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Common Names: A53T α-synuclein transgenic line M83;    
M83 transgenic mice expresses the mutant human A53T alpha-synuclein under the direction of the mouse prion protein promoter. These mice may be useful in studying human neuronal alpha-synucleinopathies, such as familial Parkinson's Disease.


Strain Information

Former Names B6;C3H-Tg(SNCA)83Vle/J    (Changed: 21-MAR-08 )
M83    (Changed: 15-DEC-04 )
Type Transgenic;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHemizygote x Hemizygote         (Female x Male)   03-JAN-07
Specieslaboratory mouse
GenerationN?+N7F7 (01-JAN-09)
Generation Definitions
Donating Investigator Virginia M Lee,   University of Pennsylvania

Mice homozygous for the transgenic insert are viable and normal in size. These transgenic mice express human A53T variant alpha-synuclein (full-length, 140 amino acid isoform) under the direction of the mouse prion protein promoter. At eight months of age, some homozygous mice develop a progressively severe motor phenotype. Presentation of the phenotype may manifest at 14-15 months of age (on average). Lax grooming, weight loss and diminished mobility precede movement impairment, partial limb paralysis, trembling and inability to stand. Immunohistochemistry analysis of mutants between eight to 12 months of age reveals widely distributed alpha-synuclein inclusions, with dense accumulation in the spinal cord, brainstem, cerebellum and thalamus. The appearance of alpha-synuclein aggregate inclusions parallels the onset of the motor impairment phenotype. Axons and myelin sheaths exhibit progressive ultrastructural degeneration. Immunoelectron microscopy and biochemical analysis show the inclusions in neurons are comprised primarily of 10-16 nm fibrils of alpha-synuclein. The structure, location and onset of the inclusions seen in the mutant mice resemble characteristics seen in human neuronal alpha-synucleinopathies, such as familial Parkinson's Disease. In addition, mice exhibit impaired odor discrimination and detection beginning at 6 months of age. Mice hemizygous for the transgenic insert develop similar phenotypic traits, but onset occurs later, between 22 and 28 months of age. Homozygous mice have a high incidence of nonproductive matings.

A transgenic construct containing the mouse prion protein promoter, its 5' and 3' untranslated regions and human alpha-synuclein A53T mutation cDNA sequence was injected into fertilized B6C3H mouse eggs. Transgenic animals are maintained on a mixed B6C3H background.

Control Information

   100010 B6C3F1/J (approximate)
  Considerations for Choosing Controls

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020783   B6.Cg-Tg(Prnp-FUS)17Ljh/J
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019728   B6.Cg-Tg(Prnp-FUS*R495X)78Ljh/J
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007182   B6.Cg-Tg(Prnp-ITM2B/APP695*42)A12Emcg/J
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View Strains carrying other alleles of SNCA     (30 strains)

Additional Web Information

JAX® NOTES, Fall 2003; 491. Novel Familial Parkinson's Disease Model.
JAX® NOTES, Summer 2007; 506. New Parkinson's Disease Mouse Model Resource.
Visit the Parkinson's Disease Resource site for helpful information on Parkinson's 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.
Parkinson Disease 1, Autosomal Dominant; PARK1
- 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.
Dementia, Lewy Body; DLB   (SNCA)
Parkinson Disease 4, Autosomal Dominant; PARK4   (SNCA)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype


        involves: C3H * C57BL/6
  • behavior/neurological phenotype
  • abnormal motor capabilities/coordination/movement   (MGI Ref ID J:127923)
    • develop the severe and complex motor impairment leading to paralysis and death that is seen in homozygous transgenics, however onset is delayed from 16 months of age to 22-28 months of age   (MGI Ref ID J:76657)
  • nervous system phenotype
  • abnormal nervous system morphology
    • develop a similar neurodegenerative disease that is observed in homozygous transgenic mice, however onset is delayed from 16 months of age to 22-28 months of age   (MGI Ref ID J:76657)
    • mice develop some inclusions that are composed of both tau and alpha-synuclein   (MGI Ref ID J:127923)
    • alpha-synuclein inclusion body
      • mice exhibit formation of abundant alpha-synuclein inclusions   (MGI Ref ID J:127923)
    • tau protein deposits
      • about 25% of diseased mutants accumulate abundant tau-positive threads, grains and spheroids in regions of the pons, midbrain, and spinal core   (MGI Ref ID J:127923)
      • rare perikaryal tau inclusions with morphology of a pre-tangle are seen   (MGI Ref ID J:127923)
      • less frequent tau inclusions are present in another 25% of symptomatic mutants but none are seen in the rest 50% of diseased mutants   (MGI Ref ID J:127923)


  • behavior/neurological phenotype
  • abnormal habituation to a novel odor
    • 6 and 10 month, but not 3 month, old mice do not sniff novel scent more than familiar scent   (MGI Ref ID J:219329)
  • homeostasis/metabolism phenotype
  • decreased acetylcholinesterase activity
    • decrease in acetylcholinesterase activity in olfactory bulb in 6 and 10 month old mice   (MGI Ref ID J:219329)
  • nervous system phenotype
  • abnormal olfactory bulb glomerular layer morphology
    • increase in dopaminergic neurons in olfactory bulb glomerular layer in 10 month old mice   (MGI Ref ID J:219329)
  • abnormal olfactory bulb mitral cell layer morphology
    • decreased numbers of cholinergic neurons are found in the olfactory bulb mitral layer in 10 month old mice   (MGI Ref ID J:219329)
  • decreased neuron number
    • decreased numbers of cholinergic neurons are found in the olfactory bulb mitral layer in 10 month old mice   (MGI Ref ID J:219329)
  • increased dopaminergic neuron number
    • increase in dopaminergic neurons in olfactory bulb glomerular layer in 10 month old mice   (MGI Ref ID J:219329)
  • taste/olfaction phenotype
  • impaired olfaction
    • time to locate buried food is increased in 6 and 10 month, but not 3 month, old mice as compared to wild-type   (MGI Ref ID J:219329)


        involves: C3H * C57BL/6
  • mortality/aging
  • premature death   (MGI Ref ID J:76657)
  • growth/size/body phenotype
  • weight loss
    • by 8 months of age, begin to lose weight   (MGI Ref ID J:76657)
  • behavior/neurological phenotype
  • abnormal motor capabilities/coordination/movement   (MGI Ref ID J:76657)
    • abnormal gait
      • reduced ambulation by 8 months of age   (MGI Ref ID J:76657)
    • akinesia
      • by 8 months of age, exhibit severe movement impairment with resistance to passive movement and partial paralysis of limbs, accompanied by periods of freezing of hindlimb   (MGI Ref ID J:76657)
    • hunched posture
      • develop hunched backs by 8 months of age   (MGI Ref ID J:76657)
    • impaired righting response
      • unable to right themselves when placed on their sides   (MGI Ref ID J:76657)
    • paresis
      • partial paralysis of limbs is observed by 8 months of age, beginning at a hindleg but affecting all limbs within a few days   (MGI Ref ID J:76657)
    • tremors
      • temulous motion is seen in some mice, possibly related to attempted muscular activity   (MGI Ref ID J:76657)
    • weakness
      • eventually are unable to stand up and support their own body weight   (MGI Ref ID J:76657)
  • aphagia
    • over time become unable to feed themselves   (MGI Ref ID J:76657)
  • decreased grooming behavior
    • by 8 months of age, grooming is neglected   (MGI Ref ID J:76657)
  • nervous system phenotype
  • abnormal myelination
    • following axonal degeneration, the myelin sheath loosens and unravels   (MGI Ref ID J:76657)
  • abnormal spinal nerve morphology
    • endoneurial space is increased and axons are filled with vacuoles in the ventral roots of aged mice   (MGI Ref ID J:76657)
  • alpha-synuclein inclusion body
    • develop age-dependent intracytoplasmic neuronal alpha-synuclein inclusions that contain 10-16 nm wide fibrils similar to those seen in human alpha-synucleinopathies, with dense accumulation in the spinal cord, brainstem, cerebellum, and thalamus   (MGI Ref ID J:76657)
  • gliosis
    • astrocytic gliosis   (MGI Ref ID J:76657)
  • neurodegeneration
    • show signs of neurodegeneration by 8 months of age and develop neurodegenerative disease within 16 months of age   (MGI Ref ID J:76657)
    • axon degeneration
      • significant axonal degeneration in aged mice   (MGI Ref ID J:76657)
  • muscle phenotype
  • abnormal gastrocnemius morphology
    • exhibit sparse neurogenic muscle atrophy   (MGI Ref ID J:76657)
View Research Applications

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

Neurobiology Research
Parkinson's Disease
      synuclein mutants

Sensorineural Research

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Tg(Prnp-SNCA*A53T)83Vle
Allele Name transgene insertion 83, Virginia M-Y Lee
Allele Type Transgenic (Humanized sequence, Inserted expressed sequence)
Common Name(s) A53T alpha-synuclein PRP; M83; PrP-alpha-syn mice (line M83); Prp-alphaSynA53T; Tg(SNCA)83Vle; alphaS+;
Mutation Made By John Trojanowski,   Dept. Pathology and Laboratory Med
Strain of OriginC57BL/6 x C3H
Expressed Gene SNCA, synuclein, alpha (non A4 component of amyloid precursor), human
Promoter Prnp, prion protein, mouse, laboratory
General Note This line was originally designated M83. Line M91 was also generated.
Molecular Note The transgene contains the mouse prion protein promoter, its 5' and 3' untranslated regions, and a human alpha synuclein cDNA sequence encoding a mutated protein with an Ala53Thr mutation. Transgene expression was detected in the cerebral cortex, spinalcord, and cerebellum. [MGI Ref ID J:76657]


Genotyping Information

Genotyping Protocols

Tg(Prnp-SNCA*A53T)83Vle, QPCR
Tg(Prnp-SNCA*A53T)83Vle, Standard PCR
Tlr4Lps-d EP, End Point Analysis

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

Giasson BI; Duda JE; Quinn SM; Zhang B; Trojanowski JQ; Lee VM. 2002. Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein. Neuron 34(4):521-33. [PubMed: 12062037]  [MGI Ref ID J:76657]

Additional References

Tg(Prnp-SNCA*A53T)83Vle related

Belal C; Ameli NJ; El Kommos A; Bezalel S; Al'khafaji AM; Mughal MR; Mattson MP; Kyriazis GA; Tyrberg B; Chan SL. 2012. The homocysteine-inducible endoplasmic reticulum (ER) stress protein Herp counteracts mutant alpha-synuclein-induced ER stress via the homeostatic regulation of ER-resident calcium release channel proteins. Hum Mol Genet 21(5):963-77. [PubMed: 22045699]  [MGI Ref ID J:180616]

Ben Gedalya T; Loeb V; Israeli E; Altschuler Y; Selkoe DJ; Sharon R. 2009. Alpha-synuclein and polyunsaturated fatty acids promote clathrin-mediated endocytosis and synaptic vesicle recycling. Traffic 10(2):218-34. [PubMed: 18980610]  [MGI Ref ID J:150319]

Clinton LK; Blurton-Jones M; Myczek K; Trojanowski JQ; LaFerla FM. 2010. Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline. J Neurosci 30(21):7281-9. [PubMed: 20505094]  [MGI Ref ID J:160821]

Emmanouilidou E; Elenis D; Papasilekas T; Stranjalis G; Gerozissis K; Ioannou PC; Vekrellis K. 2011. Assessment of alpha-synuclein secretion in mouse and human brain parenchyma. PLoS One 6(7):e22225. [PubMed: 21779395]  [MGI Ref ID J:175787]

Emmer KL; Waxman EA; Covy JP; Giasson BI. 2011. E46K human alpha-synuclein transgenic mice develop Lewy-like and tau pathology associated with age-dependent, detrimental motor impairment. J Biol Chem 286(40):35104-18. [PubMed: 21846727]  [MGI Ref ID J:177590]

Farrell KF; Krishnamachari S; Villanueva E; Lou H; Alerte TN; Peet E; Drolet RE; Perez RG. 2014. Non-motor parkinsonian pathology in aging A53T alpha-Synuclein mice is associated with progressive synucleinopathy and altered enzymatic function. J Neurochem 128(4):536-46. [PubMed: 24117685]  [MGI Ref ID J:206612]

Frake RA; Ricketts T; Menzies FM; Rubinsztein DC. 2015. Autophagy and neurodegeneration. J Clin Invest 125(1):65-74. [PubMed: 25654552]  [MGI Ref ID J:219892]

Gao HM; Kotzbauer PT; Uryu K; Leight S; Trojanowski JQ; Lee VM. 2008. Neuroinflammation and oxidation/nitration of alpha-synuclein linked to dopaminergic neurodegeneration. J Neurosci 28(30):7687-98. [PubMed: 18650345]  [MGI Ref ID J:138194]

Giasson BI; Forman MS; Higuchi M; Golbe LI; Graves CL; Kotzbauer PT; Trojanowski JQ; Lee VM. 2003. Initiation and synergistic fibrillization of tau and alpha-synuclein. Science 300(5619):636-40. [PubMed: 12714745]  [MGI Ref ID J:127923]

Graham DR; Sidhu A. 2010. Mice expressing the A53T mutant form of human alpha-synuclein exhibit hyperactivity and reduced anxiety-like behavior. J Neurosci Res 88(8):1777-83. [PubMed: 20077428]  [MGI Ref ID J:162178]

Gui YX; Wang XY; Kang WY; Zhang YJ; Zhang Y; Zhou Y; Quinn TJ; Liu J; Chen SD. 2012. Extracellular signal-regulated kinase is involved in alpha-synuclein-induced mitochondrial dynamic disorders by regulating dynamin-like protein 1. Neurobiol Aging 33(12):2841-54. [PubMed: 22445325]  [MGI Ref ID J:191254]

Hung LW; Villemagne VL; Cheng L; Sherratt NA; Ayton S; White AR; Crouch PJ; Lim S; Leong SL; Wilkins S; George J; Roberts BR; Pham CL; Liu X; Chiu FC; Shackleford DM; Powell AK; Masters CL; Bush AI; O'Keefe G; Culvenor JG; Cappai R; Cherny RA; Donnelly PS; Hill AF; Finkelstein DI; Barnham KJ. 2012. The hypoxia imaging agent CuII(atsm) is neuroprotective and improves motor and cognitive functions in multiple animal models of Parkinson's disease. J Exp Med 209(4):837-54. [PubMed: 22473957]  [MGI Ref ID J:183851]

Ihara M; Yamasaki N; Hagiwara A; Tanigaki A; Kitano A; Hikawa R; Tomimoto H; Noda M; Takanashi M; Mori H; Hattori N; Miyakawa T; Kinoshita M. 2007. Sept4, a component of presynaptic scaffold and Lewy bodies, is required for the suppression of alpha-synuclein neurotoxicity. Neuron 53(4):519-33. [PubMed: 17296554]  [MGI Ref ID J:136786]

Israeli E; Yakunin E; Zarbiv Y; Hacohen-Solovich A; Kisos H; Loeb V; Lichtenstein M; Ben-Gedalya T; Sabag O; Pikarsky E; Lorberboum-Galski H; Sharon R. 2011. alpha-Synuclein Expression Selectively Affects Tumorigenesis in Mice Modeling Parkinson's Disease. PLoS One 6(5):e19622. [PubMed: 21611169]  [MGI Ref ID J:172735]

Kisos H; Pukass K; Ben-Hur T; Richter-Landsberg C; Sharon R. 2012. Increased neuronal alpha-synuclein pathology associates with its accumulation in oligodendrocytes in mice modeling alpha-synucleinopathies. PLoS One 7(10):e46817. [PubMed: 23077527]  [MGI Ref ID J:192215]

Li L; Nadanaciva S; Berger Z; Shen W; Paumier K; Schwartz J; Mou K; Loos P; Milici AJ; Dunlop J; Hirst WD. 2013. Human A53T alpha-synuclein causes reversible deficits in mitochondrial function and dynamics in primary mouse cortical neurons. PLoS One 8(12):e85815. [PubMed: 24392030]  [MGI Ref ID J:211110]

Loeb V; Yakunin E; Saada A; Sharon R. 2010. The transgenic overexpression of alpha-synuclein and not its related pathology associates with complex I inhibition. J Biol Chem 285(10):7334-43. [PubMed: 20053987]  [MGI Ref ID J:160720]

Luk KC; Kehm VM; Zhang B; O'Brien P; Trojanowski JQ; Lee VM. 2012. Intracerebral inoculation of pathological alpha-synuclein initiates a rapidly progressive neurodegenerative alpha-synucleinopathy in mice. J Exp Med 209(5):975-86. [PubMed: 22508839]  [MGI Ref ID J:185142]

Mougenot AL; Nicot S; Bencsik A; Morignat E; Verchere J; Lakhdar L; Legastelois S; Baron T. 2012. Prion-like acceleration of a synucleinopathy in a transgenic mouse model. Neurobiol Aging 33(9):2225-8. [PubMed: 21813214]  [MGI Ref ID J:188195]

Norris EH; Uryu K; Leight S; Giasson BI; Trojanowski JQ; Lee VM. 2007. Pesticide exposure exacerbates alpha-synucleinopathy in an A53T transgenic mouse model. Am J Pathol 170(2):658-66. [PubMed: 17255333]  [MGI Ref ID J:117818]

Oaks AW; Frankfurt M; Finkelstein DI; Sidhu A. 2013. Age-dependent effects of A53T alpha-synuclein on behavior and dopaminergic function. PLoS One 8(4):e60378. [PubMed: 23560093]  [MGI Ref ID J:199878]

Paumier KL; Sukoff Rizzo SJ; Berger Z; Chen Y; Gonzales C; Kaftan E; Li L; Lotarski S; Monaghan M; Shen W; Stolyar P; Vasilyev D; Zaleska M; D Hirst W; Dunlop J. 2013. Behavioral characterization of A53T mice reveals early and late stage deficits related to Parkinson's disease. PLoS One 8(8):e70274. [PubMed: 23936403]  [MGI Ref ID J:205776]

Ramsey CP; Tsika E; Ischiropoulos H; Giasson BI. 2010. DJ-1 deficient mice demonstrate similar vulnerability to pathogenic Ala53Thr human alpha-syn toxicity. Hum Mol Genet 19(8):1425-37. [PubMed: 20089532]  [MGI Ref ID J:158368]

Sacino AN; Brooks M; Thomas MA; McKinney AB; Lee S; Regenhardt RW; McGarvey NH; Ayers JI; Notterpek L; Borchelt DR; Golde TE; Giasson BI. 2014. Intramuscular injection of alpha-synuclein induces CNS alpha-synuclein pathology and a rapid-onset motor phenotype in transgenic mice. Proc Natl Acad Sci U S A 111(29):10732-7. [PubMed: 25002524]  [MGI Ref ID J:212256]

Sardi SP; Clarke J; Viel C; Chan M; Tamsett TJ; Treleaven CM; Bu J; Sweet L; Passini MA; Dodge JC; Yu WH; Sidman RL; Cheng SH; Shihabuddin LS. 2013. Augmenting CNS glucocerebrosidase activity as a therapeutic strategy for parkinsonism and other Gaucher-related synucleinopathies. Proc Natl Acad Sci U S A 110(9):3537-42. [PubMed: 23297226]  [MGI Ref ID J:193256]

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Uryu K; Richter-Landsberg C; Welch W; Sun E; Goldbaum O; Norris EH; Pham CT; Yazawa I; Hilburger K; Micsenyi M; Giasson BI; Bonini NM; Lee VM; Trojanowski JQ. 2006. Convergence of heat shock protein 90 with ubiquitin in filamentous alpha-synuclein inclusions of alpha-synucleinopathies. Am J Pathol 168(3):947-61. [PubMed: 16507910]  [MGI Ref ID J:106557]

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Watts JC; Stohr J; Bhardwaj S; Wille H; Oehler A; Dearmond SJ; Giles K; Prusiner SB. 2011. Protease-resistant prions selectively decrease Shadoo protein. PLoS Pathog 7(11):e1002382. [PubMed: 22163178]  [MGI Ref ID J:183163]

Wills J; Credle J; Haggerty T; Lee JH; Oaks AW; Sidhu A. 2011. Tauopathic changes in the striatum of A53T alpha-synuclein mutant mouse model of Parkinson's disease. PLoS One 6(3):e17953. [PubMed: 21445308]  [MGI Ref ID J:171676]

Xie W; Chung KK. 2012. Alpha-synuclein impairs normal dynamics of mitochondria in cell and animal models of Parkinson's disease. J Neurochem :. [PubMed: 22537068]  [MGI Ref ID J:186510]

Zarbiv Y; Simhi-Haham D; Israeli E; Elhadi SA; Grigoletto J; Sharon R. 2014. Lysine residues at the first and second KTKEGV repeats mediate alpha-Synuclein binding to membrane phospholipids. Neurobiol Dis 70:90-8. [PubMed: 24905915]  [MGI Ref ID J:218358]

Zhang S; Xiao Q; Le W. 2015. Olfactory Dysfunction and Neurotransmitter Disturbance in Olfactory Bulb of Transgenic Mice Expressing Human A53T Mutant alpha-Synuclein. PLoS One 10(3):e0119928. [PubMed: 25799501]  [MGI Ref ID J:219329]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX11

Colony Maintenance

Breeding & HusbandryThe strain is maintained as a hemizygote on the same background. Homozygous mice have a high incidence of nonproductive matings. Coat color expected from breeding is Agouti.
Mating SystemHemizygote x Hemizygote         (Female x Male)   03-JAN-07
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


This strain is currently On Hold.
Register Interest

To request more information use the Customer Support Contact Form or call 1-800-422-6423 or 1-207-288-5845

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Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $232.00Female or MaleHemizygous for Tg(Prnp-SNCA*A53T)83Vle  
$232.00Female or MaleHomozygous for Tg(Prnp-SNCA*A53T)83Vle  
Price per Pair (US dollars $)Pair Genotype
$464.00Hemizygous for Tg(Prnp-SNCA*A53T)83Vle x Hemizygous for Tg(Prnp-SNCA*A53T)83Vle  

Standard Supply

This strain is currently on HOLD - Contact Customer Service for more information.


Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

This strain is currently on HOLD - Contact Customer Service for more information.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $301.60Female or MaleHemizygous for Tg(Prnp-SNCA*A53T)83Vle  
$301.60Female or MaleHomozygous for Tg(Prnp-SNCA*A53T)83Vle  
Price per Pair (US dollars $)Pair Genotype
$603.20Hemizygous for Tg(Prnp-SNCA*A53T)83Vle x Hemizygous for Tg(Prnp-SNCA*A53T)83Vle  

Standard Supply

This strain is currently on HOLD - Contact Customer Service for more information.


Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

This strain is currently on HOLD - Contact Customer Service for more information.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

This strain is currently on HOLD - Contact Customer Service for more information.

General Supply Notes

  • 4/13/15 - Due to decreased productivity this strain [Stock Number 004479], is undergoing expansion and will be on hold until June.

Control Information

   100010 B6C3F1/J (approximate)
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.

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.
Ordering Information
JAX® Mice
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JAX® Services
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Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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Terms of Use

Terms of Use

General Terms and Conditions

For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

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.