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Strain Name:

B6.129P2-Apoetm1Unc/J

Stock Number:

002052

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General Terms and Conditions

Genes & Alleles   Apoe;   Apoetm1Unc;

Product Information

Strain Details

Type JAX® GEMM® Strain - Congenic
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Mutant Strain
Type JAX® GEMM® Strain - Targeted Mutation
Mating SystemHomozygote x Homozygote         (Female x Male)
Specieslaboratory mouse
Background Strain C57BL/6
Donor Strain 129P2 via E14TG2a ES cell line
Donating Investigator Nobuyo Maeda,   Univ of North Carolina at Chapel Hill
GenerationN12F17 (03-JAN-08)

Appearance
black
Related Genotype: a/a

Strain Description
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.

Strain Development
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 C57BL/6J strain was produced by backcrossing the Apoetm1Unc mutation 10 times to C57BL/6J mice. Previously mice backcrossed 6 times (N6) to C57BL/6J mice were distributed solely. Mice from the N6 generation are homozygous for pink-eyed dilution p giving them pink eyes and a silver coat color. The E14Tg2a ES cell line carries this recessive mutation which remains linked to the targeted Apoe gene on Chromosome 7 at this backcross generation. Mice from the N6 colony are no longer available for distribution.

Mammalian Phenotype Terms assigned by genotype

Apoetm1Unc/Apoetm1Unc

        B6.129P2-Apoetm1Unc/J
  • life span-post-weaning/aging
  • premature death (J:73202)
    • 35% dead by 18 months
  • cardiovascular system phenotype
  • abnormal aorta morphology (J:101576)
    • 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
    • the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet
    • endothelial nitric oxide synthase (eNOS) in mutant aortic wall is distinctly reduced
  • abnormal blood flow velocity (J:108154)
    • 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
    • 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
    • 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
    • however, homozygotes show alterations in aortic arch acceleration suggestive of increased peripheral wave reflections
  • abnormal blood-brain barrier function (J:69455)
    • impairment of blood-brain barrier (BBB) function
    • impairment of blood-nerve barrier (BNB) function
  • abnormal cardiac stroke volume (J:108154)
    • under anesthesia, homozygotes appear to exhibit significantly increased stroke volume
  • abnormal spiral modiolar artery morphology (J:101576)
    • homozygotes fed an atherosclerotic diet develop atherosclerotic alterations in the spiral modiolar artery (SMA)
    • in contrast, no such changes are detected in the SMA of homozygotes fed a normal diet
    • spiral modiolar artery stenosis (J:101576)
      • lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal diet
  • arteriosclerosis (J:108154)
    • 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
    • atherosclerotic lesions (J:73202)
      • advanced atherosclerotic lesions
      • at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation
      • lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions
      • 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
      • 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
      • the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet
      • plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes
      • increased susceptibility to atherosclerosis (J:101576)
        • 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
  • cardiac hypertrophy (J:108154)
    • at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild type mice
  • decreased systemic vascular resistance (J:108154)
    • under anesthesia, homozygotes appear to exhibit significantly reduced peripheral vascular resistance and compliance in the presence of normal blood pressures
  • decreased vasodilation (J:101576)
    • 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
  • increased cardiac output (J:108154)
    • under anesthesia, homozygotes exhibit elevated flow velocities suggesting elevated cardiac output
  • increased heart weight (J:108154)
    • at 13 months, homozygotes show a 23% increase in heart weight relative to wild type mice (186 ± 7.1 vs. 151 ± 2.5 mg)
  • vascular stenosis (J:101576)
    • vascular stenosis is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet
    • spiral modiolar artery stenosis (J:101576)
      • lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal diet
  • homeostasis/metabolism phenotype
  • abnormal circulating cholesterol level (J:73202)
    • decreased HDL/total cholesterol ratio
    • decreased HDL/LDL ratio
    • increased circulating cholesterol level (J:73202)
      • increasing with age
      • 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
      • on a normal diet, homozygotes display significantly increased plasma total cholesterol (TC) levels relative to C57BL/6J control mice
      • on an atherosclerotic diet, homozygotes show a further significant increase in plasma TC levels relative to homozygotes on a normal diet
      • increased circulating LDL cholesterol level (J:93987)
        • on a normal diet, homozygotes display significantly increased plasma LDL cholesterol levels relative to C57BL/6J control mice
        • on an atherosclerotic diet, homozygotes show a further significant increase in plasma LDL levels relative to homozygotes on a normal diet
      • increased circulating VLDL cholesterol level (J:93987)
        • on a normal diet, homozygotes display significantly increased plasma VLDL cholesterol levels relative to C57BL/6J control mice
        • on an atherosclerotic diet, homozygotes show a further significant increase in plasma VLDL cholesterol levels relative to homozygotes on a normal diet
  • abnormal circulating homocysteine level (J:73202)
    • decreased plasma total homocysteine levels
  • decreased circulating glucose level (J:73202)
    • in plasma
  • decreased circulating triglyceride level (J:93987)
  • hyperlipidemia (J:101576)
    • 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
  • increased circulating triglyceride level (J:73202)
    • in plasma
    • on a normal diet, homozygotes display significantly increased plasma triglyceride levels relative to C57BL/6J control mice
    • on an atherosclerotic diet, homozygotes show a further significant increase in plasma triglyceride levels relative to homozygotes on a normal diet
  • skin/coat/nails phenotype
  • skin lesions (J:73202)
    • eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components
  • growth/size phenotype
  • decreased body weight (J:108154)
    • 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)
  • hematopoietic system phenotype
  • decreased hematocrit (J:108154)
    • 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)
  • cellular phenotype
  • oxidative stress (J:97385)
    • regular exercise fails to reduce endogenous oxidant load and mitochondrial damage in hypercholesterolemic mutant mice
    • in contrast, regular exercise results in reduced mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities in normocholesterolemic control mice
  • hearing/vestibular/ear phenotype
  • abnormal cochlea morphology (J:101576)
    • endothelial nitric oxide synthase (eNOS) in mutant cochlea is distinctly reduced
    • abnormal basilar membrane (J:101576)
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic basilar membrane
    • abnormal stria vascularis (J:101576)
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic stria vascularis
    • abnormal tectorial membrane morphology (J:101576)
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic tectorial membrane
    • cochlear inner hair cell degeneration (J:101576)
      • 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
      • IHC loss at the base turn is exacerbated by an atherosclerotic diet
    • cochlear outer hair cell degeneration (J:101576)
      • 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
      • OHC loss at the base turn is exacerbated by an atherosclerotic diet
    • organ of Corti degeneration (J:101576)
      • 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
      • degeneration of the organ of Corti is excerbated by an atherosclerotic diet, with complete loss noted in the basal turn in some animals
  • deafness (J:101576)
    • homozygotes fed a normal diet display hearing loss esp. at high frequencies as compared with C57BL/6J control mice
    • 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
  • decreased brainstem auditory evoked potential (J:101576)
    • 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
    • homozygotes fed an atherosclerotic diet show higher ABR thresholds than homozygotes fed a normal diet
  • nervous system phenotype
  • abnormal blood-brain barrier function (J:69455)
    • impairment of blood-brain barrier (BBB) function
    • impairment of blood-nerve barrier (BNB) function
  • cochlear ganglion degeneration (J:101576)
    • at 24 weeks, homozygotes fed a normal diet show a reduced number of spiral ganglion cells in the basal turn of the cochlea
    • loss of ganglion cells is excerbated by an atherosclerotic diet
  • cochlear inner hair cell degeneration (J:101576)
    • 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
    • IHC loss at the base turn is exacerbated by an atherosclerotic diet
  • cochlear outer hair cell degeneration (J:101576)
    • 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
    • OHC loss at the base turn is exacerbated by an atherosclerotic diet

Apoetm1Unc/Apoetm1Unc

        either: B6.129P2-Apoetm1Unc/J or (involves: 129P2/OlaHsd * C57BL/6J * ICR)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype (J:100975)
    • no alterations in passive avoidance learning are observed; coordination levels measured in rotorod tests are similar to wild-type
    • abnormal spatial learning (J:100975)
      • 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
    • decreased vertical activity (J:100975)
      • mice have fewer rearing events and shorter rearing times than wild-type controls
  • nervous system phenotype
  • *normal* nervous system phenotype (J:100975)
    • mice exhibit age-dependent loss of synaptophysin-reactive terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus
    • 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
    • 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)

Apoetm1Unc/Apoetm1Unc

        B6.129P2-Apoetm1Unc
  • immune system phenotype
  • abnormal cell-mediated immunity (J:125366)
    • the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response
    • 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
    • abnormal dendritic cell physiology (J:125366)
      • 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
      • 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
      • CD8alpha-, but not CD8alpha+, dendritic cells are defective in their ability to produce IL-12p40
      • 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
      • however, CD8alpha+ dendritic cells produce normal amounts of Il-12p70 and -12p40
      • 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%)
      • 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
  • increased CD4-positive T cell number (J:125366)
    • mice maintained on a high fat diet and infect with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild type mice
  • increased susceptibility to parasitic infection (J:125366)
    • mice maintained on a high fat diet and infect with Leishmania major produce more IL-4 and IL-5 producing CD4+ T cells compared to wild type mice
    • the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response
    • mice maintained on a high fat diet or regular chow and infect with Leishmania major exhibit an increased swelling and parasitic burden at the site of infection (footpad)
  • homeostasis/metabolism phenotype
  • abnormal lipid level (J:125366)
    • mice have increased levels of circulating oxidized lipids compared to wild type mice
  • behavior/neurological phenotype
  • abnormal locomotor activity (J:71062)
    • mice spend more time than Tg(GFAP-APOE*4)Hol Apoetm1Unc/Apoetm1Unc in the center of an open field
  • abnormal response to new environment (J:71062)
    • mice consume food slower in a new environment than Tg(GFAP-APOE*4)Hol Apoetm1Unc/Apoetm1Unc and wild type mice
    • mice require more time to habituate to a novel environment compared to wild type mice
    • mice are less reluctant than wild type mice to move into an open area
  • abnormal spatial learning (J:71062)
    • at 14 to 17 months of age, mice perform better than Tg(GFAP-APOE*4)Hol Apoetm1Unc/Apoetm1Unc and wild type mice in a rotating holeboard test
  • decreased startle reflex (J:71062)
  • hearing/vestibular/ear phenotype
  • decreased startle reflex (J:71062)
  • hematopoietic system phenotype
  • increased CD4-positive T cell number (J:125366)
    • mice maintained on a high fat diet and infect with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild type mice

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Apoetm1Unc/Apoetm1Unc

        either: 129P2/OlaHsd-Apoetm1Unc or (involves: 129P2/OlaHsd * C57BL/6J)
  • cardiovascular system phenotype
  • atherosclerotic lesions (J:43846)
  • homeostasis/metabolism phenotype
  • xanthoma (J:43846)
    • 3 of 15 aged mice (17 months) fed conventional chow exhibit small choroidal xanthomas
    • aged mice (15 - 23 months) kept on a high fat/high cholesterol diet from age 17 weeks exhibit cerebral xanthomatous lesions, consisting of crystalline cholesterol clefts, lipid globules and foam cells

Apoetm1Unc/Apoetm1Unc

        involves: 129P2/OlaHsd * C57BL/6
  • cardiovascular system phenotype
  • atherosclerotic lesions (J:80689)
    • greater than in wild-type
  • homeostasis/metabolism phenotype
  • hyperlipidemia (J:80689)
    • relative to wild-type
  • increased circulating cholesterol level (J:80689)
    • relative to wild-type
  • increased circulating triglyceride level (J:80689)
    • relative to wild-type
  • nervous system phenotype
  • abnormal glial cell physiology (J:58019)
    • astrocytes secrete less phospholipids or free cholesterol compared to wild type astrocytes

Apoetm1Unc/Apoetm1Unc

        involves: 129P2/OlaHsd
  • behavior/neurological phenotype
  • increased anxiety-related response (J:101973)
    • 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
    • effect is age-dependent; phenotype is present in older mice, but not in young 2-4 month-old mice
  • increased startle reflex (J:101973)
    • response is higher in mice at 6 months of age compared to wild-type
  • hearing/vestibular/ear phenotype
  • increased startle reflex (J:101973)
    • response is higher in mice at 6 months of age compared to wild-type
  • homeostasis/metabolism phenotype
  • decreased cerebral infarction size (J:133156)
    • compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice
  • increased circulating corticosterone level (J:101973)
    • all males have higher plasma concentrations than wild-type after behavioral testing
  • nervous system phenotype
  • abnormal dendrite morphology (J:101973)
    • mutants have lower levels of MAP 2-positive neuronal dendrites than wild-type; at 3 months, levels are similar in mutants and controls
  • decreased cerebral infarction size (J:133156)
    • compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice
  • cardiovascular system phenotype
  • increased susceptibility to atherosclerosis (J:107390)
    • bone marrow transplanted into Apoa1tm1Unc homozygotes confer susceptibility to atherosclerosis

Apoetm1Unc/Apoetm1Unc

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

Gene & Allele Details

Allele Symbol Apoetm1Unc
Allele Name targeted mutation 1, University of North Carolina
Common Name(s) AopE(-); ApoE-KO; Apoetm1Un; apoE-; apoE0; epsilon-;
Mutation Made By Nobuyo Maeda,   Univ 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; LPG; MGC1571; apoprotein; expressed sequence AI255918;
General Note

In Apoetm1Unc mutant mice also carrying Csf1op, atherotic lesions of the proximal aorta were abolished or significantly reduced in size relative to Apoe mutants homozygous for the normal allele at Csf1 (J:40136). The results may have been due to reduced macrophages or M-CSF, but were not due to reductions in circulating lipoprotein (J:40136).

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. [J:1050]

Control Information

  Allele   Control
 Apoetm1Unc  000664 C57BL/6J
 
  Considerations for Choosing Controls

Genotyping Protocols

Apoetm1Unc

Colony Maintenance

Diet Information JAX West and Bar Harbor Diets

Related Strains

View Strains carrying   Apoetm1Unc     (9 strains)

Phenotypic Data

Body Weight Information - JAX® Mice Strain B6.129P2-Apoetm1Unc/J (002052)
(This chart reflects the typical correlation between body weight and age for mice maintained in production colonies at The Jackson Laboratory.)
Mouse Phenome Database
NEW -- JAX® Physiological Data Summary
NEW -- JAX® Physiological Data Protocol

Additional Web Information

NEW -- JAX® Physiological Data Protocol
NEW -- JAX® Physiological Data Summary
Congenic Nomenclature
Genetic Quality Control Annual Report
JAX Notes, Fall 2003; 491. JAX West Expansion
Visit the Alzheimer's Disease Mouse Model Resource site for helpful information on Alzheimer's Disease and research resources.

Animal Health Reports

Room Number           AX1
Room Number           AX3
Room Number           MP14
Room Number           MP15
Room Number           WR3

Research Applications

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

Diabetes and Obesity Research
Obesity Without Diabetes (diet-induced)

Neurobiology Research
Alzheimer's Disease
Behavioral and Learning Defects
Neurodegeneration

Apoetm1Unc related

Cardiovascular Research
Atherosclerosis
Hypercholesterolemia

Mouse/Human Gene Homologs
Alzheimer's
hyperlipoproteinemia, type III

References

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]  [J:1050]

Additional References

Price and Supply Information

Strain Name: B6.129P2-Apoetm1Unc/J
Stock Number: 002052

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Supply Details

Standard SupplyLevel 1. JAX Ready Strain® (readily available).
Supply Notes Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
Strains that must be genotyped are not available until five to seven weeks of age.
This strain is available from some international Charles River Laboratories (CRL) breeding facilities in Japan and/or Europe. For more information, see the Worldwide Distributor List for JAX® Mice.
This strain is included in the Induced Mutant Resource Colony collection.
Genomic DNA is available for this strain from the Mouse DNA Resource.
LicensingSee General Terms and Conditions below  
Control InformationView Control Information in Strain Details.

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