Strain Name:



Cryopreserved - Ready for recovery     Available at the JAX MMRRC

Use Restrictions Apply, see Terms of Use
Common Names: APPK670N/M671L;    
Please refer to the Mutant Mouse Regional Resource Center (MMRRC) for ordering information and strain details on B6.129-Tg(APPSw)40Btla/Mmjax MMRRC Stock Number 034831.
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.
These R1.40 transgenic mice (formerly JAX Stock No. 005300) express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L, and may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.


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

Former Names B6.129-Tg(APPSw)40Btla/J    (Changed: 10-AUG-11 )
Type Congenic; Transgenic;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
Donating Investigator Bruce Lamb,   The Cleveland Clinic Foundation

These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is two to three fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. Levels of the beta- secretase generated human APP derivative, C-terminal 13.5kDA fragment, are elevated in brain tissue. ELISA enzyme-linked immunosorbent assay (ELISA) analysis of brain homogenates show a significant increase in total amyloid-beta peptides and 42 amino acid length amyloid beta peptides. By 14 months of age, homozygous mice develop both parenchymal and vascular amyloid beta deposits, which first appear in the frontal cortex and then spread into the hippocampus. The donating investigator reports increased mortality in young homozygous animals (higher incidence in females). 3 to 4 month old transgenic mice, maintained on a C57BL/6J background, exhibit spontaneous seizure-like events (abnormal spiking) in EEG readings, without abnormal behavior and are more susceptible to kainic acid induced seizures (Vogt et al. Neurobiol Aging 2009). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.

A publication (Lehman et al. 2003 Hum Mol Genet 12:2949) compares the well characterized B6-R1.40 strain (B6.129-Tg(APPSw)40Btla/Mmjax) with two additional congenic strains, D2-R1.40 (D2.129(B6)-Tg(APPSw)40Btla/Mmjax) and 129S1-R1.40 (129S1.129(Cg)-Tg(APPSw)40Btla/Mmjax). While these three congenic strains have similar levels of holo-APP in brain tissue, the levels of brain APP C-terminal fragments (CTFs) vary depending upon genetic background. Brain and plasma levels of amyloid beta-40 and -42 are variable as well (B6-R1.40> 129S1-R1.40> D2-R1.40). In addition, the congenic strains exhibited dramatic alterations in the age of onset of amyloid beta deposition; in contrast to 14 month old homozygous B6-R1.40 mice, homozygous D2-R1.40 and 129S1-R1.40 mice do not develop amyloid beta deposits in the parietal or frontal cortex even by 20 months of age. The donating investigator further reports that the A-R1.40 strain (A.129(B6)-Tg(APPSw)40Btla/Mmjax) exhibits levels of amyloid beta comparable to the B6-R1.40 strain, but with later onset. Therefore, APP processing and amyloid beta metabolism and deposition are modified by the genetic background. While the 129S1-R1.40 strain can be easily maintained as homozygotes, the donating investigator reports increased mortality in young homozygotes on the other genetic backgrounds, with D2-R1.40 and A-R1.40 more severely affected than B6-R1.40.

A 650 kb YAC transgene containing the entire human amyloid beta (A4) precursor protein (APP) gene, and approximately 250 kb of flanking sequence, was altered to include the Swiss mutation APPK670N/M671L associated with Familial Alzheimer's Disease. This transgene was injected into (129X1/SvJ x 129S1/Sv)F1-derived R1 embryonic stem (ES) cells. Founder animals (line R1.40) were backcrossed to C57BL/6J for 21 generations prior to arrival at the MMRRC at The Jackson Laboratory.

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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
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
007067   D2.129P2(B6)-Apoetm1Unc/J
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)

Strains carrying   Tg(APPSw)40Btla allele
006409   129S1.129(Cg)-Tg(APPSw)40Btla/Mmjax
006555   A.129(B6)-Tg(APPSw)40Btla/Mmjax
006472   D2.129(B6)-Tg(APPSw)40Btla/Mmjax
View Strains carrying   Tg(APPSw)40Btla     (3 strains)

View Strains carrying other alleles of APP     (13 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; 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.
Cerebral Amyloid Angiopathy, App-Related   (APP)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype


  • nervous system phenotype
  • amyloid beta deposits
    • all animals show amyloid beta (Abeta) deposits in the parietal cortex at 13.5 months of age, but no animals have deposits at 5 months   (MGI Ref ID J:86629)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits
    • all animals show amyloid beta (Abeta) deposits in the parietal cortex at 13.5 months of age, but no animals have deposits at 5 months   (MGI Ref ID J:86629)

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


        involves: 129S1/Sv * 129X1/SvJ
  • nervous system phenotype
  • amyloid beta deposits
    • mice have higher levels of total A-beta protein and the cleaved A-beta 1-42(43) peptide than Tg(APP)8.9Btla mice, but levels are lower than those in Tg(APPSwLon)96Btla mice   (MGI Ref ID J:42613)
    • mice have 7- to 8-fold higher levels of Abeta1-42 peptide in their brains compared to Tg(PSEN1H163R)G9Btla hemizygotes   (MGI Ref ID J:58050)
    • diffuse amyloid beta deposits are detected in the hippocampus and frontal cortex at 24-26 months of age   (MGI Ref ID J:58050)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits
    • mice have higher levels of total A-beta protein and the cleaved A-beta 1-42(43) peptide than Tg(APP)8.9Btla mice, but levels are lower than those in Tg(APPSwLon)96Btla mice   (MGI Ref ID J:42613)
    • mice have 7- to 8-fold higher levels of Abeta1-42 peptide in their brains compared to Tg(PSEN1H163R)G9Btla hemizygotes   (MGI Ref ID J:58050)
    • diffuse amyloid beta deposits are detected in the hippocampus and frontal cortex at 24-26 months of age   (MGI Ref ID J:58050)


  • nervous system phenotype
  • *normal* nervous system phenotype
    • no amyloid beta deposits are observed in 13.5 month-old mice   (MGI Ref ID J:86629)
View Research Applications

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

Neurobiology Research
Alzheimer's Disease
      strains expressing mutant APP
      electroconvulsive seizures
      increased susceptibility to kainate-induced seizures

Research Tools
Neurobiology Research

APP related

Neurobiology Research
Alzheimer's Disease

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Tg(APPSw)40Btla
Allele Name transgene insertion 40, Bruce Lamb
Allele Type Transgenic (Humanized sequence, Inserted expressed sequence)
Common Name(s) APPK670/M671; APPK670N/M671L; R1.40; R1.40-YAC;
Mutation Made By Bruce Lamb,   The Cleveland Clinic Foundation
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line NameR1
ES Cell Line Strain(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Expressed Gene APP, amyloid beta (A4) precursor protein, human
Promoter APP, amyloid beta (A4) precursor protein, human
Molecular Note The transgenic insertion comprises four to eight copies of a 650-kb YAC containing the entire 400-kb human amyloid precursor protein gene with the Swiss familial Alzheimer disease (FAD) mutation and approximately 250 kb of flanking human DNA. The double mutation (K670N/M671N) comprises a G-to-A transition converting the lysine codon at position 670 to an asparagine codon and an A-to-C transversion replacing the methionine at amino acid 671 with leucine. RT-PCR and western blot analysis revealed that hemizygous transgenic mice express all major human APP mRNA and protein isoforms in brain, in parallel with the corresponding mouse versions, at approximately three times the levels of the latter. Total brain levels of the Alzheimer disease- associated 42-amino acid amyloid-beta peptide detected by ELISA are 7-8-fold and 15-20-fold higher, respectively, in mice hemizygous and homozygous for the mutant gene than in hemizygotes for the wildtype human gene. Levels of a cell-associated, beta-secretase-generated 13.5 kDa C-terminal peptide containing the amyloid beta domain and of soluble amyloid beta peptides are significantly elevated in brains of mice with the mutant, versus wildtype, transgene, while alpha-secretase products are diminished. [MGI Ref ID J:42613] [MGI Ref ID J:58050] [MGI Ref ID J:73622]


Genotyping Information

Genotyping Protocols

Tg(APPSw)40Btla, High Resolution Melting
Tg(APPSw)40Btla, Standard PCR

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

Lamb BT; Call LM; Slunt HH; Bardel KA; Lawler AM; Eckman CB; Younkin SG; Holtz G; Wagner SL; Price DL; Sisodia SS; Gearhart JD. 1997. Altered metabolism of familial Alzheimer's disease-linked amyloid precursor protein variants in yeast artificial chromosome transgenic mice. Hum Mol Genet 6(9):1535-41. [PubMed: 9285791]  [MGI Ref ID J:42613]

Additional References

Tg(APPSw)40Btla related

Adwan L; Subaiea GM; Zawia NH. 2014. Tolfenamic acid downregulates BACE1 and protects against lead-induced upregulation of Alzheimer's disease related biomarkers. Neuropharmacology 79:596-602. [PubMed: 24462621]  [MGI Ref ID J:215369]

Chen J; Herrup K. 2012. Glutamine acts as a neuroprotectant against DNA damage, beta-amyloid and H2O2-induced stress. PLoS One 7(3):e33177. [PubMed: 22413000]  [MGI Ref ID J:186926]

Chiocco MJ; Lamb BT. 2007. Spatial and temporal control of age-related APP processing in genomic-based beta-secretase transgenic mice. Neurobiol Aging 28(1):75-84. [PubMed: 16387391]  [MGI Ref ID J:117963]

Ghosal K; Stathopoulos A; Pimplikar SW. 2010. APP intracellular domain impairs adult neurogenesis in transgenic mice by inducing neuroinflammation. PLoS One 5(7):e11866. [PubMed: 20689579]  [MGI Ref ID J:163067]

Kulnane LS; Lamb BT. 2001. Neuropathological characterization of mutant amyloid precursor protein yeast artificial chromosome transgenic mice. Neurobiol Dis 8(6):982-92. [PubMed: 11741394]  [MGI Ref ID J:73622]

Lamb BA; Bardel KA; Kulnane LS; Anderson JJ; Holtz G; Wagner SL; Sisodia SS; Hoeger EJ. 1999. Amyloid production and deposition in mutant amyloid precursor protein and presenilin-1 yeast artificial chromosome transgenic mice. Nat Neurosci 2(8):695-7. [PubMed: 10412057]  [MGI Ref ID J:58050]

Lehman EJ; Kulnane LS; Gao Y; Petriello MC; Pimpis KM; Younkin L; Dolios G; Wang R; Younkin SG; Lamb BT. 2003. Genetic background regulates beta-amyloid precursor protein processing and beta-amyloid deposition in the mouse. Hum Mol Genet 12(22):2949-56. [PubMed: 14506131]  [MGI Ref ID J:86629]

Ryman D; Gao Y; Lamb BT. 2008. Genetic loci modulating amyloid-beta levels in a mouse model of Alzheimer's disease. Neurobiol Aging 29(8):1190-8. [PubMed: 17400334]  [MGI Ref ID J:140915]

Sagare AP; Bell RD; Srivastava A; Sengillo JD; Singh I; Nishida Y; Chow N; Zlokovic BV. 2013. A lipoprotein receptor cluster IV mutant preferentially binds amyloid-beta and regulates its clearance from the mouse brain. J Biol Chem 288(21):15154-66. [PubMed: 23580652]  [MGI Ref ID J:199624]

Salehi A; Delcroix JD; Belichenko PV; Zhan K; Wu C; Valletta JS; Takimoto-Kimura R; Kleschevnikov AM; Sambamurti K; Chung PP; Xia W; Villar A; Campbell WA; Kulnane LS; Nixon RA; Lamb BT; Epstein CJ; Stokin GB; Goldstein LS; Mobley WC. 2006. Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration. Neuron 51(1):29-42. [PubMed: 16815330]  [MGI Ref ID J:122937]

Subaiea GM; Adwan LI; Ahmed AH; Stevens KE; Zawia NH. 2013. Short-term treatment with tolfenamic acid improves cognitive functions in Alzheimer's disease mice. Neurobiol Aging 34(10):2421-30. [PubMed: 23639209]  [MGI Ref ID J:211730]

Varvel NH; Bhaskar K; Kounnas MZ; Wagner SL; Yang Y; Lamb BT; Herrup K. 2009. NSAIDs prevent, but do not reverse, neuronal cell cycle reentry in a mouse model of Alzheimer disease. J Clin Invest 119(12):3692-702. [PubMed: 19907078]  [MGI Ref ID J:155100]

Varvel NH; Bhaskar K; Patil AR; Pimplikar SW; Herrup K; Lamb BT. 2008. Abeta oligomers induce neuronal cell cycle events in Alzheimer's disease. J Neurosci 28(43):10786-93. [PubMed: 18945886]  [MGI Ref ID J:144634]

Vogt DL; Thomas D; Galvan V; Bredesen DE; Lamb BT; Pimplikar SW. 2009. Abnormal neuronal networks and seizure susceptibility in mice overexpressing the APP intracellular domain. Neurobiol Aging :. [PubMed: 19828212]  [MGI Ref ID J:169998]

Wilkinson BL; Cramer PE; Varvel NH; Reed-Geaghan E; Jiang Q; Szabo A; Herrup K; Lamb BT; Landreth GE. 2012. Ibuprofen attenuates oxidative damage through NOX2 inhibition in Alzheimer's disease. Neurobiol Aging 33(1):197.e21-32. [PubMed: 20696495]  [MGI Ref ID J:188232]

Yang Y; Varvel NH; Lamb BT; Herrup K. 2006. Ectopic cell cycle events link human Alzheimer's disease and amyloid precursor protein transgenic mouse models. J Neurosci 26(3):775-84. [PubMed: 16421297]  [MGI Ref ID J:104514]

Health & husbandry

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.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, transgenic carriers may be bred together, to wildtype siblings, or to C57BL/6J inbred mice. Because of the increased mortality in young homozygous animals (higher incidence in females), maintaining the colony by breeding homozygotes together is only recommended when sufficient colony size is permitted.

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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

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JAX® Mice, Products & Services Conditions of Use

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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.