Strain Name:

B6.Cg-Usp14ax-J/J

Stock Number:

000518

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Description

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.Cg-axJ    (Changed: 15-DEC-04 )
Type Congenic; Mutant Strain;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BL/6
Donor Strain Mixed cross
Generation+N1
Generation Definitions

Description
The first outward sign of homozygosity for the recessive mutation Usp14ax-J is an unsteady gait, particularly in the hind quarters, that can be detected by approximately 2 weeks of age. These pups often show difficulty in righting themselves when turned on their backs. They have a rapid tremor that is most apparent when they are active. Extensor paralysis progresses and wasting of the hind quarters ensues until the hind quarters are not functional and the mouse can not sit upright or move except through the use of onlyits front limbs. Although death is premature, viability in the first two to three weeks is not diminished. At 18 days of age these mutants weigh an average of 15% less than wildtype controls and by 45 days this difference is increased such that they weigh 50-60% less than wildtype controls. Homozygotes do not breed. The lumbar vertebrae are slightly shorter than normal with shorter spinous processes and more elongate foramen. These homozygotes have defects in synaptic transmission in the central and peripheral nervous systems. End plate potentials are altered at neuromuscular junctions. D'Amato et al. published an extensive histological assessment of the Usp14ax-J/Usp14ax-J brain in which they reported that the corpus collosum, cingulum, and hippocampal commissureare underdeveloped as are particular nuclei and long tracts of the brain stem. The pons is shorter longitudinally and deficiencies are also found in the trapezoid body, as well as spinal nerves and spinal cord white matter. The medial lemniscus is smaller than normal only from the ventral beginning in the medulla to an area rostral to the substantia nigra and cerebral peduncles (for more detail see D'Amato et al., 1965.). A.M. Burt described abnormalities in the differentiation of the dendritic trees of CA1 pyramidal cells of the hippocampus and granule cells of the dentate gyrus. This is consistent with altered developmental apoptosis. Ohgoh et al. subsequently found significant apoptosis in the granule cell layer of the cerebellum but not the dentate gyrus or olfactory bulb. Ohgoh et al. also found no TUNEL staining of Purkinje cells, but the early report by D'Amato et al. identified disordered development and degenerative deformities of Purkinje cells. (Lyon, 1955; D'Amato and Hicks, 1965; Burt, 1980; Ohgoh et al., 2000; Wilson et al., 2002.)

Development
The mutation ataxia, Usp14ax, arose spontaneously in 1950 in CBA/H at Edinburgh, Scotland in the control series of a gamma ray mutagenesis experiment. In 1952 the kreisler mutation (Mafbkr) in a multiple recessive stock was imported into The Jackson Laboratory from Dr. Mary Lyon then at Edinburgh. This pair was mated and a female offspring was then mated back to the imported father and produced two ataxic type offspring. This newly identified mutation was called "paralytic" and was maintained by test matings within stock. In 1961 heterozygotes for "paralytic" were sent to Dr. Mary Lyon for allele testing with ataxia because of the similar phenotype. The test was positive and the "paralytic" mutation was then re-named ataxia Jackson (Usp14ax-J). In 1999 the possibility of ataxia Jackson being the same as the original ataxia was considered, and Dr. Lyon was asked to check the original pairs of kreisler mice for the presence of ataxia. She found that the imported male (#SU71.175) was homozygous for kreisler and heterozygous for ataxia (Usp14ax), having come from an ataxic mother, and the imported female (#SU88.197) was heterozygous for kreisler and a possible carrier of ataxia. Therefore, Usp14ax-J is probably the same mutation as the original Usp14ax.

This strain is congenic. In 1959 a "paralytic&" (ataxia Jackson) carrier female was outcrossed to a C57BL/6J male and backcrossing to C57BL/6J was continued to N6 after which the strain was sibling bred as tested pairs, reaching N6F25 in 1971 as ataxia Jackson stock. In 1971 Dr. Eva Eicher maintained ataxia Jackson by backcrossing to C57BL/6JEi via ovarian transplant using B6CBAF1 hosts. This strain was cryopreserved in 1984 by mating C57BL/6J females with heterozygous congenic males at N18F1.

Control Information

  Control
   Untyped from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Usp14
005750   B6;CByJ-Usp14nmf375/J
View Strains carrying other alleles of Usp14     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Usp14ax-J/Usp14ax-J

        B6.Cg-Usp14ax-J/J
  • nervous system phenotype
  • abnormal cerebellar granule cell morphology
    • TUNEL staining at 38 days of age shows increased apoptosis in cerebellar granule neurons in homozygotes and this is more severe in the anterior lobules than the posterior lobules   (MGI Ref ID J:108034)
  • abnormal synaptic transmission   (MGI Ref ID J:79322)
    • abnormal miniature endplate potential
      • significantly lower frequency and higher amplitude of miniature endplate potentials (MEPPs) in diaphragm muscle   (MGI Ref ID J:79322)
      • some MEPPs are larger and have significantly slower rise times   (MGI Ref ID J:79322)
      • input resistance and size of muscle fibers is not different from controls indicating lack of muscle degeneration   (MGI Ref ID J:79322)
    • abnormal neurotransmitter secretion
      • the amplitude of stimulus evoked endplate currents is smaller in diaphragm muscle   (MGI Ref ID J:79322)
      • the amplitude of spontaneous miniature endplate currents is larger in diaphragm muscle   (MGI Ref ID J:79322)
      • 53% lower quantal content in mutant mice   (MGI Ref ID J:79322)
    • decreased paired-pulse facilitation
      • lower levels of PPF at short interpulse intervals indicating defect in presynaptic calcium handling machinery   (MGI Ref ID J:79322)
      • there is significant depression of the PPF ratio for the first four inter-stimulus intervals in testing of the hippocampus region   (MGI Ref ID J:142436)
    • decreased post-tetanic potentiation
      • lower transient PTP immediately after high frequency stimulation   (MGI Ref ID J:79322)
    • increased synaptic depression
      • have increased synaptic short-term depression immediately following low frequency stimulation   (MGI Ref ID J:142436)
    • reduced long term potentiation
      • reduced early phase LTP after high frequency stimulation   (MGI Ref ID J:79322)
  • impaired synaptic plasticity
    • changes in short-term plasticity suggestive of a learning impairment; could not be tested due to motor defects of animals   (MGI Ref ID J:79322)
  • increased neuron apoptosis   (MGI Ref ID J:108034)
  • cellular phenotype
  • increased neuron apoptosis   (MGI Ref ID J:108034)

Usp14ax-J/Usp14ax-J

        B6.Cg-Usp14ax-J
  • mortality/aging
  • premature death
    • mice die by 2 months   (MGI Ref ID J:203043)
  • nervous system phenotype
  • abnormal neuromuscular synapse morphology
    • large accumulation of neurofilaments in terminals   (MGI Ref ID J:203043)
  • growth/size/body phenotype
  • decreased body weight   (MGI Ref ID J:203043)

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

Usp14ax-J/Usp14ax-J

        involves: STOCK Mafbkr
  • mortality/aging
  • premature death
    • death occurs at approximately 3 months of age   (MGI Ref ID J:27868)
    • death does not appear to be due to neuromuscular defects   (MGI Ref ID J:27868)
  • growth/size/body phenotype
  • decreased body size   (MGI Ref ID J:12283)
    • smaller than control siblings   (MGI Ref ID J:27868)
  • postnatal growth retardation
    • slowing of growth from birth is noted   (MGI Ref ID J:27868)
    • at one week, animals weigh 10% less than controls, 25% less at 3 weeks, and half as much at 5-6 weeks of age   (MGI Ref ID J:27868)
  • behavior/neurological phenotype
  • ataxia   (MGI Ref ID J:12283)
    • abnormalities noted at 1 week of age and classifiable at 18 days of age   (MGI Ref ID J:27868)
    • at 1 week of age, mice are more active than control siblings and hold legs straight when walking   (MGI Ref ID J:27868)
    • animals lift bodies clear of the ground when walking while control siblings crawl with the belly resting on the ground   (MGI Ref ID J:27868)
    • occasional tremor or disturbance of the normal diagonal sequence of limb movement is seen   (MGI Ref ID J:27868)
  • paralysis   (MGI Ref ID J:12283)
    • first seen at 3 weeks of age with a steadily increasing paralysis up to 3 months of age   (MGI Ref ID J:27868)
    • by 5-6 weeks the ability to sit on haunches is lost and the gait is slower   (MGI Ref ID J:27868)
    • in the end state, animals lay on one side and cannot balance in the normal prone position   (MGI Ref ID J:27868)
  • tremors   (MGI Ref ID J:12283)
    • some tremors of the head and body and limbs are observed   (MGI Ref ID J:27868)
  • weakness   (MGI Ref ID J:12283)
    • progressive limb weakness   (MGI Ref ID J:27868)
    • developed in parallel with loss of coordination   (MGI Ref ID J:27868)
  • muscle phenotype
  • muscular atrophy
    • evident at 3 weeks of age by reduction in muscle fiber diameter and presence of centrally located nuclei   (MGI Ref ID J:12283)
  • reproductive system phenotype
  • female infertility   (MGI Ref ID J:27868)
  • male infertility   (MGI Ref ID J:27868)
  • priapism
    • common in males after a few months of age   (MGI Ref ID J:12283)
    • full urinary bladders often seen upon autopsy   (MGI Ref ID J:12283)
  • nervous system phenotype
  • abnormal brain morphology   (MGI Ref ID J:12283)
    • abnormal brain commissure morphology   (MGI Ref ID J:12283)
      • decreased corpus callosum size   (MGI Ref ID J:12283)
      • decreased hippocampal commissure size   (MGI Ref ID J:12283)
    • abnormal cingulum morphology
      • reduced size of cingulum   (MGI Ref ID J:12283)
    • abnormal hindbrain morphology   (MGI Ref ID J:12283)
      • Purkinje cell degeneration
        • degeneration in Purkinje cell axons and dendrites   (MGI Ref ID J:12283)
      • abnormal pons morphology
        • longitudinally shorter than normal   (MGI Ref ID J:12283)
        • pontine neurons are smaller than in controls   (MGI Ref ID J:12283)
      • small cerebellum
        • deficiency of white matter in the lobules   (MGI Ref ID J:12283)
    • abnormal limbic system morphology
      • underdeveloped structures associated with the limbic system, and some nuclei and tracts of the brainstem   (MGI Ref ID J:12283)
      • abnormal dentate gyrus morphology
        • reduced in cross-sectional area   (MGI Ref ID J:6389)
        • dendritic trees of granule cells of the dentate gyrus are shorter than normal   (MGI Ref ID J:6389)
      • abnormal hippocampus pyramidal cell morphology
        • dendritic trees of hippocampal cells show marked reduction in height and lateral spread between 19 and 41 days of age   (MGI Ref ID J:6389)
      • small hippocampus
        • reduced in cross-sectional area   (MGI Ref ID J:6389)
    • decreased midbrain size
      • smaller size is more apparent at the tegmentum than the base   (MGI Ref ID J:12283)
  • abnormal spinal cord white matter morphology
    • deficient white matter   (MGI Ref ID J:12283)
  • abnormal spinal nerve morphology
    • axis cylinders are smaller than normal and myelin sheaths are correspondingly small   (MGI Ref ID J:12283)
  • skeleton phenotype
  • abnormal lumbar vertebrae morphology
    • short spinous processes and elongated foramen for exit of spinal nerves   (MGI Ref ID J:12283)
    • short lumbar vertebrae
      • shorter than normal   (MGI Ref ID J:12283)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • no significant differences from normal are found in the major brain lipid classes, fatty acids, nucleic acids, or neurokeratin amino acid content   (MGI Ref ID J:5066)

Usp14ax-J/Usp14ax-J

        C.Cg-Usp14ax-J
  • mortality/aging
  • complete perinatal lethality
    • mice on a pseudocongenic C57BL/6 background die at or before birth unlike mice on a BALB/c background   (MGI Ref ID J:203043)
View Research Applications

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

Usp14ax-J related

Apoptosis Research

Cell Biology Research
Protein Processing
      degradation

Developmental Biology Research
Internal/Organ Defects
      brain
Neurodevelopmental Defects
Skeletal Defects

Neurobiology Research
Ataxia (Movement) Defects
Cerebellar Defects
Neurodegeneration
Neurodevelopmental Defects
Neuromuscular Defects
Neurotransmitter Receptor and Synaptic Vesicle Defects
Tremor Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Usp14ax-J
Allele Name ataxia Jackson
Allele Type Spontaneous (Hypomorph)
Common Name(s) Usp14asJ; Usp14axJ; ax; axJ; paralytic; pr;
Strain of OriginSTOCK Mafb
Gene Symbol and Name Usp14, ubiquitin specific peptidase 14
Chromosome 18
Gene Common Name(s) 2610005K12Rik; 2610037B11Rik; AW107924; C78769; NMF375; RIKEN cDNA 2610005K12 gene; RIKEN cDNA 2610037B11 gene; TGT; ataxia; ax; dUB-type TGT; expressed sequence AW107924; expressed sequence C78769; neuroscience mutagenesis facility, 375; nmf375;
General Note There is sufficient reason to believe that axJand ax represent the same mutation. The kreisler stock was imported to The Jackson Laboratory from Edinburgh in 1952. The axJ mutation arose at The Jackson Laboratory in the kreisler stock in 1953 and was originally called paralytic. Mary Lyon, also in Edinburgh, reported the ataxia mutation shortly thereafter. Paralytic heterozygotes were sent to Mary Lyon and found to be allelic with her ataxia mutant. Thus the name was changed from paralytic to ataxia. The Jackson Laboratory investigated the possibility that ax and axJ were really the same strain. Examination of the original shipping records and pedigree numbers showed that the original kreisler male and female mice shippedto the laboratory in 1952, were potentially heterozygote for the ax mutation (J:58683).
Molecular Note The mutation underlying this phenotypic mutant has been identified as an IAP insertion into intron 5 of the Usp14 gene. The insertion results in a number of aberrant splice products containing stop codons immediately following the splice junction. Low levels of wild-type transcript are observed in homozygous mutant animals, suggesting that this allele is hypomorphic. [MGI Ref ID J:79322]

Genotyping

Genotyping Information

Genotyping Protocols

Usp14ax-J, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Wilson SM; Bhattacharyya B; Rachel RA; Coppola V; Tessarollo L; Householder DB; Fletcher CF; Miller RJ; Copeland NG; Jenkins NA. 2002. Synaptic defects in ataxia mice result from a mutation in Usp14, encoding a ubiquitin-specific protease. Nat Genet 32(3):420-5. [PubMed: 12368914]  [MGI Ref ID J:79322]

Usp14ax-J related

Anderson C; Crimmins S; Wilson JA; Korbel GA; Ploegh HL; Wilson SM. 2005. Loss of Usp14 results in reduced levels of ubiquitin in ataxia mice. J Neurochem 95(3):724-31. [PubMed: 16190881]  [MGI Ref ID J:102268]

Bhattacharyya BJ; Wilson SM; Jung H; Miller RJ. 2012. Altered neurotransmitter release machinery in mice deficient for the deubiquitinating enzyme Usp14. Am J Physiol Cell Physiol 302(4):C698-708. [PubMed: 22075695]  [MGI Ref ID J:180610]

Burt AM. 1980. Morphologic abnormalities in the postnatal differentiation of CA1 pyramidal cells and granule cells in the hippocampal formation of the ataxic mouse. Anat Rec 196(1):61-9. [PubMed: 7416502]  [MGI Ref ID J:6389]

Carter TC. 1950. New mutants Mouse News Lett 2:1.  [MGI Ref ID J:24770]

Chen PC; Bhattacharyya BJ; Hanna J; Minkel H; Wilson JA; Finley D; Miller RJ; Wilson SM. 2011. Ubiquitin homeostasis is critical for synaptic development and function. J Neurosci 31(48):17505-13. [PubMed: 22131412]  [MGI Ref ID J:178142]

Chen PC; Qin LN; Li XM; Walters BJ; Wilson JA; Mei L; Wilson SM. 2009. The proteasome-associated deubiquitinating enzyme Usp14 is essential for the maintenance of synaptic ubiquitin levels and the development of neuromuscular junctions. J Neurosci 29(35):10909-19. [PubMed: 19726649]  [MGI Ref ID J:152454]

Concepcion D; Flores-Garcia L; Hamilton BA. 2009. Multipotent genetic suppression of retrotransposon-induced mutations by Nxf1 through fine-tuning of alternative splicing. PLoS Genet 5(5):e1000484. [PubMed: 19436707]  [MGI Ref ID J:149430]

Crimmins S; Jin Y; Wheeler C; Huffman AK; Chapman C; Dobrunz LE; Levey A; Roth KA; Wilson JA; Wilson SM. 2006. Transgenic rescue of ataxia mice with neuronal-specific expression of ubiquitin-specific protease 14. J Neurosci 26(44):11423-31. [PubMed: 17079671]  [MGI Ref ID J:114696]

D'Amato CJ; Hicks SP. 1965. Neuropathologic alterations in the ataxia (paralytic) mouse. Arch Pathol 80(6):604-12. [PubMed: 5855800]  [MGI Ref ID J:12283]

Donahue LR. 1999. Evidence that ax-J and ax alleles are the same strain Personal Communication :.  [MGI Ref ID J:58683]

Jin YN; Chen PC; Watson JA; Walters BJ; Phillips SE; Green K; Schmidt R; Wilson JA; Johnson GV; Roberson ED; Dobrunz LE; Wilson SM. 2012. Usp14 deficiency increases tau phosphorylation without altering tau degradation or causing tau-dependent deficits. PLoS One 7(10):e47884. [PubMed: 23144711]  [MGI Ref ID J:192359]

Lane PW. 1962. Allelism of pr and ax Mouse News Lett 26:35.  [MGI Ref ID J:180]

Lane PW; Searle AG; Beechey CV; Eicher E. 1981. Chromosome 18 of the house mouse. J Hered 72(6):409-12. [PubMed: 6949984]  [MGI Ref ID J:6710]

Lappe-Siefke C; Loebrich S; Hevers W; Waidmann OB; Schweizer M; Fehr S; Fritschy JM; Dikic I; Eilers J; Wilson SM; Kneussel M. 2009. The ataxia (axJ) mutation causes abnormal GABAA receptor turnover in mice. PLoS Genet 5(9):e1000631. [PubMed: 19759851]  [MGI Ref ID J:154119]

Lyon MF. 1955. Ataxia - A new recessive mutant of the house mouse J Hered 46(2):77-80.  [MGI Ref ID J:27868]

Marshall AG; Watson JA; Hallengren JJ; Walters BJ; Dobrunz LE; Francillon L; Wilson JA; Phillips SE; Wilson SM. 2013. Genetic background alters the severity and onset of Neuromuscular Disease caused by the loss of ubiquitin-specific protease 14 (Usp14) PLoS ONE 8(12):e84042.  [MGI Ref ID J:203043]

Marshall AG; Watson JA; Hallengren JJ; Walters BJ; Dobrunz LE; Francillon L; Wilson JA; Phillips SE; Wilson SM. 2013. Genetic background alters the severity and onset of neuromuscular disease caused by the loss of ubiquitin-specific protease 14 (usp14). PLoS One 8(12):e84042. [PubMed: 24358326]  [MGI Ref ID J:211136]

Ohgoh M; Yamazaki K; Ogura H; Nishizawa Y; Tanaka I. 2000. Apoptotic cell death of cerebellar granule neurons in genetically ataxia (ax) mice. Neurosci Lett 288(3):167-70. [PubMed: 10889334]  [MGI Ref ID J:108034]

Walters BJ; Campbell SL; Chen PC; Taylor AP; Schroeder DG; Dobrunz LE; Artavanis-Tsakonas K; Ploegh HL; Wilson JA; Cox GA; Wilson SM. 2008. Differential effects of Usp14 and Uch-L1 on the ubiquitin proteasome system and synaptic activity. Mol Cell Neurosci 39(4):539-48. [PubMed: 18771733]  [MGI Ref ID J:142436]

Weber MB. 1968. A study of brain lipids, nucleic acids and proteins in the ataxic (axJ) mouse. Neurology 18(3):243-9. [PubMed: 5689664]  [MGI Ref ID J:5066]

Wilson SM; Bhattacharyya B; Rachel RA; Coppola V; Tessarollo L; Householder DB; Fletcher CF; Miller RJ; Copeland NG; Jenkins NA. 2002. Synaptic defects in ataxia mice result from a mutation in Usp14, encoding a ubiquitin-specific protease. Nat Genet 32(3):420-5. [PubMed: 12368914]  [MGI Ref ID J:79322]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3300.00
Animals Provided

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

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

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

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

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4290.00
Animals Provided

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

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

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

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

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

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

Control Information

  Control
   Untyped from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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.


(6.6)