Strain Name:



Repository- Live     Available at the JAX MMRRC

Use Restrictions Apply, see Terms of Use
Common Names: 5XFAD;    
This strain is now distributed by the Mutant Mouse Regional Resource Center. Please refer to the Mutant Mouse Regional Resource Center (MMRRC) for ordering information and strain details on (B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax MMRRC Stock Number 034848.
As a designated MMRRC center, The Jackson Laboratory will continue to distribute these mice at the same high health and
quality standards but ordering is exclusively provided through the MMRRC.
5XFAD transgenic mice (formerly JAX Stock No. 008730) overexpress both mutant human APP(695) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations and human PS1 harboring two FAD mutations, M146L and L286V. Expression of both transgenes is regulated by neural-specific elements of the mouse Thy1 promoter to drive overexpression in the brain. These 5XFAD transgenic mice rapidly recapitulate major features of Alzheimer's Disease amyloid pathology and may be useful models of intraneuronal Aβ-42 induced neurodegeneration and amyloid plaque formation.


Strain Information

Former Names B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/J    (Changed: 11-AUG-11 )
Type Congenic; Transgenic;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemNoncarrier x Hemizygote         (Female x Male)   28-OCT-13
Specieslaboratory mouse
GenerationN6+N1F1 (24-APR-15)
Generation Definitions
Donating Investigator IMR Colony,   The Jackson Laboratory

Hemizygous mice are viable and fertile. These 5XFAD transgenic mice overexpress both mutant human APP(695) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations and human PS1 harboring two FAD mutations, M146L and L286V. Expression of both transgenes is regulated by neural-specific elements of the mouse Thy1 promoter to drive overexpression in the brain. Mice from this founder line have high APP expression correlating with high burden and accelerated accumulation of the 42 amino acid species of beta-amyloid (Aβ-42). 5XFAD mice generate Aβ-42 almost exclusively and rapidly accumulate massive cerebral levels. On the B6SJL F1 genetic background (see MMRRC stock 34840), intraneuronal Abeta;-42 accumulation is observed starting at 1.5 months of age, just prior to amyloid deposition and gliosis, which begins at two months of age. On a congenic C57BL/6J genetic background (see MMRRC stock 34848) it has been the observation of the MMRRC that this phenotype is not as robust as that demonstrated in the B6SJL hybrid background (view data). In addition, these mice have reduced synaptic marker protein levels, increased p25 levels, neuron loss, and memory impairment in the Y-maze test. 5XFAD transgenic mice rapidly recapitulate major features of Alzheimer's Disease amyloid pathology and may be useful models of intraneuronal Aβ-42 induced neurodegeneration and amyloid plaque formation.

This strain does not carry the retinal degeneration allele Pde6brd1.

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.

A transgene was designed with a mutant human amyloid beta (A4) precursor protein (APP) cDNA sequence (altered to include the APP K670N/M671L (Swedish) + I716V (Florida) + V717I (London) Familial Alzheimer's Disease (FAD) mutations) inserted into exon 2 of the mouse Thy1 gene. A second transgene was designed with a mutant human presenilin 1 (Alzheimer disease 3) (PSEN1 or PS1) cDNA sequence (altered to include the PS1 M146L + L286V FAD mutations) inserted into exon 2 of the mouse Thy1 gene. Both transgenes were added together in equal proportions and co-injected into the pronuclei of single-cell "C57/B6XSJL" hybrid embryos. Founders from the highest APP expressing line (Tg6799) were bred with (B6/SJL)F1 for more than 10 generations with stable germ-line transmission and expression of both transgenes, demonstrating that these "5XFAD" mice breed as single transgenics. The mice were then backcrossed to C57BL/6J mice using a speed congenic protocol and the retinal degeneration allele Pde6brd1 was bred out of the strain. Of note, the APP transgene includes the 5' untranslated region and thus contains a putative interleukin-1beta translational enhancer element.

Control Information

   000664 C57BL/6J
  Considerations for Choosing Controls

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006410   B6;129S6-Chattm2(cre)Lowl/J
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006554   B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
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002328   C.129S2-Plautm1Mlg/J
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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
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004779   STOCK Mapttm1(EGFP)Klt/J
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View Alzheimer's Disease Models     (111 strains)

Strains carrying   Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas allele
006554   B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
View Strains carrying   Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas     (1 strain)

View Strains carrying other alleles of APP695     (9 strains)

View Strains carrying other alleles of PSEN1     (5 strains)

Strains carrying other alleles of Thy1
005895   B10.Cg-Thy1a H2d Tg(TcraCl1,TcrbCl1)1Shrm/J
001317   B6.Cg-Gpi1a Thy1a Igha/J
017798   B6.Cg-Mapttm1Hnd Tg(Thy1-MAPT*)3610Gds/Mmjax
009126   B6.Cg-Nos2tm1Lau Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
025855   B6.Cg-Ptprca Lag3tm1Doi Tg(CAG-luc,-GFP)L2G85Chco Thy1a/J
014550   B6.Cg-Thy1a Tg(TcraCWM5,TcrbCWM5)1807Wuth/J
005023   B6.Cg-Thy1a/Cy Tg(TcraTcrb)8Rest/J
007901   B6.Cg-Tg(Thy1-Brainbow1.0)HLich/J
007911   B6.Cg-Tg(Thy1-Brainbow1.1)MLich/J
007921   B6.Cg-Tg(Thy1-Brainbow2.1)RLich/J
003710   B6.Cg-Tg(Thy1-CFP)23Jrs/J
014131   B6.Cg-Tg(Thy1-CFP)IJrs/GfngJ
007940   B6.Cg-Tg(Thy1-CFP/COX8A)C1Lich/J
007967   B6.Cg-Tg(Thy1-CFP/COX8A)S2Lich/J
012597   B6.Cg-Tg(Thy1-COL25A1)861Yfu/J
007612   B6.Cg-Tg(Thy1-COP4/EYFP)18Gfng/J
007615   B6.Cg-Tg(Thy1-COP4/EYFP)9Gfng/J
013161   B6.Cg-Tg(Thy1-Clomeleon)1Gjau/J
007919   B6.Cg-Tg(Thy1-EGFP)OJrs/GfngJ
005630   B6.Cg-Tg(Thy1-EYFP)15Jrs/J
009611   B6.Cg-Tg(Thy1-Nlgn1)6Hnes/J
009612   B6.Cg-Tg(Thy1-Nlgn2)6Hnes/J
021069   B6.Cg-Tg(Thy1-PA-GFP)5Rmpl/J
021070   B6.Cg-Tg(Thy1-PA-GFP)6Rmpl/J
003709   B6.Cg-Tg(Thy1-YFP)16Jrs/J
003782   B6.Cg-Tg(Thy1-YFP)HJrs/J
005627   B6.Cg-Tg(Thy1-YFP/Syp)10Jrs/J
007606   B6.Cg-Tg(Thy1-cre/ERT2,-EYFP)AGfng/J
025854   B6.FVB-Ptprca Tg(CAG-luc,-GFP)L2G85Chco Thy1a/J
000406   B6.PL-Thy1a/CyJ
000983   B6.PL/(84NS)CyJ
004807   B6;129-Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Mmjax
007910   B6;CBA-Tg(Thy1-Brainbow1.0)LLich/J
011070   B6;CBA-Tg(Thy1-EGFP)SJrs/NdivJ
017892   B6;CBA-Tg(Thy1-GCaMP2.2c)8Gfng/J
017893   B6;CBA-Tg(Thy1-GCaMP3)6Gfng/J
014130   B6;CBA-Tg(Thy1-YFP)GJrs/GfngJ
014651   B6;CBA-Tg(Thy1-spH)21Vnmu/J
015814   B6;CBA-Tg(Thy1-spH)64Vnmu/FrkJ
012341   B6;SJL-Tg(Thy1-COP3/EYFP)1Gfng/J
012344   B6;SJL-Tg(Thy1-COP3/EYFP)4Gfng/J
012348   B6;SJL-Tg(Thy1-COP3/EYFP)8Gfng/J
012350   B6;SJL-Tg(Thy1-COP4*H134R/EYFP)20Gfng/J
008004   B6;SJL-Tg(Thy1-ECFP/VAMP2)1Sud/J
012836   B6;SJL-Tg(Thy1-TARDBP)4Singh/J
007610   B6;SJL-Tg(Thy1-cre/ERT2,-EYFP)VGfng/J
012332   B6;SJL-Tg(Thy1-hop/EYFP)2Gfng/J
012334   B6;SJL-Tg(Thy1-hop/EYFP)4Gfng/J
025401   B6SJL-Tg(Thy1-COX8A/Dendra)57Gmnf/J
017590   B6SJL-Tg(Thy1-DCTN1*G59S)M2Pcw/J
007880   B6SJL-Tg(Thy1-Stx1a/EYFP)1Sud/J
007856   B6SJL-Tg(Thy1-Syt1/ECFP)1Sud/J
017589   B6SJL-Tg(Thy1-TARDBP*G298S)S97Pcw/J
017351   BKa.Cg-Ptprcb Bmi1tm1Ilw Thy1a/J
007687   BKa.Cg-Sox17tm1Sjm Ptprcb Thy1a/J
007686   BKa.Cg-Sox17tm2Sjm Ptprcb Thy1a/J
024703   C3A.Cg-Pde6b+Tg(Thy1-CFP)23Jrs/SjJ
007027   C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
027258   C57BL/6-Tg(Thy1-EGFP/SQSTM1)02Mcwo/J
010800   C57BL/6-Tg(Thy1-PTGS2)300Kand/J
010703   C57BL/6-Tg(Thy1-PTGS2)303Kand/J
012769   C57BL/6-Tg(Thy1-Sncg)HvP36Putt/J
024339   C57BL/6J-Tg(Thy1-GCaMP6f)GP5.11Dkim/J
025393   C57BL/6J-Tg(Thy1-GCaMP6f)GP5.17Dkim/J
024276   C57BL/6J-Tg(Thy1-GCaMP6f)GP5.5Dkim/J
025776   C57BL/6J-Tg(Thy1-GCaMP6s)GP4.12Dkim/J
024275   C57BL/6J-Tg(Thy1-GCaMP6s)GP4.3Dkim/J
025533   C57BL/6N-Sncatm1Mjff Tg(Thy1-SNCA)15Mjff/J
016936   C57BL/6N-Tg(Thy1-SNCA)12Mjff/J
017682   C57BL/6N-Tg(Thy1-SNCA)15Mjff/J
005307   CBy.Cg-Thy1a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ
005922   CBy.Cg-Thy1a Tg(TcraCl1,TcrbCl1)1Shrm/J
005443   CBy.PL(B6)-Thy1a/ScrJ
024704   D2.Cg-Gpnmb+Tg(Thy1-CFP)23Jrs/SjJ
025018   D2.Cg-Gpnmb+Tg(Thy1-YFP)HJrs/SjJ
026854   D2.Cg-Tg(Thy1-Brainbow1.0)LLich/SjJ
018671   D2.Cg-Tg(Thy1-CFP)23Jrs/SjJ
024705   D2.Cg-Tg(Thy1-YFP)HJrs/SjJ
008230   FVB(Cg)-Tg(Thy1-SOD1*G93A)T3Hgrd/J
006143   FVB/N-Tg(Thy1-cre)1Vln/J
024476   NOD.Cg-Stat4tm1Gru Thy1a Ifngr1tm1Agt Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/LmbrJ
005686   NOD.Cg-Thy1a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ
004483   NOD.NON-Thy1a/1LtJ
002721   NOD.NON-Thy1a/J
005651   SJL.AK-Thy1a/TseJ
003961   SJL.Cg Thy1a-Noxo1hslt/J
021226   STOCK Tg(Thy1-Brainbow3.1)18Jrs/J
021225   STOCK Tg(Thy1-Brainbow3.1)3Jrs/J
021227   STOCK Tg(Thy1-Brainbow3.2)7Jrs/J
013162   STOCK Tg(Thy1-Clomeleon)12Gjau/J
013163   STOCK Tg(Thy1-Clomeleon)13Gjau/J
007788   STOCK Tg(Thy1-EGFP)MJrs/J
012708   STOCK Tg(Thy1-cre/ERT2,-EYFP)HGfng/PyngJ
View Strains carrying other alleles of Thy1     (93 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
- Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.
Alzheimer Disease 3
Alzheimer Disease; AD
- Potential model based on transgenic expression of a human gene that is associated with this disease. Phenotypic similarity to the human disease has not been tested.
Acne Inversa, Familial, 3; ACNINV3   (PSEN1)
Cardiomyopathy, Dilated, 1u; CMD1U   (PSEN1)
Frontotemporal Dementia; FTD   (PSEN1)
Pick Disease of Brain   (PSEN1)
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: C57BL/6 * SJL
  • behavior/neurological phenotype
  • abnormal spatial learning
    • by 4-5 months of age, defects in Y-maze alternation are detected in transgenic mice, indicating impaired spatial learning/memory   (MGI Ref ID J:112949)
  • nervous system phenotype
  • abnormal hippocampus morphology
    • cortical layer 1 is significantly thinner than in control brains   (MGI Ref ID J:112949)
    • abnormal subiculum morphology
      • neurons in subiculum are very pale, or absent   (MGI Ref ID J:112949)
  • abnormal neuron morphology
    • some neurons contain intraneuronal aggregates and display disrupted morphology   (MGI Ref ID J:112949)
    • decreased cerebral cortex pyramidal cell number
      • large neurons in cortical layer 5 are reduced in number   (MGI Ref ID J:112949)
  • amyloid beta deposits
    • mice show Abeta42 deposits at 2 months of age; Abeta40 levels are lower in amyloid deposits; mice show robust intraneuronal amyloid deposition   (MGI Ref ID J:112949)
    • amyloid deposition increases rapidly with increasing age   (MGI Ref ID J:112949)
    • plaques appear first in deep cortical layers and in subiculum, and spread with age to fill most of cortex, subiculum and hippocampus; also, less numerous deposits are observed in thalamus, brainstem and olfactory bulb in older mice   (MGI Ref ID J:112949)
  • brain inflammation
    • transgenic mice display neuroinflammation   (MGI Ref ID J:112949)
  • gliosis
    • microgliosis and astrogliosis is seen in plaque-bearing regions of the brain by 2 months of age; numbers of activated astrocytes and microglia increases with age   (MGI Ref ID J:112949)
  • neurodegeneration
    • synapse degeneration begins at 4 months of age, compared to nontransgenic controls, as shown by reduction in levels of synaptic markers; neurodeneration marker p25 level is ~150% of control at 9 and 12 months   (MGI Ref ID J:112949)
  • immune system phenotype
  • brain inflammation
    • transgenic mice display neuroinflammation   (MGI Ref ID J:112949)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits
    • mice show Abeta42 deposits at 2 months of age; Abeta40 levels are lower in amyloid deposits; mice show robust intraneuronal amyloid deposition   (MGI Ref ID J:112949)
    • amyloid deposition increases rapidly with increasing age   (MGI Ref ID J:112949)
    • plaques appear first in deep cortical layers and in subiculum, and spread with age to fill most of cortex, subiculum and hippocampus; also, less numerous deposits are observed in thalamus, brainstem and olfactory bulb in older mice   (MGI Ref ID J:112949)


        involves: C57BL/6 * C57BL/6J * CBA * SJL
  • mortality/aging
  • premature death
    • decreased survival at 10 months of age   (MGI Ref ID J:201809)
  • nervous system phenotype
  • amyloid beta deposits   (MGI Ref ID J:201809)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits   (MGI Ref ID J:201809)


  • homeostasis/metabolism phenotype
  • amyloid beta deposits
    • retinal amyloid beta accumulates in the retinal pigment epithelial (RPE) layer and amyloid beta deposits are seen beneath the RPE layer   (MGI Ref ID J:214858)
  • nervous system phenotype
  • amyloid beta deposits
    • retinal amyloid beta accumulates in the retinal pigment epithelial (RPE) layer and amyloid beta deposits are seen beneath the RPE layer   (MGI Ref ID J:214858)
  • pigmentation phenotype
  • abnormal retinal pigment epithelium morphology
    • abundant intracellular amyloid beta is seen in the cytosol of RPE and with increasing intracellular accumulation of amyloid beta, tight junction integrity is attenuated and disorganized   (MGI Ref ID J:214858)
    • abnormal retinal pigmentation
      • 12 month old mutants show hypopigmentation in the RPE layer   (MGI Ref ID J:214858)
  • vision/eye phenotype
  • abnormal eye morphology
    • drusen-like deposit is seen between the retinal pigment epithelium (RPE) layer and Bruch membrane in 12 month old mutants   (MGI Ref ID J:214858)
    • abnormal Bruch membrane morphology
      • thickened Bruch membrane is seen in the retina of 12 month old mutants   (MGI Ref ID J:214858)
    • abnormal retina morphology
      • large vacuoles are seen in the retina of 12 month old mutants   (MGI Ref ID J:214858)
      • abnormal retinal pigment epithelium morphology
        • abundant intracellular amyloid beta is seen in the cytosol of RPE and with increasing intracellular accumulation of amyloid beta, tight junction integrity is attenuated and disorganized   (MGI Ref ID J:214858)
        • abnormal retinal pigmentation
          • 12 month old mutants show hypopigmentation in the RPE layer   (MGI Ref ID J:214858)


        involves: 129S4/SvJae * C57BL/6 * SJL
  • mortality/aging
  • premature death
    • impaired survival compared to wild-type mice   (MGI Ref ID J:169682)
    • survive longer than transgenic mice that are also Apoa4 null   (MGI Ref ID J:169682)
  • nervous system phenotype
  • amyloid beta deposits   (MGI Ref ID J:169682)
  • neuron degeneration   (MGI Ref ID J:169682)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits   (MGI Ref ID J:169682)


        involves: C57BL/6 * SJL
  • behavior/neurological phenotype
  • abnormal response to novel object
    • poor novel object recognition   (MGI Ref ID J:208030)
  • impaired contextual conditioning behavior
    • decreased % of time freezing in contextual fear conditioning test   (MGI Ref ID J:208030)
  • impaired cued conditioning behavior
    • decreased % of time freezing in cued fear conditioning test   (MGI Ref ID J:208030)
  • hematopoietic system phenotype
  • abnormal microglial cell activation
    • increased percentage of activated microglia as compared to controls   (MGI Ref ID J:208030)
  • immune system phenotype
  • abnormal microglial cell activation
    • increased percentage of activated microglia as compared to controls   (MGI Ref ID J:208030)
  • nervous system phenotype
  • abnormal astrocyte physiology
    • increased percentage of reactive astrocytes as compared to controls   (MGI Ref ID J:208030)
  • abnormal long term depression
    • decreased magnitude of long term depression as compared to controls   (MGI Ref ID J:208030)
  • abnormal microglial cell activation
    • increased percentage of activated microglia as compared to controls   (MGI Ref ID J:208030)
  • amyloid beta deposits
    • increased plaque load and size as compared to controls   (MGI Ref ID J:208030)
    • high levels of Abeta42 and Abeta40 in the hippocampus as compared to mice that also carry Cdk5r1tm2.1Lht   (MGI Ref ID J:208030)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits
    • increased plaque load and size as compared to controls   (MGI Ref ID J:208030)
    • high levels of Abeta42 and Abeta40 in the hippocampus as compared to mice that also carry Cdk5r1tm2.1Lht   (MGI Ref ID J:208030)
View Research Applications

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

Neurobiology Research
Alzheimer's Disease
      APP and PSEN1 mutants
      Presenilin mutants
      strains expressing mutant APP

Research Tools
Neurobiology Research

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas
Allele Name transgene insertion 6799, Robert Vassar
Allele Type Transgenic (Humanized sequence, Inserted expressed sequence)
Common Name(s) 5XFAD; 5XFAD APP/PS1; 5XFAD line Tg6799; Tg-5xFAD; Tg6799;
Mutation Made By Robert Vassar,   Northwestern University
Strain of Origin(C57BL/6 x SJL)F1
Expressed Gene PSEN1, presenilin 1, human
Expressed Gene APP695, amyloid beta (A4) precursor protein (chimeric), mouse/human chimera
Promoter Thy1, thymus cell antigen 1, theta, mouse, laboratory
General Note Three transgenic lines coexpressing the APP and PSEN1 proteins at high, medium and low levels, respectively designated Tg6799, Tg7031, and Tg7092, were propagated for analysis, most of which employed Tg6799.

Phenotypic Similarity to Human Syndrome: Macular Degeneration, Age-Related J:214858.

Molecular Note Four familial Alzheimer disease- (FAD-) associated mutations were introduced into a single human amyloid precursor protein cDNA: the "Swedish" double mutation (K670N/M671L); the "Florida" mutation (I716V); and the "London" mutation (V717I). Two FAD-associated mutations, M146L and L286V, likewise were introduced into a human presenilin 1 cDNA. Each cDNA was then cloned independently into the mouse thymus cell antigen 1 gene, replacing a segment that contains thymus-specific elements so that expression of the transgenes is targeted only to the brain. Equal molar amounts of the two transgenes were coinjected into pronuclei of single-celled embryos. [MGI Ref ID J:112949] [MGI Ref ID J:32213]


Genotyping Information

Genotyping Protocols

Generic Human PSEN1 cDNA Multiplex1, Melt Curve Analysis
Generic Tg(APP), Standard PCR
Tg(PSEN1), Standard PCR

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

Oakley H; Cole SL; Logan S; Maus E; Shao P; Craft J; Guillozet-Bongaarts A; Ohno M; Disterhoft J; Van Eldik L; Berry R; Vassar R. 2006. Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. J Neurosci 26(40):10129-40. [PubMed: 17021169]  [MGI Ref ID J:112949]

Additional References

Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas related

Ahn HJ; Glickman JF; Poon KL; Zamolodchikov D; Jno-Charles OC; Norris EH; Strickland S. 2014. A novel Abeta-fibrinogen interaction inhibitor rescues altered thrombosis and cognitive decline in Alzheimer's disease mice. J Exp Med 211(6):1049-62. [PubMed: 24821909]  [MGI Ref ID J:213119]

Avrahami L; Farfara D; Shaham-Kol M; Vassar R; Frenkel D; Eldar-Finkelman H. 2013. Inhibition of glycogen synthase kinase-3 ameliorates beta-amyloid pathology and restores lysosomal acidification and mammalian target of rapamycin activity in the Alzheimer disease mouse model: in vivo and in vitro studies. J Biol Chem 288(2):1295-306. [PubMed: 23155049]  [MGI Ref ID J:193739]

Aytan N; Choi JK; Carreras I; Kowall NW; Jenkins BG; Dedeoglu A. 2013. Combination therapy in a transgenic model of Alzheimer's disease. Exp Neurol 250:228-38. [PubMed: 24120437]  [MGI Ref ID J:206610]

Baik SH; Cha MY; Hyun YM; Cho H; Hamza B; Kim DK; Han SH; Choi H; Kim KH; Moon M; Lee J; Kim M; Irimia D; Mook-Jung I. 2014. Migration of neutrophils targeting amyloid plaques in Alzheimer's disease mouse model. Neurobiol Aging 35(6):1286-92. [PubMed: 24485508]  [MGI Ref ID J:213882]

Bhattacharya S; Haertel C; Maelicke A; Montag D. 2014. Galantamine slows down plaque formation and behavioral decline in the 5XFAD mouse model of Alzheimer's disease. PLoS One 9(2):e89454. [PubMed: 24586789]  [MGI Ref ID J:213824]

Brower CS; Piatkov KI; Varshavsky A. 2013. Neurodegeneration-associated protein fragments as short-lived substrates of the N-end rule pathway. Mol Cell 50(2):161-71. [PubMed: 23499006]  [MGI Ref ID J:198127]

Burgert T; Schmidt V; Caglayan S; Lin F; Fuchtbauer A; Fuchtbauer EM; Nykjaer A; Carlo AS; Willnow TE. 2013. SORLA-dependent and -independent functions for PACS1 in control of amyloidogenic processes. Mol Cell Biol 33(21):4308-20. [PubMed: 24001769]  [MGI Ref ID J:205418]

Buskila Y; Crowe SE; Ellis-Davies GC. 2013. Synaptic deficits in layer 5 neurons precede overt structural decay in 5xFAD mice. Neuroscience 254:152-9. [PubMed: 24055684]  [MGI Ref ID J:207428]

Cai Y; Xue ZQ; Zhang XM; Li MB; Wang H; Luo XG; Cai H; Yan XX. 2012. An age-related axon terminal pathology around the first olfactory relay that involves amyloidogenic protein overexpression without plaque formation. Neuroscience 215:160-73. [PubMed: 22542680]  [MGI Ref ID J:192436]

Carlo AS; Gustafsen C; Mastrobuoni G; Nielsen MS; Burgert T; Hartl D; Rohe M; Nykjaer A; Herz J; Heeren J; Kempa S; Petersen CM; Willnow TE. 2013. The pro-neurotrophin receptor sortilin is a major neuronal apolipoprotein E receptor for catabolism of amyloid-beta peptide in the brain. J Neurosci 33(1):358-70. [PubMed: 23283348]  [MGI Ref ID J:193915]

Chen R; Zhang J; Wu Y; Wang D; Feng G; Tang YP; Teng Z; Chen C. 2012. Monoacylglycerol lipase is a therapeutic target for Alzheimer's disease. Cell Rep 2(5):1329-39. [PubMed: 23122958]  [MGI Ref ID J:196345]

Cho WH; Park JC; Chung C; Jeon WK; Han JS. 2014. Learning strategy preference of 5XFAD transgenic mice depends on the sequence of place/spatial and cued training in the water maze task. Behav Brain Res 273:116-22. [PubMed: 25078295]  [MGI Ref ID J:217100]

Cho WH; Park JC; Kim DH; Kim MS; Lee SY; Park H; Kang JH; Yeon SW; Han JS. 2014. ID1201, the ethanolic extract of the fruit of Melia toosendan ameliorates impairments in spatial learning and reduces levels of amyloid beta in 5XFAD mice. Neurosci Lett 583:170-5. [PubMed: 25281546]  [MGI Ref ID J:218544]

Christensen DZ; Bayer TA; Wirths O. 2009. Formic acid is essential for immunohistochemical detection of aggregated intraneuronal Abeta peptides in mouse models of Alzheimer's disease. Brain Res 1301:116-25. [PubMed: 19751708]  [MGI Ref ID J:158791]

Cortes-Canteli M; Paul J; Norris EH; Bronstein R; Ahn HJ; Zamolodchikov D; Bhuvanendran S; Fenz KM; Strickland S. 2010. Fibrinogen and beta-amyloid association alters thrombosis and fibrinolysis: a possible contributing factor to Alzheimer's disease. Neuron 66(5):695-709. [PubMed: 20547128]  [MGI Ref ID J:167873]

Crouzin N; Baranger K; Cavalier M; Marchalant Y; Cohen-Solal C; Roman FS; Khrestchatisky M; Rivera S; Feron F; Vignes M. 2013. Area-specific alterations of synaptic plasticity in the 5XFAD mouse model of Alzheimer's disease: dissociation between somatosensory cortex and hippocampus. PLoS One 8(9):e74667. [PubMed: 24069328]  [MGI Ref ID J:206029]

Crowe SE; Ellis-Davies GC. 2013. In vivo characterization of a bigenic fluorescent mouse model of Alzheimer's disease with neurodegeneration. J Comp Neurol 521(10):Spc1. [PubMed: 23605442]  [MGI Ref ID J:200729]

Crowe SE; Ellis-Davies GC. 2014. Spine pruning in 5xFAD mice starts on basal dendrites of layer 5 pyramidal neurons. Brain Struct Funct 219(2):571-80. [PubMed: 23417057]  [MGI Ref ID J:214142]

Cui Y; Huang M; He Y; Zhang S; Luo Y. 2011. Genetic Ablation of Apolipoprotein A-IV Accelerates Alzheimer's Disease Pathogenesis in a Mouse Model. Am J Pathol 178(3):1298-308. [PubMed: 21356380]  [MGI Ref ID J:169682]

Devi L; Ohno M. 2013. Deletion of the eIF2alpha Kinase GCN2 fails to rescue the memory decline associated with Alzheimer's disease. PLoS One 8(10):e77335. [PubMed: 24146979]  [MGI Ref ID J:209106]

Devi L; Ohno M. 2010. Genetic reductions of beta-site amyloid precursor protein-cleaving enzyme 1 and amyloid-beta ameliorate impairment of conditioned taste aversion memory in 5XFAD Alzheimer's disease model mice. Eur J Neurosci 31(1):110-8. [PubMed: 20092558]  [MGI Ref ID J:158363]

Devi L; Ohno M. 2012. Mitochondrial dysfunction and accumulation of the beta-secretase-cleaved C-terminal fragment of APP in Alzheimer's disease transgenic mice. Neurobiol Dis 45(1):417-24. [PubMed: 21933711]  [MGI Ref ID J:179837]

Devi L; Ohno M. 2014. PERK mediates eIF2alpha phosphorylation responsible for BACE1 elevation, CREB dysfunction and neurodegeneration in a mouse model of Alzheimer's disease. Neurobiol Aging 35(10):2272-81. [PubMed: 24889041]  [MGI Ref ID J:218077]

Devi L; Ohno M. 2010. Phospho-eIF2alpha level is important for determining abilities of BACE1 reduction to rescue cholinergic neurodegeneration and memory defects in 5XFAD mice. PLoS One 5(9):e12974. [PubMed: 20886088]  [MGI Ref ID J:165103]

Dinkins MB; Dasgupta S; Wang G; Zhu G; Bieberich E. 2014. Exosome reduction in vivo is associated with lower amyloid plaque load in the 5XFAD mouse model of Alzheimer's disease. Neurobiol Aging 35(8):1792-800. [PubMed: 24650793]  [MGI Ref ID J:214860]

Fragkouli A; Tsilibary EC; Tzinia AK. 2014. Neuroprotective role of MMP-9 overexpression in the brain of Alzheimer's 5xFAD mice. Neurobiol Dis 70:179-89. [PubMed: 25008761]  [MGI Ref ID J:215635]

Frost JL; Le KX; Cynis H; Ekpo E; Kleinschmidt M; Palmour RM; Ervin FR; Snigdha S; Cotman CW; Saido TC; Vassar RJ; George-Hyslop PS; Ikezu T; Schilling S; Demuth HU; Lemere CA. 2013. Pyroglutamate-3 Amyloid-beta Deposition in the Brains of Humans, Non-Human Primates, Canines, and Alzheimer Disease-Like Transgenic Mouse Models. Am J Pathol 183(2):369-81. [PubMed: 23747948]  [MGI Ref ID J:199082]

Graff J; Rei D; Guan JS; Wang WY; Seo J; Hennig KM; Nieland TJ; Fass DM; Kao PF; Kahn M; Su SC; Samiei A; Joseph N; Haggarty SJ; Delalle I; Tsai LH. 2012. An epigenetic blockade of cognitive functions in the neurodegenerating brain. Nature 483(7388):222-6. [PubMed: 22388814]  [MGI Ref ID J:181683]

Guo Z; Zhang L; Wu Z; Chen Y; Wang F; Chen G. 2014. In Vivo direct reprogramming of reactive glial cells into functional neurons after brain injury and in an Alzheimer's disease model. Cell Stem Cell 14(2):188-202. [PubMed: 24360883]  [MGI Ref ID J:210106]

Heraud C; Goufak D; Ando K; Leroy K; Suain V; Yilmaz Z; De Decker R; Authelet M; Laporte V; Octave JN; Brion JP. 2013. Increased misfolding and truncation of tau in APP/PS1/tau transgenic mice compared to mutant tau mice. Neurobiol Dis 62C:100-112. [PubMed: 24076100]  [MGI Ref ID J:201809]

Hillmann A; Hahn S; Schilling S; Hoffmann T; Demuth HU; Bulic B; Schneider-Axmann T; Bayer TA; Weggen S; Wirths O. 2012. No improvement after chronic ibuprofen treatment in the 5XFAD mouse model of Alzheimer's disease. Neurobiol Aging 33(4):833.e39-50. [PubMed: 21943956]  [MGI Ref ID J:188189]

Jawhar S; Trawicka A; Jenneckens C; Bayer TA; Wirths O. 2012. Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal Abeta aggregation in the 5XFAD mouse model of Alzheimer's disease. Neurobiol Aging 33(1):196.e29-40. [PubMed: 20619937]  [MGI Ref ID J:188235]

Jawhar S; Wirths O; Schilling S; Graubner S; Demuth HU; Bayer TA. 2011. Overexpression of glutaminyl cyclase, the enzyme responsible for pyroglutamate A{beta} formation, induces behavioral deficits, and glutaminyl cyclase knock-out rescues the behavioral phenotype in 5XFAD mice. J Biol Chem 286(6):4454-60. [PubMed: 21148560]  [MGI Ref ID J:169481]

Kalinin S; Polak PE; Lin SX; Sakharkar AJ; Pandey SC; Feinstein DL. 2012. The noradrenaline precursor L-DOPS reduces pathology in a mouse model of Alzheimer's disease. Neurobiol Aging 33(8):1651-63. [PubMed: 21705113]  [MGI Ref ID J:188202]

Katsouri L; Georgopoulos S. 2011. Lack of LDL receptor enhances amyloid deposition and decreases glial response in an Alzheimer's disease mouse model. PLoS One 6(7):e21880. [PubMed: 21755005]  [MGI Ref ID J:174945]

Kim C; Nam DW; Park SY; Song H; Hong HS; Boo JH; Jung ES; Kim Y; Baek JY; Kim KS; Cho JW; Mook-Jung I. 2013. O-linked beta-N-acetylglucosaminidase inhibitor attenuates beta-amyloid plaque and rescues memory impairment. Neurobiol Aging 34(1):275-85. [PubMed: 22503002]  [MGI Ref ID J:191369]

Kimura R; Devi L; Ohno M. 2010. Partial reduction of BACE1 improves synaptic plasticity, recent and remote memories in Alzheimer's disease transgenic mice. J Neurochem 113(1):248-61. [PubMed: 20089133]  [MGI Ref ID J:174832]

Kimura R; Ohno M. 2009. Impairments in remote memory stabilization precede hippocampal synaptic and cognitive failures in 5XFAD Alzheimer mouse model. Neurobiol Dis 33(2):229-35. [PubMed: 19026746]  [MGI Ref ID J:144743]

Kook SY; Hong HS; Moon M; Ha CM; Chang S; Mook-Jung I. 2012. Abeta1-42-RAGE Interaction Disrupts Tight Junctions of the Blood-Brain Barrier Via Ca2+-Calcineurin Signaling. J Neurosci 32(26):8845-54. [PubMed: 22745485]  [MGI Ref ID J:185647]

Lee JE; Han PL. 2013. An update of animal models of Alzheimer disease with a reevaluation of plaque depositions. Exp Neurobiol 22(2):84-95. [PubMed: 23833557]  [MGI Ref ID J:202532]

Leroy K; Ando K; Laporte V; Dedecker R; Suain V; Authelet M; Heraud C; Pierrot N; Yilmaz Z; Octave JN; Brion JP. 2012. Lack of tau proteins rescues neuronal cell death and decreases amyloidogenic processing of APP in APP/PS1 mice. Am J Pathol 181(6):1928-40. [PubMed: 23026200]  [MGI Ref ID J:190305]

Mijatovic J; Piltonen M; Alberton P; Mannisto PT; Saarma M; Piepponen TP. 2011. Constitutive Ret signaling is protective for dopaminergic cell bodies but not for axonal terminals. Neurobiol Aging 32(8):1486-94. [PubMed: 19767128]  [MGI Ref ID J:176716]

Moechars D; Lorent K; De Strooper B; Dewachter I; Van Leuven F. 1996. Expression in brain of amyloid precursor protein mutated in the alpha-secretase site causes disturbed behavior, neuronal degeneration and premature death in transgenic mice. EMBO J 15(6):1265-74. [PubMed: 8635459]  [MGI Ref ID J:32213]

Moon M; Jeong I; Kim CH; Kim J; Lee PK; Mook-Jung I; Leblanc P; Kim KS. 2015. Correlation between orphan nuclear receptor Nurr1 expression and amyloid deposition in 5XFAD mice, an animal model of Alzheimer's disease. J Neurochem 132(2):254-62. [PubMed: 25156412]  [MGI Ref ID J:217828]

Noh H; Park C; Park S; Lee YS; Cho SY; Seo H. 2014. Prediction of miRNA-mRNA associations in Alzheimer's disease mice using network topology. BMC Genomics 15:644. [PubMed: 25086961]  [MGI Ref ID J:214603]

Noh H; Seo H. 2014. Age-dependent effects of valproic acid in Alzheimer's disease (AD) mice are associated with nerve growth factor (NGF) regulation. Neuroscience 266:255-65. [PubMed: 24568732]  [MGI Ref ID J:210335]

Ohno M. 2009. Failures to reconsolidate memory in a mouse model of Alzheimer's disease. Neurobiol Learn Mem 92(3):455-9. [PubMed: 19435612]  [MGI Ref ID J:154421]

Ohno M; Cole SL; Yasvoina M; Zhao J; Citron M; Berry R; Disterhoft JF; Vassar R. 2007. BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice. Neurobiol Dis 26(1):134-45. [PubMed: 17258906]  [MGI Ref ID J:119002]

Ou-Yang MH; Xu F; Liao MC; Davis J; Robinson JK; Van Nostrand WE. 2015. The N-terminal region of myelin basic protein reduces fibrillar amyloid-beta deposition in Tg-5xFAD mice. Neurobiol Aging 36(2):801-11. [PubMed: 25457550]  [MGI Ref ID J:219504]

Park SW; Kim JH; Mook-Jung I; Kim KW; Park WJ; Park KH; Kim JH. 2014. Intracellular amyloid beta alters the tight junction of retinal pigment epithelium in 5XFAD mice. Neurobiol Aging 35(9):2013-20. [PubMed: 24709310]  [MGI Ref ID J:214858]

Peretti D; Bastide A; Radford H; Verity N; Molloy C; Martin MG; Moreno JA; Steinert JR; Smith T; Dinsdale D; Willis AE; Mallucci GR. 2015. RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration. Nature 518(7538):236-9. [PubMed: 25607368]  [MGI Ref ID J:219567]

Pietri M; Dakowski C; Hannaoui S; Alleaume-Butaux A; Hernandez-Rapp J; Ragagnin A; Mouillet-Richard S; Haik S; Bailly Y; Peyrin JM; Launay JM; Kellermann O; Schneider B. 2013. PDK1 decreases TACE-mediated alpha-secretase activity and promotes disease progression in prion and Alzheimer's diseases. Nat Med 19(9):1124-31. [PubMed: 23955714]  [MGI Ref ID J:202038]

Rojas S; Herance JR; Gispert JD; Abad S; Torrent E; Jimenez X; Pareto D; Perpina U; Sarroca S; Rodriguez E; Ortega-Aznar A; Sanfeliu C. 2013. In vivo evaluation of amyloid deposition and brain glucose metabolism of 5XFAD mice using positron emission tomography. Neurobiol Aging 34(7):1790-8. [PubMed: 23402900]  [MGI Ref ID J:211692]

Sadleir KR; Eimer WA; Kaufman RJ; Osten P; Vassar R. 2014. Genetic inhibition of phosphorylation of the translation initiation factor eIF2alpha does not block Abeta-dependent elevation of BACE1 and APP levels or reduce amyloid pathology in a mouse model of Alzheimer's disease. PLoS One 9(7):e101643. [PubMed: 24992504]  [MGI Ref ID J:218929]

Sadleir KR; Vassar R. 2012. Cdk5 protein inhibition and Abeta42 increase BACE1 protein level in primary neurons by a post-transcriptional mechanism: implications of CDK5 as a therapeutic target for Alzheimer disease. J Biol Chem 287(10):7224-35. [PubMed: 22223639]  [MGI Ref ID J:182773]

Saul A; Sprenger F; Bayer TA; Wirths O. 2013. Accelerated tau pathology with synaptic and neuronal loss in a novel triple transgenic mouse model of Alzheimer's disease. Neurobiol Aging 34(11):2564-73. [PubMed: 23747045]  [MGI Ref ID J:211723]

Seo J; Giusti-Rodriguez P; Zhou Y; Rudenko A; Cho S; Ota KT; Park C; Patzke H; Madabhushi R; Pan L; Mungenast AE; Guan JS; Delalle I; Tsai LH. 2014. Activity-Dependent p25 Generation Regulates Synaptic Plasticity and Abeta-Induced Cognitive Impairment. Cell 157(2):486-98. [PubMed: 24725413]  [MGI Ref ID J:208030]

Sesele K; Thanopoulou K; Paouri E; Tsefou E; Klinakis A; Georgopoulos S. 2013. Conditional inactivation of nicastrin restricts amyloid deposition in an Alzheimer's disease mouse model. Aging Cell 12(6):1032-40. [PubMed: 23826707]  [MGI Ref ID J:210209]

Sethi M; Joshi SS; Webb RL; Beckett TL; Donohue KD; Murphy MP; O'Hara BF; Duncan MJ. 2015. Increased fragmentation of sleep-wake cycles in the 5XFAD mouse model of Alzheimer's disease. Neuroscience 290:80-9. [PubMed: 25637807]  [MGI Ref ID J:221806]

Tagawa K; Homma H; Saito A; Fujita K; Chen X; Imoto S; Oka T; Ito H; Motoki K; Yoshida C; Hatsuta H; Murayama S; Iwatsubo T; Miyano S; Okazawa H. 2015. Comprehensive phosphoproteome analysis unravels the core signaling network that initiates the earliest synapse pathology in preclinical Alzheimer's disease brain. Hum Mol Genet 24(2):540-58. [PubMed: 25231903]  [MGI Ref ID J:217304]

Torres M; Price SL; Fiol-Deroque MA; Marcilla-Etxenike A; Ahyayauch H; Barcelo-Coblijn G; Teres S; Katsouri L; Ordinas M; Lopez DJ; Ibarguren M; Goni FM; Busquets X; Vitorica J; Sastre M; Escriba PV. 2014. Membrane lipid modifications and therapeutic effects mediated by hydroxydocosahexaenoic acid on Alzheimer's disease. Biochim Biophys Acta 1838(6):1680-92. [PubMed: 24374316]  [MGI Ref ID J:210860]

Wang Q; Xiao B; Cui S; Song H; Qian Y; Dong L; An H; Cui Y; Zhang W; He Y; Zhang J; Yang J; Zhang F; Hu G; Gong X; Yan Z; Zheng Y; Wang X. 2014. Triptolide treatment reduces Alzheimer's disease (AD)-like pathology through inhibition of BACE1 in a transgenic mouse model of AD. Dis Model Mech 7(12):1385-95. [PubMed: 25481013]  [MGI Ref ID J:217376]

Wirths O; Erck C; Martens H; Harmeier A; Geumann C; Jawhar S; Kumar S; Multhaup G; Walter J; Ingelsson M; Degerman-Gunnarsson M; Kalimo H; Huitinga I; Lannfelt L; Bayer TA. 2010. Identification of low molecular weight pyroglutamate A{beta} oligomers in Alzheimer disease: a novel tool for therapy and diagnosis. J Biol Chem 285(53):41517-24. [PubMed: 20971852]  [MGI Ref ID J:167567]

Wittnam JL; Portelius E; Zetterberg H; Gustavsson MK; Schilling S; Koch B; Demuth HU; Blennow K; Wirths O; Bayer TA. 2012. Pyroglutamate amyloid beta (Abeta) aggravates behavioral deficits in transgenic amyloid mouse model for Alzheimer disease. J Biol Chem 287(11):8154-62. [PubMed: 22267726]  [MGI Ref ID J:182761]

Woo DC; Lee SH; Lee DW; Kim SY; Kim GY; Rhim HS; Choi CB; Kim HY; Lee CU; Choe BY. 2010. Regional metabolic alteration of Alzheimer's disease in mouse brain expressing mutant human APP-PS1 by 1H HR-MAS. Behav Brain Res 211(1):125-31. [PubMed: 20307581]  [MGI Ref ID J:159678]

You H; Tsutsui S; Hameed S; Kannanayakal TJ; Chen L; Xia P; Engbers JD; Lipton SA; Stys PK; Zamponi GW. 2012. Abeta neurotoxicity depends on interactions between copper ions, prion protein, and N-methyl-D-aspartate receptors. Proc Natl Acad Sci U S A 109(5):1737-42. [PubMed: 22307640]  [MGI Ref ID J:182028]

Youmans KL; Tai LM; Nwabuisi-Heath E; Jungbauer L; Kanekiyo T; Gan M; Kim J; Eimer WA; Estus S; Rebeck GW; Weeber EJ; Bu G; Yu C; Ladu MJ. 2012. APOE4-specific changes in Abeta accumulation in a new transgenic mouse model of Alzheimer disease. J Biol Chem 287(50):41774-86. [PubMed: 23060451]  [MGI Ref ID J:193422]

Yun SM; Cho SJ; Song JC; Song SY; Jo SA; Jo C; Yoon K; Tanzi RE; Choi EJ; Koh YH. 2013. SUMO1 modulates Abeta generation via BACE1 accumulation. Neurobiol Aging 34(3):650-62. [PubMed: 22975420]  [MGI Ref ID J:194511]

Zamolodchikov D; Chen ZL; Conti BA; Renne T; Strickland S. 2015. Activation of the factor XII-driven contact system in Alzheimer's disease patient and mouse model plasma. Proc Natl Acad Sci U S A 112(13):4068-73. [PubMed: 25775543]  [MGI Ref ID J:220675]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX12

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, hemizygous mice may be bred to C57BL/6J mice.
Mating SystemNoncarrier x Hemizygote         (Female x Male)   28-OCT-13
Diet Information New Diet as of April 7, 2014: Lab Diet® 5K0Q

Pricing and Purchasing

Supply Notes

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

See Terms of Use tab for General Terms and Conditions

The Jackson Laboratory's Genotype Promise

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.

Terms of Use

Terms of Use

General Terms and Conditions

For Licensing and Use Restrictions view the link(s) below:
- Strain(s) not available to companies or for-profit entities.

Contact information

General inquiries regarding Terms of Use

Contracts Administration


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.