref ID J:133156)
  • increased circulating corticosterone level
    • all males have higher plasma concentrations than wild-type after behavioral testing   (MGI Ref ID J:101973)
  • nervous system phenotype
  • abnormal dendrite morphology
    • mutants have lower levels of MAP 2-positive neuronal dendrites than wild-type; at 3 months, levels are similar in mutants and controls   (MGI Ref ID J:101973)
  • decreased cerebral infarction size
    • compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice   (MGI Ref ID J:133156)
  • cardiovascular system phenotype
  • altered susceptibility to atherosclerosis
    • atherosclerotic lesions begin to form in the left common carotid by 2 weeks after partial ligation of the left common carotid   (MGI Ref ID J:154332)
    • atherosclerotic lesion development is well advanced by 4-6 weeks after partial ligation of the left common carotid   (MGI Ref ID J:154332)
    • increased susceptibility to atherosclerosis
      • bone marrow transplanted into Apoa1tm1Unc homozygotes confer susceptibility to atherosclerosis   (MGI Ref ID J:107390)
  • decreased vasodilation
    • impaired vasodilation induced by sodium nitroprusside 7 days after partial ligation of the left common carotid   (MGI Ref ID J:154332)
  • muscle phenotype
  • decreased vasodilation
    • impaired vasodilation induced by sodium nitroprusside 7 days after partial ligation of the left common carotid   (MGI Ref ID J:154332)


  • immune system phenotype
  • abnormal cell-mediated immunity
    • the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response   (MGI Ref ID J:125366)
    • in an adoptive transfer experiment, the proliferation of Tg(TcrLCMV)2Aox CD45.2+ cell in mice fed a high fat diet and receiving then immunized with GP61-80 peptide with CpG is reduced compared to in wild-type mice similarly treated   (MGI Ref ID J:125366)
    • abnormal dendritic cell physiology
      • dendrictic cells mount reduced IL-12p40 and TNF-alpha responses to stimulation with zymosan, poly(I:C), LPS, imiquimod, and a combination of anti-CD40 antibodies and CpG compared to wild-type mice but similar to wild-type mice fed a high fat diet   (MGI Ref ID J:125366)
      • in mice fed a high fat diet, dendritic cell production of IL-12p40, IL-6 and TNF-alpha after 35 to 40 weeks, but not after 6 to 10 weeks, is severely impaired compared to wild-type cells in response to CpG/anti-CD-40 stimulation   (MGI Ref ID J:125366)
      • CD8alpha-, but not CD8alpha+, dendritic cells are defective in their ability to produce IL-12p40   (MGI Ref ID J:125366)
      • dendritic cells from mice on a high fat diet are severely impaired in their ability to produce Il-12p40, -12p70, -6, and TNF-alpha compared to dendritic cells from wild-type mice on a high fat diet   (MGI Ref ID J:125366)
      • however, CD8alpha+ dendritic cells produce normal amounts of Il-12p70 and -12p40   (MGI Ref ID J:125366)
      • mice fed a high fat diet and co-stimulated with CpG or LPS have fewer IL-12p40-producing CD8alpha- dendritic cells (4.6+/-1.1%) than wild-type mice fed a high fat diet (15.3+/-2.4%)   (MGI Ref ID J:125366)
      • however, the immune responses of bone marrow derived dendritic cells from mice fed a high fat diet or splenic dendritic cells from mice fed a regular diet are normal   (MGI Ref ID J:125366)
  • increased CD4-positive, alpha beta T cell number
    • mice maintained on a high fat diet and infected with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice   (MGI Ref ID J:125366)
  • increased susceptibility to parasitic infection
    • mice maintained on a high fat diet and infected with Leishmania major produce more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice   (MGI Ref ID J:125366)
    • the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response   (MGI Ref ID J:125366)
    • mice maintained on a high fat diet or regular chow and infected with Leishmania major exhibit an increased swelling and parasitic burden at the site of infection (footpad)   (MGI Ref ID J:125366)
  • homeostasis/metabolism phenotype
  • abnormal lipid level
    • mice have increased levels of circulating oxidized lipids compared to wild-type mice   (MGI Ref ID J:125366)
    • increased circulating cholesterol level
      • mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks)   (MGI Ref ID J:61287)
  • decreased circulating leptin level
    • plasma leptin levels are low at both 6 and 18 months   (MGI Ref ID J:60585)
  • behavior/neurological phenotype
  • abnormal kindling response
    • after-discharge duration is significantly prolonged by the sixth trial   (MGI Ref ID J:118390)
    • delayed rekindling after 3-4 weeks   (MGI Ref ID J:118390)
  • abnormal locomotor behavior
    • mice spend more time than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc in the center of an open field   (MGI Ref ID J:71062)
  • abnormal response to new environment
    • mice consume food slower in a new environment than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice   (MGI Ref ID J:71062)
    • mice require more time to habituate to a novel environment compared to wild-type mice   (MGI Ref ID J:71062)
    • mice are less reluctant than wild-type mice to move into an open area   (MGI Ref ID J:71062)
    • decreased exploration in new environment
      • reduced exploratory behavior in an open field test by 12 months although normal earlier   (MGI Ref ID J:60585)
      • exploratory behavior remains constant over several days whereas controls show higher initial exploratory behavior which drops off quickly   (MGI Ref ID J:60585)
  • abnormal spatial learning
    • at 14 to 17 months of age, mice perform better than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice in a rotating holeboard test   (MGI Ref ID J:71062)
  • abnormal thermal nociception
    • 41% increase in foot withdrawal latency from painful thermal stimuli   (MGI Ref ID J:106368)
    • 100% slower tail withdrawal latency   (MGI Ref ID J:106368)
  • decreased startle reflex   (MGI Ref ID J:71062)
  • increased anxiety-related response
    • at 6 months as measured in an elevated plus maze   (MGI Ref ID J:60585)
  • increased fluid intake
    • increased water intake at 18 months   (MGI Ref ID J:60585)
  • increased food intake
    • increased food intake at 12 and 18 months but not earlier   (MGI Ref ID J:60585)
  • hematopoietic system phenotype
  • increased CD4-positive, alpha beta T cell number
    • mice maintained on a high fat diet and infected with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice   (MGI Ref ID J:125366)
  • nervous system phenotype
  • abnormal kindling response
    • after-discharge duration is significantly prolonged by the sixth trial   (MGI Ref ID J:118390)
    • delayed rekindling after 3-4 weeks   (MGI Ref ID J:118390)
  • abnormal myelin sheath morphology
    • very little Schwann cell cytoplasm   (MGI Ref ID J:106368)
    • blurring of lipid membrane border between axons and Schwann cells   (MGI Ref ID J:106368)
  • abnormal sciatic nerve morphology
    • cross-section of unmyelinated axons is irregular   (MGI Ref ID J:106368)
    • very little Schwann cell cytoplasm   (MGI Ref ID J:106368)
    • blurring of lipid membrane border between axons and Schwann cells   (MGI Ref ID J:106368)
    • reduced number of unmyelinated axons   (MGI Ref ID J:106368)
    • ratio of unmyelinated to myelinated axons is reduced   (MGI Ref ID J:106368)
  • abnormal synaptic vesicle morphology
    • synaptophysin levels are somewhat more reduced than in controls after entorhinal cortex lesion   (MGI Ref ID J:118390)
  • hypopituitarism
    • restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels   (MGI Ref ID J:60585)
  • endocrine/exocrine gland phenotype
  • abnormal adrenal gland morphology   (MGI Ref ID J:60585)
    • abnormal adrenal cortex morphology
      • increased lipid droplets seen at six months   (MGI Ref ID J:60585)
    • abnormal adrenal medulla morphology
      • increased lipid droplets seen at six months   (MGI Ref ID J:60585)
  • abnormal gland physiology   (MGI Ref ID J:60585)
    • hypersecretion of corticosterone
      • fter 10 min of restraint stress plasma levels are elevated at six months but not at three months   (MGI Ref ID J:60585)
      • elevated adrenal levels at six months but not earlier   (MGI Ref ID J:60585)
    • hypopituitarism
      • restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels   (MGI Ref ID J:60585)
  • adipose tissue phenotype
  • decreased brown adipose tissue amount
    • decreased interscapular brown fat at 18 but not at 6 months   (MGI Ref ID J:60585)
  • decreased white adipose tissue amount
    • epididymal white fat reduced at both 6 and 18 months   (MGI Ref ID J:60585)
  • cardiovascular system phenotype
  • atherosclerotic lesions
    • cellular composition of lesions is similar among Serpine1-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age   (MGI Ref ID J:61287)
  • integument phenotype
  • abnormal thermal nociception
    • 41% increase in foot withdrawal latency from painful thermal stimuli   (MGI Ref ID J:106368)
    • 100% slower tail withdrawal latency   (MGI Ref ID J:106368)


        involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
  • cardiovascular system phenotype
  • atherosclerotic lesions
    • most severe in the aortic arch region   (MGI Ref ID J:66419)


        involves: 129P2/OlaHsd * C57BL/6 * FVB/N
  • cardiovascular system phenotype
  • atherosclerotic lesions
    • lesions are observed in aortas of nontransgenic mice   (MGI Ref ID J:130658)


        involves: 129P2/OlaHsd * C57BL/6 * DBA
  • homeostasis/metabolism phenotype
  • abnormal circulating protein level
    • increase in APOB-48   (MGI Ref ID J:75567)
  • abnormal lipid homeostasis
    • the HDL phospholipid fraction is enriched in 16:0 and 18:0 species and contains less 20:4 and 22:6 species compared to Ldlrtm1Her single mutants   (MGI Ref ID J:75567)
    • abnormal cholesterol homeostasis
      • increase in the APOB lipoprotein cholesterol level compared to wild-type controls   (MGI Ref ID J:75567)
      • there is a 2.3 fold increase in the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species compared to Ldlrtm1Her single mutants   (MGI Ref ID J:75567)
      • the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species in the LDL fraction is significantly increased compared to Ldlrtm1Her single mutants   (MGI Ref ID J:75567)
      • decreased circulating HDL cholesterol level
        • about a 50% decrease in HDL compared to controls   (MGI Ref ID J:75567)
      • increased circulating cholesterol level
        • increased total cholesterol and esterfied cholesterol levels in the plasma   (MGI Ref ID J:75567)
    • increased circulating phospholipid level   (MGI Ref ID J:75567)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Diabetes and Obesity Research
Obesity Without Diabetes

Neurobiology Research
Alzheimer's Disease
      APOE mutants
Behavioral and Learning Defects

Apoetm1Unc related

Cardiovascular Research

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Apoetm1Unc
Allele Name targeted mutation 1, University of North Carolina
Allele Type Targeted (Null/Knockout)
Common Name(s) APOE KO; AopE(-); ApoE-KO; Apoetm1Un; apoE-; apoE0; epsilon-; mE-; mEKO;
Mutation Made ByDr. Nobuyo Maeda,   University of North Carolina at Chapel Hill
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14TG2a
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Apoe, apolipoprotein E
Chromosome 7
Gene Common Name(s) AD2; AI255918; APO-E; APOEA; LDLCQ5; LPG; expressed sequence AI255918;
General Note Phenotypic Similarity to Human Syndrome: Coronary Artery Disease (CAD) in mice homozygous for Apoe tm1Unc and Scarb1 tm1Kri on a mixed 129, BALB/c and C57BL/6 background (J:201999)
Phenotypic Similarity to Human Syndrome: Metabolic Syndrome in mice homozygous for Apoetm1Unc and Cyp19a1tm1Esi (J:184647)
Phenotypic Similarity to Human Syndrome: Metabolic Syndrome in mice homozygous for Apoetm1Unc and heterozygous for Ay and a (J:177084)
Molecular Note Insertion of a neomycin resistance cassette deleted part of exon 3 and part of intron 3 of the Apoe gene. Plasma from homozygous mutant mice gave no detectable immunoprecipitate by the Ouchterlony double immunodiffusion test using a rabbit antibody to rat APOE. [MGI Ref ID J:1050]


Genotyping Information

Genotyping Protocols

Apoetm1Unc, High Resolution Melting
Apoetm1Unc, Standard PCR

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

Piedrahita JA; Zhang SH; Hagaman JR; Oliver PM; Maeda N. 1992. Generation of mice carrying a mutant apolipoprotein E gene inactivated by gene targeting in embryonic stem cells. Proc Natl Acad Sci U S A 89(10):4471-5. [PubMed: 1584779]  [MGI Ref ID J:1050]

Additional References

Apoetm1Unc related

't Hoen PA; Van der Lans CA; Van Eck M; Bijsterbosch MK; Van Berkel TJ; Twisk J. 2003. Aorta of ApoE-deficient mice responds to atherogenic stimuli by a prelesional increase and subsequent decrease in the expression of antioxidant enzymes. Circ Res 93(3):262-9. [PubMed: 12829615]  [MGI Ref ID J:115676]

A-Gonzalez N; Bensinger SJ; Hong C; Beceiro S; Bradley MN; Zelcer N; Deniz J; Ramirez C; Diaz M; Gallardo G; de Galarreta CR; Salazar J; Lopez F; Edwards P; Parks J; Andujar M; Tontonoz P; Castrillo A. 2009. Apoptotic cells promote their own clearance and immune tolerance through activation of the nuclear receptor LXR. Immunity 31(2):245-58. [PubMed: 19646905]  [MGI Ref ID J:151872]

Abd Alla J; Langer A; Elzahwy SS; Arman-Kalcek G; Streichert T; Quitterer U. 2010. Angiotensin-converting enzyme inhibition down-regulates the pro-atherogenic chemokine receptor 9 (CCR9)-chemokine ligand 25 (CCL25) axis. J Biol Chem 285(30):23496-505. [PubMed: 20504763]  [MGI Ref ID J:165997]

Accad M; Smith SJ; Newland DL; Sanan DA; King LE Jr; Linton MF; Fazio S; Farese RV Jr. 2000. Massive xanthomatosis and altered composition of atherosclerotic lesions in hyperlipidemic mice lacking acyl CoA:cholesterol acyltransferase 1 [see comments] J Clin Invest 105(6):711-9. [PubMed: 10727439]  [MGI Ref ID J:61147]

Adachi H; Fujiwara Y; Kondo T; Nishikawa T; Ogawa R; Matsumura T; Ishii N; Nagai R; Miyata K; Tabata M; Motoshima H; Furukawa N; Tsuruzoe K; Kawashima J; Takeya M; Yamashita S; Koh GY; Nagy A; Suda T; Oike Y; Araki E. 2009. Angptl 4 deficiency improves lipid metabolism, suppresses foam cell formation and protects against atherosclerosis. Biochem Biophys Res Commun 379(4):806-11. [PubMed: 19094966]  [MGI Ref ID J:145171]

Agrawal S; Febbraio M; Podrez E; Cathcart MK; Stark GR; Chisolm GM. 2007. Signal transducer and activator of transcription 1 is required for optimal foam cell formation and atherosclerotic lesion development. Circulation 115(23):2939-47. [PubMed: 17533179]  [MGI Ref ID J:137115]

Ahluwalia N; Lin AY; Tager AM; Pruitt IE; Anderson TJ; Kristo F; Shen D; Cruz AR; Aikawa M; Luster AD; Gerszten RE. 2007. Inhibited aortic aneurysm formation in BLT1-deficient mice. J Immunol 179(1):691-7. [PubMed: 17579092]  [MGI Ref ID J:143153]

Aihara K; Azuma H; Akaike M; Ikeda Y; Sata M; Takamori N; Yagi S; Iwase T; Sumitomo Y; Kawano H; Yamada T; Fukuda T; Matsumoto T; Sekine K; Sato T; Nakamichi Y; Yamamoto Y; Yoshimura K; Watanabe T; Nakamura T; Oomizu A; Tsukada M; Hayashi H; Sudo T; KatoS; Matsumoto T. 2007. Strain-dependent embryonic lethality and exaggerated vascular remodeling in heparin cofactor II-deficient mice. J Clin Invest 117(6):1514-26. [PubMed: 17549254]  [MGI Ref ID J:122173]

Aikawa E; Nahrendorf M; Sosnovik D; Lok VM; Jaffer FA; Aikawa M; Weissleder R. 2007. Multimodality molecular imaging identifies proteolytic and osteogenic activities in early aortic valve disease. Circulation 115(3):377-86. [PubMed: 17224478]  [MGI Ref ID J:130156]

Alberts-Grill N; Rezvan A; Son DJ; Qiu H; Kim CW; Kemp ML; Weyand CM; Jo H. 2012. Dynamic immune cell accumulation during flow-induced atherogenesis in mouse carotid artery: an expanded flow cytometry method. Arterioscler Thromb Vasc Biol 32(3):623-32. [PubMed: 22247254]  [MGI Ref ID J:195958]

Alexander MR; Knowles JW; Nishikimi T; Maeda N. 2003. Increased atherosclerosis and smooth muscle cell hypertrophy in natriuretic peptide receptor A-/-apolipoprotein E-/- mice. Arterioscler Thromb Vasc Biol 23(6):1077-82. [PubMed: 12702516]  [MGI Ref ID J:103054]

Alexander MR; Moehle CW; Johnson JL; Yang Z; Lee JK; Jackson CL; Owens GK. 2012. Genetic inactivation of IL-1 signaling enhances atherosclerotic plaque instability and reduces outward vessel remodeling in advanced atherosclerosis in mice. J Clin Invest 122(1):70-9. [PubMed: 22201681]  [MGI Ref ID J:184390]

Ali K; Middleton M; Pure E; Rader DJ. 2005. Apolipoprotein E suppresses the type I inflammatory response in vivo. Circ Res 97(9):922-7. [PubMed: 16179587]  [MGI Ref ID J:114634]

Ali ZA; de Jesus Perez V; Yuan K; Orcholski M; Pan S; Qi W; Chopra G; Adams C; Kojima Y; Leeper NJ; Qu X; Zaleta-Rivera K; Kato K; Yamada Y; Oguri M; Kuchinsky A; Hazen SL; Jukema JW; Ganesh SK; Nabel EG; Channon K; Leon MB; Charest A; Quertermous T; Ashley EA. 2014. Oxido-reductive regulation of vascular remodeling by receptor tyrosine kinase ROS1. J Clin Invest 124(12):5159-74. [PubMed: 25401476]  [MGI Ref ID J:219378]

Alkemade FE; van Vliet P; Henneman P; van Dijk KW; Hierck BP; van Munsteren JC; Scheerman JA; Goeman JJ; Havekes LM; Gittenberger-de Groot AC; van den Elsen PJ; DeRuiter MC. 2010. Prenatal exposure to apoE deficiency and postnatal hypercholesterolemia are associated with altered cell-specific lysine methyltransferase and histone methylation patterns in the vasculature. Am J Pathol 176(2):542-8. [PubMed: 20035052]  [MGI Ref ID J:156605]

Alp NJ; McAteer MA; Khoo J; Choudhury RP; Channon KM. 2004. Increased endothelial tetrahydrobiopterin synthesis by targeted transgenic GTP-cyclohydrolase I overexpression reduces endothelial dysfunction and atherosclerosis in ApoE-knockout mice. Arterioscler Thromb Vasc Biol 24(3):445-50. [PubMed: 14707037]  [MGI Ref ID J:102062]

Amar S; Wu SC; Madan M. 2009. Is Porphyromonas gingivalis cell invasion required for atherogenesis? Pharmacotherapeutic implications. J Immunol 182(3):1584-92. [PubMed: 19155507]  [MGI Ref ID J:144322]

Amigo L; Quinones V; Mardones P; Zanlungo S; Miquel JF; Nervi F; Rigotti A. 2000. Impaired biliary cholesterol secretion and decreased gallstone formation in apolipoprotein E-deficient mice fed a high-cholesterol diet. Gastroenterology 118(4):772-9. [PubMed: 10734029]  [MGI Ref ID J:107676]

Amirbekian S; Long RC Jr; Consolini MA; Suo J; Willett NJ; Fielden SW; Giddens DP; Taylor WR; Oshinski JN. 2009. In vivo assessment of blood flow patterns in abdominal aorta of mice with MRI: implications for AAA localization. Am J Physiol Heart Circ Physiol 297(4):H1290-5. [PubMed: 19684182]  [MGI Ref ID J:154334]

An G; Miwa T; Song WL; Lawson JA; Rader DJ; Zhang Y; Song WC. 2009. CD59 but not DAF deficiency accelerates atherosclerosis in female ApoE knockout mice. Mol Immunol 46(8-9):1702-9. [PubMed: 19297024]  [MGI Ref ID J:148359]

An G; Wang H; Tang R; Yago T; McDaniel JM; McGee S; Huo Y; Xia L. 2008. P-selectin glycoprotein ligand-1 is highly expressed on Ly-6Chi monocytes and a major determinant for Ly-6Chi monocyte recruitment to sites of atherosclerosis in mice. Circulation 117(25):3227-37. [PubMed: 18519846]  [MGI Ref ID J:155081]

Anderson DR; Tsutsui JM; Xie F; Radio SJ; Porter TR. 2007. The role of complement in the adherence of microbubbles to dysfunctional arterial endothelium and atherosclerotic plaque. Cardiovasc Res 73(3):597-606. [PubMed: 17196951]  [MGI Ref ID J:119533]

Anderson R; Barnes JC; Bliss TV; Cain DP; Cambon K; Davies HA; Errington ML; Fellows LA; Gray RA; Hoh T; Stewart M; Large CH; Higgins GA. 1998. Behavioural, physiological and morphological analysis of a line of apolipoprotein E knockout mouse. Neuroscience 85(1):93-110. [PubMed: 9607706]  [MGI Ref ID J:118390]

Anderson R; Higgins GA. 1997. Absence of central cholinergic deficits in ApoE knockout mice. Psychopharmacology (Berl) 132(2):135-44. [PubMed: 9266610]  [MGI Ref ID J:127860]

Andersson IJ; Jiang YY; Davidge ST. 2009. Maternal stress and development of atherosclerosis in the adult apolipoprotein E-deficient mouse offspring. Am J Physiol Regul Integr Comp Physiol 296(3):R663-71. [PubMed: 19129374]  [MGI Ref ID J:145701]

Ando Y; Shimizugawa T; Takeshita S; Ono M; Shimamura M; Koishi R; Furukawa H. 2003. A decreased expression of angiopoietin-like 3 is protective against atherosclerosis in apoE-deficient mice. J Lipid Res 44(6):1216-23. [PubMed: 12671033]  [MGI Ref ID J:84022]

Andre P; Morooka T; Sim D; Abe K; Lowell C; Nanda N; Delaney S; Siu G; Yan Y; Hollenbach S; Pandey A; Gao H; Wang Y; Nakajima K; Parikh SA; Shi C; Phillips D; Owen W; Sinha U; Simon DI. 2011. Critical role for Syk in responses to vascular injury. Blood 118(18):5000-10. [PubMed: 21881044]  [MGI Ref ID J:178801]

Andrews-Zwilling Y; Bien-Ly N; Xu Q; Li G; Bernardo A; Yoon SY; Zwilling D; Yan TX; Chen L; Huang Y. 2010. Apolipoprotein E4 causes age- and Tau-dependent impairment of GABAergic interneurons, leading to learning and memory deficits in mice. J Neurosci 30(41):13707-17. [PubMed: 20943911]  [MGI Ref ID J:165492]

Angeli V; Llodra J; Rong JX; Satoh K; Ishii S; Shimizu T; Fisher EA; Randolph GJ. 2004. Dyslipidemia associated with atherosclerotic disease systemically alters dendritic cell mobilization. Immunity 21(4):561-74. [PubMed: 15485633]  [MGI Ref ID J:93917]

Aono J; Suzuki J; Iwai M; Horiuchi M; Nagai T; Nishimura K; Inoue K; Ogimoto A; Okayama H; Higaki J. 2012. Deletion of the angiotensin II type 1a receptor prevents atherosclerotic plaque rupture in apolipoprotein E-/- mice. Arterioscler Thromb Vasc Biol 32(6):1453-9. [PubMed: 22460554]  [MGI Ref ID J:196922]

Apostolov EO; Ray D; Savenka AV; Shah SV; Basnakian AG. 2010. Chronic uremia stimulates LDL carbamylation and atherosclerosis. J Am Soc Nephrol 21(11):1852-7. [PubMed: 20947625]  [MGI Ref ID J:185898]

Aprahamian T; Bonegio R; Rizzo J; Perlman H; Lefer DJ; Rifkin IR; Walsh K. 2006. Simvastatin treatment ameliorates autoimmune disease associated with accelerated atherosclerosis in a murine lupus model. J Immunol 177(5):3028-34. [PubMed: 16920939]  [MGI Ref ID J:139547]

Aprahamian T; Bonegio RG; Richez C; Yasuda K; Chiang LK; Sato K; Walsh K; Rifkin IR. 2009. The peroxisome proliferator-activated receptor gamma agonist rosiglitazone ameliorates murine lupus by induction of adiponectin. J Immunol 182(1):340-6. [PubMed: 19109165]  [MGI Ref ID J:142895]

Aprahamian T; Rifkin I; Bonegio R; Hugel B; Freyssinet JM; Sato K; Castellot JJ Jr; Walsh K. 2004. Impaired Clearance of Apoptotic Cells Promotes Synergy between Atherogenesis and Autoimmune Disease. J Exp Med 199(8):1121-31. [PubMed: 15096538]  [MGI Ref ID J:91058]

Arakawa M; Mita T; Azuma K; Ebato C; Goto H; Nomiyama T; Fujitani Y; Hirose T; Kawamori R; Watada H. 2010. Inhibition of monocyte adhesion to endothelial cells and attenuation of atherosclerotic lesion by a glucagon-like peptide-1 receptor agonist, exendin-4. Diabetes 59(4):1030-7. [PubMed: 20068138]  [MGI Ref ID J:164336]

Arsenescu V; Arsenescu R; Parulkar M; Karounos M; Zhang X; Baker N; Cassis LA. 2011. Polychlorinated biphenyl 77 augments angiotensin II-induced atherosclerosis and abdominal aortic aneurysms in male apolipoprotein E deficient mice. Toxicol Appl Pharmacol 257(1):148-54. [PubMed: 21925196]  [MGI Ref ID J:178556]

Ashida N; Senbanerjee S; Kodama S; Foo SY; Coggins M; Spencer JA; Zamiri P; Shen D; Li L; Sciuto T; Dvorak A; Gerszten RE; Lin CP; Karin M; Rosenzweig A. 2011. IKKbeta regulates essential functions of the vascular endothelium through kinase-dependent and -independent pathways. Nat Commun 2:318. [PubMed: 21587235]  [MGI Ref ID J:205654]

Ason B; van der Hoorn JW; Chan J; Lee E; Pieterman EJ; Nguyen KK; Di M; Shetterly S; Tang J; Yeh WC; Schwarz M; Jukema JW; Scott R; Wasserman SM; Princen HM; Jackson S. 2014. PCSK9 inhibition fails to alter hepatic LDLR, circulating cholesterol, and atherosclerosis in the absence of ApoE. J Lipid Res 55(11):2370-9. [PubMed: 25258384]  [MGI Ref ID J:216603]

Atkins GB; Wang Y; Mahabeleshwar GH; Shi H; Gao H; Kawanami D; Natesan V; Lin Z; Simon DI; Jain MK. 2008. Hemizygous deficiency of Kruppel-like factor 2 augments experimental atherosclerosis. Circ Res 103(7):690-3. [PubMed: 18757824]  [MGI Ref ID J:155153]

Atkinson RD; Coenen KR; Plummer MR; Gruen ML; Hasty AH. 2008. Macrophage-derived apolipoprotein E ameliorates dyslipidemia and atherosclerosis in obese apolipoprotein E-deficient mice. Am J Physiol Endocrinol Metab 294(2):E284-90. [PubMed: 18029445]  [MGI Ref ID J:133332]

Auger A; Truong TQ; Rhainds D; Lapointe J; Letarte F; Brissette L. 2001. Low and high density lipoprotein metabolism in primary cultures of hepatic cells from normal and apolipoprotein E knockout mice. Eur J Biochem 268(8):2322-30. [PubMed: 11298750]  [MGI Ref ID J:115588]

Austin SA; Combs CK. 2010. Amyloid precursor protein mediates monocyte adhesion in AD tissue and apoE(-)/(-) mice. Neurobiol Aging 31(11):1854-66. [PubMed: 19058878]  [MGI Ref ID J:165242]

Avraham-Davidi I; Ely Y; Pham VN; Castranova D; Grunspan M; Malkinson G; Gibbs-Bar L; Mayseless O; Allmog G; Lo B; Warren CM; Chen TT; Ungos J; Kidd K; Shaw K; Rogachev I; Wan W; Murphy PM; Farber SA; Carmel L; Shelness GS; Iruela-Arispe ML; Weinstein BM; Yaniv K. 2012. ApoB-containing lipoproteins regulate angiogenesis by modulating expression of VEGF receptor 1. Nat Med 18(6):967-73. [PubMed: 22581286]  [MGI Ref ID J:187459]

Azevedo OG; Bolick DT; Roche JK; Pinkerton RF; Lima AA; Vitek MP; Warren CA; Oria RB; Guerrant RL. 2014. Apolipoprotein E plays a key role against cryptosporidial infection in transgenic undernourished mice. PLoS One 9(2):e89562. [PubMed: 24586873]  [MGI Ref ID J:213815]

Azuma K; Ichimura K; Mita T; Nakayama S; Jin WL; Hirose T; Fujitani Y; Sumiyoshi K; Shimada K; Daida H; Sakai T; Mitsumata M; Kawamori R; Watada H. 2009. Presence of alpha-smooth muscle actin-positive endothelial cells in the luminal surface of adult aorta. Biochem Biophys Res Commun 380(3):620-6. [PubMed: 19285011]  [MGI Ref ID J:147062]

Baba SP; Barski OA; Ahmed Y; O'Toole TE; Conklin DJ; Bhatnagar A; Srivastava S. 2009. Reductive metabolism of AGE precursors: a metabolic route for preventing AGE accumulation in cardiovascular tissue. Diabetes 58(11):2486-97. [PubMed: 19651811]  [MGI Ref ID J:154389]

Babaev VR; Ding L; Reese J; Morrow JD; Breyer MD; Dey SK; Fazio S; Linton MF. 2006. Cyclooxygenase-1 deficiency in bone marrow cells increases early atherosclerosis in apolipoprotein E- and low-density lipoprotein receptor-null mice. Circulation 113(1):108-17. [PubMed: 16380543]  [MGI Ref ID J:121507]

Babaev VR; Li L; Shah S; Fazio S; Linton MF; May JM. 2010. Combined vitamin C and vitamin E deficiency worsens early atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 30(9):1751-7. [PubMed: 20558818]  [MGI Ref ID J:179551]

Bagavant H; Scindia Y; Nackiewicz D; Rao Nandula S; Doran A; Cutchins A; Oldham S; Deshmukh U; McNamara C. 2011. Deficiency of a transcriptional regulator, inhibitor of differentiation 3, induces glomerulonephritis in apolipoprotein e-deficient mice a model linking hyperlipidemia and renal disease. Am J Pathol 179(2):651-60. [PubMed: 21801865]  [MGI Ref ID J:174603]

Bai B; Liang Y; Xu C; Lee MY; Xu A; Wu D; Vanhoutte PM; Wang Y. 2012. Cyclin-dependent kinase 5-mediated hyperphosphorylation of sirtuin-1 contributes to the development of endothelial senescence and atherosclerosis. Circulation 126(6):729-40. [PubMed: 22753194]  [MGI Ref ID J:202201]

Baldan A; Pei L; Lee R; Tarr P; Tangirala RK; Weinstein MM; Frank J; Li AC; Tontonoz P; Edwards PA. 2006. Impaired development of atherosclerosis in hyperlipidemic Ldlr-/- and ApoE-/- mice transplanted with Abcg1-/- bone marrow. Arterioscler Thromb Vasc Biol 26(10):2301-7. [PubMed: 16888235]  [MGI Ref ID J:128048]

Bales KR; Liu F; Wu S; Lin S; Koger D; DeLong C; Hansen JC; Sullivan PM; Paul SM. 2009. Human APOE isoform-dependent effects on brain beta-amyloid levels in PDAPP transgenic mice. J Neurosci 29(21):6771-9. [PubMed: 19474305]  [MGI Ref ID J:149522]

Bales KR; Verina T; Cummins DJ; Du Y; Dodel RC; Saura J; Fishman CE; DeLong CA; Piccardo P; Petegnief V; Ghetti B; Paul SM. 1999. Apolipoprotein E is essential for amyloid deposition in the APP(V717F) transgenic mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A 96(26):15233-8. [PubMed: 10611368]  [MGI Ref ID J:59078]

Bales KR; Verina T; Dodel RC; Du Y; Altstiel L; Bender M; Hyslop P; Johnstone EM; Little SP; Cummins DJ; Piccardo P; Ghetti B; Paul SM. 1997. Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition [letter] [see comments] Nat Genet 17(3):263-4. [PubMed: 9354781]  [MGI Ref ID J:43845]

Baltgalvis KA; White K; Li W; Claypool MD; Lang W; Alcantara R; Singh BK; Friera AM; McLaughlin J; Hansen D; McCaughey K; Nguyen H; Smith IJ; Godinez G; Shaw SJ; Goff D; Singh R; Markovtsov V; Sun TQ; Jenkins Y; Uy G; Li Y; Pan A; Gururaja T; Lau D; ParkG; Hitoshi Y; Payan DG; Kinsella TM. 2014. Exercise performance and peripheral vascular insufficiency improve with AMPK activation in high-fat diet-fed mice. Am J Physiol Heart Circ Physiol 306(8):H1128-45. [PubMed: 24561866]  [MGI Ref ID J:210750]

Barajas B; Che N; Yin F; Rowshanrad A; Orozco LD; Gong KW; Wang X; Castellani LW; Reue K; Lusis AJ; Araujo JA. 2011. NF-E2-related factor 2 promotes atherosclerosis by effects on plasma lipoproteins and cholesterol transport that overshadow antioxidant protection. Arterioscler Thromb Vasc Biol 31(1):58-66. [PubMed: 20947826]  [MGI Ref ID J:184195]

Barile GR; Pachydaki SI; Tari SR; Lee SE; Donmoyer CM; Ma W; Rong LL; Buciarelli LG; Wendt T; Horig H; Hudson BI; Qu W; Weinberg AD; Yan SF; Schmidt AM. 2005. The RAGE axis in early diabetic retinopathy. Invest Ophthalmol Vis Sci 46(8):2916-24. [PubMed: 16043866]  [MGI Ref ID J:103714]

Barlic J; Murphy PM. 2007. Chemokine regulation of atherosclerosis. J Leukoc Biol 82(2):226-36. [PubMed: 17329566]  [MGI Ref ID J:123530]

Barry-Lane PA; Patterson C; van der Merwe M; Hu Z; Holland SM; Yeh ET; Runge MS. 2001. p47phox is required for atherosclerotic lesion progression in ApoE(-/-) mice. J Clin Invest 108(10):1513-22. [PubMed: 11714743]  [MGI Ref ID J:111638]

Bartelt A; Beil FT; Schinke T; Roeser K; Ruether W; Heeren J; Niemeier A. 2010. Apolipoprotein E-dependent inverse regulation of vertebral bone and adipose tissue mass in C57Bl/6 mice: modulation by diet-induced obesity. Bone 47(4):736-45. [PubMed: 20633710]  [MGI Ref ID J:165157]

Bartelt A; Orlando P; Mele C; Ligresti A; Toedter K; Scheja L; Heeren J; Di Marzo V. 2011. Altered endocannabinoid signalling after a high-fat diet in Apoe (-/-) mice: relevance to adipose tissue inflammation, hepatic steatosis and insulin resistance. Diabetologia 54(11):2900-10. [PubMed: 21847582]  [MGI Ref ID J:178356]

Barton M; Haudenschild CC; d'Uscio LV; Shaw S; Munter K; Luscher TF. 1998. Endothelin ETA receptor blockade restores NO-mediated endothelial function and inhibits atherosclerosis in apolipoprotein E-deficient mice. Proc Natl Acad Sci U S A 95(24):14367-72. [PubMed: 9826706]  [MGI Ref ID J:51282]

Bates KA; Fonte J; Robertson TA; Martins RN; Harvey AR. 2002. Chronic gliosis triggers Alzheimer's disease-like processing of amyloid precursor protein. Neuroscience 113(4):785-96. [PubMed: 12182886]  [MGI Ref ID J:120711]

Baumgartl J; Baudler S; Scherner M; Babaev V; Makowski L; Suttles J; McDuffie M; Tobe K; Kadowaki T; Fazio S; Kahn CR; Hotamisligil GS; Krone W; Linton M; Bruning JC. 2006. Myeloid lineage cell-restricted insulin resistance protects apolipoproteinE-deficient mice against atherosclerosis. Cell Metab 3(4):247-56. [PubMed: 16581002]  [MGI Ref ID J:129654]

Bechtholt AJ; Smith R; Raber J; Cunningham CL. 2004. Enhanced ethanol-, but not cocaine-induced, conditioned place preference in Apoe(-/-) mice. Pharmacol Biochem Behav 77(4):783-92. [PubMed: 15099924]  [MGI Ref ID J:102259]

Becker LE; Koleganova N; Piecha G; Noronha IL; Zeier M; Geldyyev A; Kokeny G; Ritz E; Gross ML. 2011. Effect of paricalcitol and calcitriol on aortic wall remodeling in uninephrectomized ApoE knockout mice. Am J Physiol Renal Physiol 300(3):F772-82. [PubMed: 21159735]  [MGI Ref ID J:169320]

Beckers L; Heeneman S; Wang L; Burkly L; Rousch M; Davidson N; Gijbels M; de Winther M; Daemen M; Lutgens E. 2007. Disruption of hedgehog signalling in ApoE - /- mice reduces plasma lipid levels, but increases atherosclerosis due to enhanced lipid uptake by macrophages. J Pathol 212(4):420-8. [PubMed: 17573667]  [MGI Ref ID J:122864]

Beleznai T; Takano H; Hamill C; Yarova P; Douglas G; Channon K; Dora K. 2011. Enhanced K(+)-channel-mediated endothelium-dependent local and conducted dilation of small mesenteric arteries from ApoE(-/-) mice. Cardiovasc Res 92(2):199-208. [PubMed: 21690174]  [MGI Ref ID J:191707]

Bell RD; Winkler EA; Singh I; Sagare AP; Deane R; Wu Z; Holtzman DM; Betsholtz C; Armulik A; Sallstrom J; Berk BC; Zlokovic BV. 2012. Apolipoprotein E controls cerebrovascular integrity via cyclophilin A. Nature 485(7399):512-6. [PubMed: 22622580]  [MGI Ref ID J:184835]

Bengtsson E; To F; Hakansson K; Grubb A; Branen L; Nilsson J; Jovinge S. 2005. Lack of the cysteine protease inhibitor cystatin C promotes atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 25(10):2151-6. [PubMed: 16051881]  [MGI Ref ID J:114346]

Bennett BJ; Scatena M; Kirk EA; Rattazzi M; Varon RM; Averill M; Schwartz SM; Giachelli CM; Rosenfeld ME. 2006. Osteoprotegerin inactivation accelerates advanced atherosclerotic lesion progression and calcification in older ApoE-/- mice. Arterioscler Thromb Vasc Biol 26(9):2117-24. [PubMed: 16840715]  [MGI Ref ID J:128053]

Bennett BJ; Wang SS; Wang X; Wu X; Lusis AJ. 2009. Genetic regulation of atherosclerotic plaque size and morphology in the innominate artery of hyperlipidemic mice. Arterioscler Thromb Vasc Biol 29(3):348-55. [PubMed: 19122174]  [MGI Ref ID J:159783]

Bentzon JF; Sondergaard CS; Kassem M; Falk E. 2007. Smooth muscle cells healing atherosclerotic plaque disruptions are of local, not blood, origin in apolipoprotein E knockout mice. Circulation 116(18):2053-61. [PubMed: 17938286]  [MGI Ref ID J:142997]

Berbee JF; van der Hoogt CC; Sundararaman D; Havekes LM; Rensen PC. 2005. Severe hypertriglyceridemia in human APOC1 transgenic mice is caused by apoC-I-induced inhibition of LPL. J Lipid Res 46(2):297-306. [PubMed: 15576844]  [MGI Ref ID J:96691]

Bernhagen J; Krohn R; Lue H; Gregory JL; Zernecke A; Koenen RR; Dewor M; Georgiev I; Schober A; Leng L; Kooistra T; Fingerle-Rowson G; Ghezzi P; Kleemann R; McColl SR; Bucala R; Hickey MJ; Weber C. 2007. MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment. Nat Med 13(5):587-596. [PubMed: 17435771]  [MGI Ref ID J:121807]

Bhattacharjee PS; Neumann DM; Stark D; Thompson HW; Hill JM. 2006. Apolipoprotein E modulates establishment of HSV-1 latency and survival in a mouse ocular model. Curr Eye Res 31(9):703-8. [PubMed: 16966142]  [MGI Ref ID J:119878]

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Yang H; Roberts LJ; Shi MJ; Zhou LC; Ballard BR; Richardson A; Guo ZM. 2004. Retardation of atherosclerosis by overexpression of catalase or both Cu/Zn-superoxide dismutase and catalase in mice lacking apolipoprotein E. Circ Res 95(11):1075-81. [PubMed: 15528470]  [MGI Ref ID J:103561]

Yang J; Sato K; Aprahamian T; Brown NJ; Hutcheson J; Bialik A; Perlman H; Walsh K. 2004. Endothelial overexpression of Fas ligand decreases atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 24(8):1466-73. [PubMed: 15178561]  [MGI Ref ID J:102307]

Yang X; Peterson L; Thieringer R; Deignan JL; Wang X; Zhu J; Wang S; Zhong H; Stepaniants S; Beaulaurier J; Wang IM; Rosa R; Cumiskey AM; Luo JM; Luo Q; Shah K; Xiao J; Nickle D; Plump A; Schadt EE; Lusis AJ; Lum PY. 2010. Identification and validation of genes affecting aortic lesions in mice. J Clin Invest 120(7):2414-22. [PubMed: 20577049]  [MGI Ref ID J:163781]

Yao J; Petanceska SS; Montine TJ; Holtzman DM; Schmidt SD; Parker CA; Callahan MJ; Lipinski WJ; Bisgaier CL; Turner BA; Nixon RA; Martins RN; Ouimet C; Smith JD; Davies P; Laska E; Ehrlich ME; Walker LC; Mathews PM; Gandy S. 2004. Aging, gender and APOE isotype modulate metabolism of Alzheimer's Abeta peptides and F-isoprostanes in the absence of detectable amyloid deposits. J Neurochem 90(4):1011-8. [PubMed: 15287908]  [MGI Ref ID J:107867]

Yao Y; Bennett BJ; Wang X; Rosenfeld ME; Giachelli C; Lusis AJ; Bostrom KI. 2010. Inhibition of bone morphogenetic proteins protects against atherosclerosis and vascular calcification. Circ Res 107(4):485-94. [PubMed: 20576934]  [MGI Ref ID J:175034]

Yao Y; Watson AD; Ji S; Bostrom KI. 2009. Heat shock protein 70 enhances vascular bone morphogenetic protein-4 signaling by binding matrix Gla protein. Circ Res 105(6):575-84. [PubMed: 19661459]  [MGI Ref ID J:169973]

Ye X; Jiang X; Guo W; Clark K; Gao Z. 2013. Overexpression of NF-kappaB p65 in macrophages ameliorates atherosclerosis in apoE-knockout mice. Am J Physiol Endocrinol Metab 305(11):E1375-83. [PubMed: 24105415]  [MGI Ref ID J:205993]

Yesilaltay A; Daniels K; Pal R; Krieger M; Kocher O. 2009. Loss of PDZK1 causes coronary artery occlusion and myocardial infarction in Paigen diet-fed apolipoprotein E deficient mice. PLoS One 4(12):e8103. [PubMed: 19956623]  [MGI Ref ID J:155971]

Yet SF; Layne MD; Liu X; Chen YH; Ith B; Sibinga NE; Perrella MA. 2003. Absence of heme oxygenase-1 exacerbates atherosclerotic lesion formation and vascular remodeling. FASEB J 17(12):1759-61. [PubMed: 12958201]  [MGI Ref ID J:85417]

Yi X; Maeda N. 2006. alpha-Lipoic acid prevents the increase in atherosclerosis induced by diabetes in apolipoprotein E-deficient mice fed high-fat/low-cholesterol diet. Diabetes 55(8):2238-44. [PubMed: 16873686]  [MGI Ref ID J:116519]

Yoshimatsu M; Terasaki Y; Sakashita N; Kiyota E; Sato H; van der Laan LJ; Takeya M. 2004. Induction of macrophage scavenger receptor MARCO in nonalcoholic steatohepatitis indicates possible involvement of endotoxin in its pathogenic process. Int J Exp Pathol 85(6):335-43. [PubMed: 15566430]  [MGI Ref ID J:104609]

Yoshimura K; Aoki H; Ikeda Y; Fujii K; Akiyama N; Furutani A; Hoshii Y; Tanaka N; Ricci R; Ishihara T; Esato K; Hamano K; Matsuzaki M. 2005. Regression of abdominal aortic aneurysm by inhibition of c-Jun N-terminal kinase. Nat Med 11(12):1330-8. [PubMed: 16311603]  [MGI Ref ID J:104132]

Young CG; Knight CA; Vickers KC; Westbrook D; Madamanchi NR; Runge MS; Ischiropoulos H; Ballinger SW. 2005. Differential effects of exercise on aortic mitochondria. Am J Physiol Heart Circ Physiol 288(4):H1683-9. [PubMed: 15550530]  [MGI Ref ID J:97385]

Yu H; Zhang W; Yancey PG; Koury MJ; Zhang Y; Fazio S; Linton MF. 2006. Macrophage apolipoprotein E reduces atherosclerosis and prevents premature death in apolipoprotein E and scavenger receptor-class BI double-knockout mice. Arterioscler Thromb Vasc Biol 26(1):150-6. [PubMed: 16269665]  [MGI Ref ID J:127962]

Yu J; Deng M; Zhao J; Huang L. 2010. Decreased expression of klotho gene in uremic atherosclerosis in apolipoprotein E-deficient mice. Biochem Biophys Res Commun 391(1):261-6. [PubMed: 19912987]  [MGI Ref ID J:156734]

Yu KC; David C; Kadambi S; Stahl A; Hirata K; Ishida T; Quertermous T; Cooper AD; Choi SY. 2004. Endothelial lipase is synthesized by hepatic and aorta endothelial cells and its expression is altered in apoE-deficient mice. J Lipid Res 45(9):1614-23. [PubMed: 15175355]  [MGI Ref ID J:93268]

Yu KC; Jiang Y; Chen W; Cooper AD. 2000. Rapid initial removal of chylomicron remnants by the mouse liver does not require hepatically localized apolipoprotein E J Lipid Res 41(11):1715-27. [PubMed: 11060341]  [MGI Ref ID J:65695]

Yu M; Zhou H; Zhao J; Xiao N; Roychowdhury S; Schmitt D; Hu B; Harding CV; Hise AG; Hazen SL; DeFranco AL; Fox PL; Morton RE; Dicorleto PE; Febbraio M; Nagy LE; Smith JD; Wang JA; Li X. 2014. MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases. J Exp Med 211(5):887-907. [PubMed: 24752299]  [MGI Ref ID J:211307]

Yu Z; Crichton I; Tang SY; Hui Y; Ricciotti E; Levin MD; Lawson JA; Pure E; Fitzgerald GA. 2012. Disruption of the 5-lipoxygenase pathway attenuates atherogenesis consequent to COX-2 deletion in mice. Proc Natl Acad Sci U S A 109(17):6727-32. [PubMed: 22493243]  [MGI Ref ID J:183843]

Yuan H; Zelka S; Burkatovskaya M; Gupte R; Leeman SE; Amar S. 2013. Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss. Proc Natl Acad Sci U S A 110(52):E5059-68. [PubMed: 24324141]  [MGI Ref ID J:205495]

Yuan Z; Miyoshi T; Bao Y; Sheehan JP; Matsumoto AH; Shi W. 2009. Microarray analysis of gene expression in mouse aorta reveals role of the calcium signaling pathway in control of atherosclerosis susceptibility. Am J Physiol Heart Circ Physiol 296(5):H1336-43. [PubMed: 19304945]  [MGI Ref ID J:150880]

Yuan Z; Pei H; Roberts DJ; Zhang Z; Rowlan JS; Matsumoto AH; Shi W. 2009. Quantitative trait locus analysis of neointimal formation in an intercross between C57BL/6 and C3H/HeJ apolipoprotein E-deficient mice. Circ Cardiovasc Genet 2(3):220-228. [PubMed: 19718279]  [MGI Ref ID J:153521]

Yuan Z; Su Z; Miyoshi T; Rowlan JS; Shi W. 2008. Quantitative trait locus analysis of circulating adhesion molecules in hyperlipidemic apolipoprotein E-deficient mice. Mol Genet Genomics 280(5):375-83. [PubMed: 18704499]  [MGI Ref ID J:153398]

Yun SJ; Ha JM; Kim EK; Kim YW; Jin SY; Lee DH; Song SH; Kim CD; Shin HK; Bae SS. 2014. Akt1 isoform modulates phenotypic conversion of vascular smooth muscle cells. Biochim Biophys Acta 1842(11):2184-92. [PubMed: 25201081]  [MGI Ref ID J:218454]

Zaina S; Pettersson L; Ahren B; Branen L; Hassan AB; Lindholm M; Mattsson R; Thyberg J; Nilsson J. 2002. Insulin-like growth factor II plays a central role in atherosclerosis in a mouse model. J Biol Chem 277(6):4505-11. [PubMed: 11726660]  [MGI Ref ID J:74530]

Zanotti I; Pedrelli M; Poti F; Stomeo G; Gomaraschi M; Calabresi L; Bernini F. 2011. Macrophage, but not systemic, apolipoprotein E is necessary for macrophage reverse cholesterol transport in vivo. Arterioscler Thromb Vasc Biol 31(1):74-80. [PubMed: 20966401]  [MGI Ref ID J:184192]

Zeibig S; Li Z; Wagner S; Holthoff HP; Ungerer M; Bultmann A; Uhland K; Vogelmann J; Simmet T; Gawaz M; Munch G. 2011. Effect of the oxLDL binding protein Fc-CD68 on plaque extension and vulnerability in atherosclerosis. Circ Res 108(6):695-703. [PubMed: 21293004]  [MGI Ref ID J:183595]

Zerbi V; Wiesmann M; Emmerzaal TL; Jansen D; Van Beek M; Mutsaers MP; Beckmann CF; Heerschap A; Kiliaan AJ. 2014. Resting-state functional connectivity changes in aging apoE4 and apoE-KO mice. J Neurosci 34(42):13963-75. [PubMed: 25319693]  [MGI Ref ID J:217160]

Zernecke A; Bot I; Djalali-Talab Y; Shagdarsuren E; Bidzhekov K; Meiler S; Krohn R; Schober A; Sperandio M; Soehnlein O; Bornemann J; Tacke F; Biessen EA; Weber C. 2008. Protective role of CXC receptor 4/CXC ligand 12 unveils the importance of neutrophils in atherosclerosis. Circ Res 102(2):209-17. [PubMed: 17991882]  [MGI Ref ID J:145593]

Zernecke A; Liehn EA; Fraemohs L; von Hundelshausen P; Koenen RR; Corada M; Dejana E; Weber C. 2006. Importance of junctional adhesion molecule-A for neointimal lesion formation and infiltration in atherosclerosis-prone mice. Arterioscler Thromb Vasc Biol 26(2):e10-3. [PubMed: 16306427]  [MGI Ref ID J:127969]

Zernecke A; Liehn EA; Gao JL; Kuziel WA; Murphy PM; Weber C. 2006. Deficiency in CCR5 but not CCR1 protects against neointima formation in atherosclerosis-prone mice: involvement of IL-10. Blood 107(11):4240-3. [PubMed: 16467202]  [MGI Ref ID J:128843]

Zernecke A; Schober A; Bot I; von Hundelshausen P; Liehn EA; Mopps B; Mericskay M; Gierschik P; Biessen EA; Weber C. 2005. SDF-1alpha/CXCR4 axis is instrumental in neointimal hyperplasia and recruitment of smooth muscle progenitor cells. Circ Res 96(7):784-91. [PubMed: 15761195]  [MGI Ref ID J:137758]

Zerr M; Hechler B; Freund M; Magnenat S; Lanois I; Cazenave JP; Leon C; Gachet C. 2011. Major contribution of the P2Y(1)receptor in purinergic regulation of TNFalpha-induced vascular inflammation. Circulation 123(21):2404-13. [PubMed: 21576651]  [MGI Ref ID J:184116]

Zetterqvist AV; Berglund LM; Blanco F; Garcia-Vaz E; Wigren M; Duner P; Andersson AM; To F; Spegel P; Nilsson J; Bengtsson E; Gomez MF. 2013. Inhibition of nuclear factor of activated T-cells (NFAT) suppresses accelerated atherosclerosis in diabetic mice. PLoS One 8(6):e65020. [PubMed: 23755169]  [MGI Ref ID J:203205]

Zhang D; Jiang X; Fang P; Yan Y; Song J; Gupta S; Schafer AI; Durante W; Kruger WD; Yang X; Wang H. 2009. Hyperhomocysteinemia promotes inflammatory monocyte generation and accelerates atherosclerosis in transgenic cystathionine beta-synthase-deficient mice. Circulation 120(19):1893-902. [PubMed: 19858416]  [MGI Ref ID J:168131]

Zhang G; Thomas AL; Marshall AL; Kernan KA; Su Y; Zheng Y; Takano J; Saido TC; Eddy AA. 2011. Nicotinic acetylcholine receptor alpha1 promotes calpain-1 activation and macrophage inflammation in hypercholesterolemic nephropathy. Lab Invest 91(1):106-23. [PubMed: 20661225]  [MGI Ref ID J:167191]

Zhang L; Connelly JJ; Peppel K; Brian L; Shah SH; Nelson S; Crosslin DR; Wang T; Allen A; Kraus WE; Gregory SG; Hauser ER; Freedman NJ. 2010. Aging-related atherosclerosis is exacerbated by arterial expression of tumor necrosis factor receptor-1: evidence from mouse models and human association studies. Hum Mol Genet 19(14):2754-66. [PubMed: 20421368]  [MGI Ref ID J:161330]

Zhang L; Peppel K; Sivashanmugam P; Orman ES; Brian L; Exum ST; Freedman NJ. 2007. Expression of tumor necrosis factor receptor-1 in arterial wall cells promotes atherosclerosis. Arterioscler Thromb Vasc Biol 27(5):1087-94. [PubMed: 17442899]  [MGI Ref ID J:128059]

Zhang S; Picard MH; Vasile E; Zhu Y; Raffai RL; Weisgraber KH; Krieger M. 2005. Diet-induced occlusive coronary atherosclerosis, myocardial infarction, cardiac dysfunction, and premature death in scavenger receptor class B type I-deficient, hypomorphic apolipoprotein ER61 mice. Circulation 111(25):3457-64. [PubMed: 15967843]  [MGI Ref ID J:114611]

Zhang SH; Reddick RL; Burkey B; Maeda N. 1994. Diet-induced atherosclerosis in mice heterozygous and homozygous for apolipoprotein E gene disruption. J Clin Invest 94(3):937-45. [PubMed: 8083379]  [MGI Ref ID J:20459]

Zhang SH; Reddick RL; Piedrahita JA; Maeda N. 1992. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science 258(5081):468-71. [PubMed: 1411543]  [MGI Ref ID J:16573]

Zhang T; Dai P; Cheng D; Zhang L; Chen Z; Meng X; Zhang F; Han X; Liu J; Pan J; Yang G; Zhang C. 2014. Obesity occurring in apolipoprotein E-knockout mice has mild effects on fertility. Reproduction 147(2):141-51. [PubMed: 24196014]  [MGI Ref ID J:207680]

Zhang W; Yancey PG; Su YR; Babaev VR; Zhang Y; Fazio S; Linton MF. 2003. Inactivation of macrophage scavenger receptor class B type I promotes atherosclerotic lesion development in apolipoprotein E-deficient mice. Circulation 108(18):2258-63. [PubMed: 14581413]  [MGI Ref ID J:103014]

Zhang WJ; Bird KE; McMillen TS; LeBoeuf RC; Hagen TM; Frei B. 2008. Dietary alpha-lipoic acid supplementation inhibits atherosclerotic lesion development in apolipoprotein E-deficient and apolipoprotein E/low-density lipoprotein receptor-deficient mice. Circulation 117(3):421-8. [PubMed: 18158360]  [MGI Ref ID J:145089]

Zhang X; Thatcher SE; Rateri DL; Bruemmer D; Charnigo R; Daugherty A; Cassis LA. 2012. Transient exposure of neonatal female mice to testosterone abrogates the sexual dimorphism of abdominal aortic aneurysms. Circ Res 110(11):e73-85. [PubMed: 22539767]  [MGI Ref ID J:212660]

Zhang X; Zhu X; Chen B. 2010. Inhibition of collar-induced carotid atherosclerosis by recombinant apoA-I cysteine mutants in apoE-deficient mice. J Lipid Res 51(12):3434-42. [PubMed: 20817832]  [MGI Ref ID J:167029]

Zhao L; Pratico D; Rader DJ; Funk CD. 2005. 12/15-Lipoxygenase gene disruption and vitamin E administration diminish atherosclerosis and oxidative stress in apolipoprotein E deficient mice through a final common pathway. Prostaglandins Other Lipid Mediat 78(1-4):185-93. [PubMed: 16303615]  [MGI Ref ID J:112785]

Zhao Y; Howatt DA; Gizard F; Nomiyama T; Findeisen HM; Heywood EB; Jones KL; Conneely OM; Daugherty A; Bruemmer D. 2010. Deficiency of the NR4A orphan nuclear receptor NOR1 decreases monocyte adhesion and atherosclerosis. Circ Res 107(4):501-11. [PubMed: 20558821]  [MGI Ref ID J:175040]

Zhou C; King N; Chen KY; Breslow JL. 2009. Activation of pregnane X receptor induces hypercholesterolemia in wild-type and accelerates atherosclerosis in apolipoprotein E deficient mice. J Lipid Res 50:2004-2013. [PubMed: 19436068]  [MGI Ref ID J:154141]

Zhou J; Dimayuga PC; Zhao X; Yano J; Lio WM; Trinidad P; Honjo T; Cercek B; Shah PK; Chyu KY. 2014. CD8(+)CD25(+) T cells reduce atherosclerosis in apoE(-/-) mice. Biochem Biophys Res Commun 443(3):864-70. [PubMed: 24342615]  [MGI Ref ID J:211854]

Zhou J; Lee PL; Tsai CS; Lee CI; Yang TL; Chuang HS; Lin WW; Lin TE; Lim SH; Wei SY; Chen YL; Chien S; Chiu JJ. 2012. Force-specific activation of Smad1/5 regulates vascular endothelial cell cycle progression in response to disturbed flow. Proc Natl Acad Sci U S A 109(20):7770-5. [PubMed: 22550179]  [MGI Ref ID J:184788]

Zhou J; Lhotak S; Hilditch BA; Austin RC. 2005. Activation of the unfolded protein response occurs at all stages of atherosclerotic lesion development in apolipoprotein E-deficient mice. Circulation 111(14):1814-21. [PubMed: 15809369]  [MGI Ref ID J:109687]

Zhou X; Hansson GK. 1999. Detection of B cells and proinflammatory cytokines in atherosclerotic plaques of hypercholesterolaemic apolipoprotein E knockout mice. Scand J Immunol 50(1):25-30. [PubMed: 10404048]  [MGI Ref ID J:56605]

Zhou X; Paulsson G; Stemme S; Hansson GK. 1998. Hypercholesterolemia is associated with a T helper (Th) 1/Th2 switch of the autoimmune response in atherosclerotic apo E-knockout mice. J Clin Invest 101(8):1717-25. [PubMed: 9541503]  [MGI Ref ID J:47027]

Zhou X; Robertson AK; Rudling M; Parini P; Hansson GK. 2005. Lesion development and response to immunization reveal a complex role for CD4 in atherosclerosis. Circ Res 96(4):427-34. [PubMed: 15662027]  [MGI Ref ID J:106869]

Zhou X; Stemme S; Hansson GK. 1996. Evidence for a local immune response in atherosclerosis. CD4+ T cells infiltrate lesions of apolipoprotein-E-deficient mice [see comments] Am J Pathol 149(2):359-66. [PubMed: 8701976]  [MGI Ref ID J:34435]

Zhou Y; Cheshire A; Howell LA; Ryan DH; Harris RB. 1999. Neuroautoantibody immunoreactivity in relation to aging and stress in apolipoprotein E-deficient mice. Brain Res Bull 49(3):173-9. [PubMed: 10435780]  [MGI Ref ID J:110915]

Zhou Z; Subramanian P; Sevilmis G; Globke B; Soehnlein O; Karshovska E; Megens R; Heyll K; Chun J; Saulnier-Blache JS; Reinholz M; van Zandvoort M; Weber C; Schober A. 2011. Lipoprotein-derived lysophosphatidic acid promotes atherosclerosis by releasing CXCL1 from the endothelium. Cell Metab 13(5):592-600. [PubMed: 21531341]  [MGI Ref ID J:175811]

Zhu B; Kuhel DG; Witte DP; Hui DY. 2000. Apolipoprotein E inhibits neointimal hyperplasia after arterial injury in mice Am J Pathol 157(6):1839-48. [PubMed: 11106557]  [MGI Ref ID J:66130]

Zhu J; Chen T; Yang L; Li Z; Wong MM; Zheng X; Pan X; Zhang L; Yan H. 2012. Regulation of microRNA-155 in atherosclerotic inflammatory responses by targeting MAP3K10. PLoS One 7(11):e46551. [PubMed: 23189122]  [MGI Ref ID J:195455]

Zimmer S; Steinmetz M; Asdonk T; Motz I; Coch C; Hartmann E; Barchet W; Wassmann S; Hartmann G; Nickenig G. 2011. Activation of endothelial toll-like receptor 3 impairs endothelial function. Circ Res 108(11):1358-66. [PubMed: 21493895]  [MGI Ref ID J:185699]

d'Uscio LV; Baker TA; Mantilla CB; Smith L; Weiler D; Sieck GC; Katusic ZS. 2001. Mechanism of endothelial dysfunction in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 21(6):1017-22. [PubMed: 11397713]  [MGI Ref ID J:103189]

d'Uscio LV; Katusic ZS. 2006. Increased vascular biosynthesis of tetrahydrobiopterin in apolipoprotein E-deficient mice. Am J Physiol Heart Circ Physiol 290(6):H2466-71. [PubMed: 16428344]  [MGI Ref ID J:111845]

d'Uscio LV; Smith LA; Katusic ZS. 2001. Hypercholesterolemia impairs endothelium-dependent relaxations in common carotid arteries of apolipoprotein e-deficient mice. Stroke 32(11):2658-64. [PubMed: 11692031]  [MGI Ref ID J:104001]

ten Freyhaus H; Calay ES; Yalcin A; Vallerie SN; Yang L; Calay ZZ; Saatcioglu F; Hotamisligil GS. 2012. Stamp2 controls macrophage inflammation through nicotinamide adenine dinucleotide phosphate homeostasis and protects against atherosclerosis. Cell Metab 16(1):81-9. [PubMed: 22704678]  [MGI Ref ID J:187419]

van Gils JM; Derby MC; Fernandes LR; Ramkhelawon B; Ray TD; Rayner KJ; Parathath S; Distel E; Feig JL; Alvarez-Leite JI; Rayner AJ; McDonald TO; O'Brien KD; Stuart LM; Fisher EA; Lacy-Hulbert A; Moore KJ. 2012. The neuroimmune guidance cue netrin-1 promotes atherosclerosis by inhibiting the emigration of macrophages from plaques. Nat Immunol 13(2):136-43. [PubMed: 22231519]  [MGI Ref ID J:181210]

van Haperen R; de Waard M; van Deel E; Mees B; Kutryk M; van Aken T; Hamming J; Grosveld F; Duncker DJ; de Crom R. 2002. Reduction of blood pressure, plasma cholesterol, and atherosclerosis by elevated endothelial nitric oxide. J Biol Chem 277(50):48803-7. [PubMed: 12364322]  [MGI Ref ID J:80701]

van Meer P; Pfankuch T; Raber J. 2007. Reduced histamine levels and H3 receptor antagonist-induced histamine release in the amygdala of Apoe-/- mice. J Neurochem 103(1):124-30. [PubMed: 17573822]  [MGI Ref ID J:128042]

von Dehn G; von Dehn O; Volker W; Langer C; Weinbauer GF; Behre HM; Nieschlag E; Assmann G; von Eckardstein A. 2001. Atherosclerosis in apolipoprotein E-deficient mice is decreased by the suppression of endogenous sex hormones. Horm Metab Res 33(2):110-4. [PubMed: 11294492]  [MGI Ref ID J:68906]

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The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

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Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3435.00
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At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

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    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

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Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4465.50
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

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Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty


In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.