Strain Name:

B6;129-Trp53bp1tm1Jc/J

Stock Number:

006495

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Availability:

Cryopreserved - Ready for recovery

Use Restrictions Apply, see Terms of Use
These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways.

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

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
GenerationN?+N1+N1pN1
Generation Definitions
 
Donating Investigator Junjie Chen,   UTexas; M. D. Anderson Cancer Center

Description
Homozygous "53BP1"-deficient mice are viable and fertile, but exhibit retarded growth and generate reduced litter sizes. Protein from the targeted gene is not detected in the testes (by immunoblot) or in mouse embryonic fibroblasts (MEFs) (by immunofluorescence). Homozygotes are immunocompromised, hypersensitive to whole-body irradiation, and develop thymic lymphomas with higher frequency (8%) compared to wildtype by 4-7 months of age. MEFs from homozygous mutant mice have a defective DNA damage response with impaired Chk2 activation. These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways.

Development
A targeting vector containing a neomycin resistance gene was used to replace the exon spanning nucleotides 3777 to 4048 of the endogenous gene. The construct was electroporated into "129/SvE"-derived embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and chimeric males were mated to C57BL/6 females. The resulting heterozygous mice were interbred for many generations prior to arrival at The Jackson Laboratory.

Control Information

  Control
   101043 B6129SF1/J (approximate)
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Trp53bp1
005375   STOCK Trp53bp1hlb543/CloJ
View Strains carrying other alleles of Trp53bp1     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Trp53bp1tm1Jc/Trp53bp1tm1Jc

        involves: 129 * C57BL/6
  • mortality/aging
  • increased mortality induced by ionizing radiation
    • in response to 8 Gy of whole body ionizing radiation (IR), all homozygotes die by 14 days from radiation-induced intestinal bleeding and bone marrow failure, whereas most wild-type mice remain viable for at least 2 months after IR treatment   (MGI Ref ID J:82512)
  • premature death
    • 9% of homozygotes die at the ages of 1 to 7 months in the absence of overt detectable tumors; possibly due to opportunistic infections   (MGI Ref ID J:82512)
  • growth/size/body phenotype
  • decreased body size
    • homozygotes are significantly smaller than wild-type and heterozygous control mice   (MGI Ref ID J:82512)
    • decreased body weight
      • at 5 months of age, both male and female homozygotes weigh significantly less than their wild-type or heterozygous counterparts   (MGI Ref ID J:82512)
  • postnatal growth retardation
    • homozygotes of both sexes are growth retarded relative to wild-type or heterozygous control littermates   (MGI Ref ID J:82512)
  • immune system phenotype
  • decreased CD4-positive T cell number
    • at 6 weeks of age, homozygotes show a ~2-fold reduction in the percentage of CD4+ mature thymocytes and peripheral CD4+ T lymphocytes relative to wild-type littermates   (MGI Ref ID J:82512)
  • increased double-negative T cell number
    • at 6 weeks of age, homozygotes show a maximum 2-fold increase in the percentage of CD4- CD8- progenitors relative to wild-type littermates   (MGI Ref ID J:82512)
  • thymus hypoplasia
    • homozygotes show a 40% reduction in thymus cellularity relative to wild-type littermates   (MGI Ref ID J:82512)
  • hematopoietic system phenotype
  • decreased CD4-positive T cell number
    • at 6 weeks of age, homozygotes show a ~2-fold reduction in the percentage of CD4+ mature thymocytes and peripheral CD4+ T lymphocytes relative to wild-type littermates   (MGI Ref ID J:82512)
  • increased double-negative T cell number
    • at 6 weeks of age, homozygotes show a maximum 2-fold increase in the percentage of CD4- CD8- progenitors relative to wild-type littermates   (MGI Ref ID J:82512)
  • thymus hypoplasia
    • homozygotes show a 40% reduction in thymus cellularity relative to wild-type littermates   (MGI Ref ID J:82512)
  • cellular phenotype
  • abnormal cell cycle checkpoint function
    • several hrs after exposure to 6 Gy of ionizing radiation (IR), mutant MEFs, like wild-type MEFs, are arrested in G2 but display a delayed exit from the G2/M phase   (MGI Ref ID J:82512)
    • at 24 hrs after IR, the % of mitotic cells is ~3-fold lower in nocodazole-treated mutant MEFs than in wild-type cells, as assessed by immunostaining with anti-phospho-histone H3 antibodies   (MGI Ref ID J:82512)
    • at 30 min after exposure to 20 Gy of IR, mutant MEFs show a slight defect in intra-S-phase checkpoint regulation relative to wild-type MEFs   (MGI Ref ID J:82512)
    • however, mutant MEFs, synchronized by a cycle of serum starvation and release, show a normal G1 arrest in response to 10 to 20 Gy of IR   (MGI Ref ID J:82512)
  • aneuploidy
    • mutant MEFs (passage 3) show a tendency toward aneuploidy   (MGI Ref ID J:82512)
  • chromosomal instability
    • mutant MEFs (passage 3) show a tendency toward aneuploidy and/or tetraploidy, suggesting a defect in chromosome segregation   (MGI Ref ID J:82512)
    • however, no spontaneous chromosomal breaks are detected in mutant MEFs   (MGI Ref ID J:82512)
  • decreased cell proliferation
    • MEFs derived from E14.5 homozygous mutant embryos display a reduced proliferation rate relative to wild-type MEFs   (MGI Ref ID J:82512)
  • increased cellular sensitivity to ionizing radiation
    • mutant ES cells show a 2- to 3-fold increase in ionizing radiation sensitivity relative to wild-type ES cells, revealed by in vitro clonogenic survival assays   (MGI Ref ID J:82512)
  • tumorigenesis
  • increased lymphoma incidence
    • homozygotes exhibit an increased incidence of malignant lymphomas, putatively due to an inability to detect or repair abnormal V(D)J recombination   (MGI Ref ID J:82512)
    • increased T cell derived lymphoma incidence
      • at 4 to 7 months of age, 8% of homozygotes develop massive thymic lymphomas with or without infiltration of the lymph nodes, spleen, and kidney, not observed in wild-type or heterozygous control mice   (MGI Ref ID J:82512)
      • three of these tumors display a CD4+ CD8+ immunophenotype   (MGI Ref ID J:82512)
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • male homozygotes show no overt defects in spermatogenesis, suggesting normal meiosis   (MGI Ref ID J:82512)
    • decreased litter size
      • although both male and female homozygotes are fertile, the average litter size of homozygous mutant intercrosses is slightly reduced relative to that of wild-type intercrosses   (MGI Ref ID J:82512)
  • homeostasis/metabolism phenotype
  • increased mortality induced by ionizing radiation
    • in response to 8 Gy of whole body ionizing radiation (IR), all homozygotes die by 14 days from radiation-induced intestinal bleeding and bone marrow failure, whereas most wild-type mice remain viable for at least 2 months after IR treatment   (MGI Ref ID J:82512)
  • endocrine/exocrine gland phenotype
  • thymus hypoplasia
    • homozygotes show a 40% reduction in thymus cellularity relative to wild-type littermates   (MGI Ref ID J:82512)

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

Trp53bp1tm1Jc/Trp53bp1tm1Jc

        involves: 129
  • cellular phenotype
  • abnormal cell physiology
    • mouse embryonic cells are more sensitive to DNA damage induced by radiation compared to wild type cells   (MGI Ref ID J:194603)
    • abnormal DNA repair
      • mouse embryonic fibroblasts exhibit suppression of chromosome end fusion events at telomeres induced by expression of a dominant negative Terf2   (MGI Ref ID J:195061)
    • increased cellular sensitivity to hydroxyurea   (MGI Ref ID J:194603)
    • increased cellular sensitivity to ionizing radiation   (MGI Ref ID J:194603)
  • hematopoietic system phenotype
  • abnormal class switch recombination
    • impaired but partially rescued by short hairpin RNA inhibition of Rbbp8 and enhanced by treatment with the WRNi helicase inhibitor or to a lesser extent the ATM inhibitor Ku55933   (MGI Ref ID J:194603)
  • immune system phenotype
  • abnormal class switch recombination
    • impaired but partially rescued by short hairpin RNA inhibition of Rbbp8 and enhanced by treatment with the WRNi helicase inhibitor or to a lesser extent the ATM inhibitor Ku55933   (MGI Ref ID J:194603)
  • homeostasis/metabolism phenotype
  • abnormal DNA repair
    • mouse embryonic fibroblasts exhibit suppression of chromosome end fusion events at telomeres induced by expression of a dominant negative Terf2   (MGI Ref ID J:195061)
View Research Applications

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

Cancer Research
Increased Tumor Incidence
      Lymphomas
      Lymphomas: thymic
Other
      DNA Repair

Cell Biology Research
DNA Damage Response
Genes Regulating Growth and Proliferation

Developmental Biology Research
Growth Defects

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
      multiple immune defects
Immunodeficiency Associated with Other Defects

Internal/Organ Research
Thymus Defects

Research Tools
Cancer Research
Cell Biology Research
Immunology, Inflammation and Autoimmunity Research

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Trp53bp1tm1Jc
Allele Name targeted mutation 1, Junjie Chen
Allele Type Targeted (Null/Knockout)
Common Name(s) 53BP1-; Trp53bp1delta;
Mutation Made By Kay Minn,   Mayo Clinic College of Medicine
Strain of Origin129
Gene Symbol and Name Trp53bp1, transformation related protein 53 binding protein 1
Chromosome 2
Gene Common Name(s) 53BP1; p202; p53BP1;
Molecular Note The gene was disrupted by replacement of an exon containing nucleotides 3777 - 4048 with a neomycin resistance cassette via homologous recombination. Absence of gene expression in homozygous mutant animals was confirmed by Western blot analysis using an antibody directed against the N-terminal portion of the protein. [MGI Ref ID J:82512]

Genotyping

Genotyping Information

Genotyping Protocols

Trp53bp1tm1Jc, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Ward IM; Minn K; van Deursen J; Chen J. 2003. p53 Binding protein 53BP1 is required for DNA damage responses and tumor suppression in mice. Mol Cell Biol 23(7):2556-63. [PubMed: 12640136]  [MGI Ref ID J:82512]

Additional References

Trp53bp1tm1Jc related

Barlow JH; Faryabi RB; Callen E; Wong N; Malhowski A; Chen HT; Gutierrez-Cruz G; Sun HW; McKinnon P; Wright G; Casellas R; Robbiani DF; Staudt L; Fernandez-Capetillo O; Nussenzweig A. 2013. Identification of Early Replicating Fragile Sites that Contribute to Genome Instability. Cell 152(3):620-32. [PubMed: 23352430]  [MGI Ref ID J:193481]

Bothmer A; Robbiani DF; Feldhahn N; Gazumyan A; Nussenzweig A; Nussenzweig MC. 2010. 53BP1 regulates DNA resection and the choice between classical and alternative end joining during class switch recombination. J Exp Med 207(4):855-65. [PubMed: 20368578]  [MGI Ref ID J:159173]

Bothmer A; Rommel PC; Gazumyan A; Polato F; Reczek CR; Muellenbeck MF; Schaetzlein S; Edelmann W; Chen PL; Brosh RM Jr; Casellas R; Ludwig T; Baer R; Nussenzweig A; Nussenzweig MC; Robbiani DF. 2013. Mechanism of DNA resection during intrachromosomal recombination and immunoglobulin class switching. J Exp Med 210(1):115-23. [PubMed: 23254285]  [MGI Ref ID J:194603]

Bowman-Colin C; Xia B; Bunting S; Klijn C; Drost R; Bouwman P; Fineman L; Chen X; Culhane AC; Cai H; Rodig SJ; Bronson RT; Jonkers J; Nussenzweig A; Kanellopoulou C; Livingston DM. 2013. Palb2 synergizes with Trp53 to suppress mammary tumor formation in a model of inherited breast cancer. Proc Natl Acad Sci U S A 110(21):8632-7. [PubMed: 23657012]  [MGI Ref ID J:197442]

Buonomo SB; Wu Y; Ferguson D; de Lange T. 2009. Mammalian Rif1 contributes to replication stress survival and homology-directed repair. J Cell Biol 187(3):385-98. [PubMed: 19948482]  [MGI Ref ID J:155449]

Callen E; Di Virgilio M; Kruhlak MJ; Nieto-Soler M; Wong N; Chen HT; Faryabi RB; Polato F; Santos M; Starnes LM; Wesemann DR; Lee JE; Tubbs A; Sleckman BP; Daniel JA; Ge K; Alt FW; Fernandez-Capetillo O; Nussenzweig MC; Nussenzweig A. 2013. 53BP1 Mediates Productive and Mutagenic DNA Repair through Distinct Phosphoprotein Interactions. Cell 153(6):1266-80. [PubMed: 23727112]  [MGI Ref ID J:198413]

Callen E; Jankovic M; Difilippantonio S; Daniel JA; Chen HT; Celeste A; Pellegrini M; McBride K; Wangsa D; Bredemeyer AL; Sleckman BP; Ried T; Nussenzweig M; Nussenzweig A. 2007. ATM prevents the persistence and propagation of chromosome breaks in lymphocytes. Cell 130(1):63-75. [PubMed: 17599403]  [MGI Ref ID J:143821]

Callen E; Jankovic M; Wong N; Zha S; Chen HT; Difilippantonio S; Di Virgilio M; Heidkamp G; Alt FW; Nussenzweig A; Nussenzweig M. 2009. Essential role for DNA-PKcs in DNA double-strand break repair and apoptosis in ATM-deficient lymphocytes. Mol Cell 34(3):285-97. [PubMed: 19450527]  [MGI Ref ID J:150435]

Cao L; Xu X; Bunting SF; Liu J; Wang RH; Cao LL; Wu JJ; Peng TN; Chen J; Nussenzweig A; Deng CX; Finkel T. 2009. A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency. Mol Cell 35(4):534-41. [PubMed: 19716796]  [MGI Ref ID J:154193]

Chapman JR; Barral P; Vannier JB; Borel V; Steger M; Tomas-Loba A; Sartori AA; Adams IR; Batista FD; Boulton SJ. 2013. RIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resection. Mol Cell 49(5):858-71. [PubMed: 23333305]  [MGI Ref ID J:195061]

Dimitrova N; Chen YC; Spector DL; de Lange T. 2008. 53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility. Nature 456(7221):524-8. [PubMed: 18931659]  [MGI Ref ID J:143563]

Fradet-Turcotte A; Canny MD; Escribano-Diaz C; Orthwein A; Leung CC; Huang H; Landry MC; Kitevski-LeBlanc J; Noordermeer SM; Sicheri F; Durocher D. 2013. 53BP1 is a reader of the DNA-damage-induced H2A Lys 15 ubiquitin mark. Nature 499(7456):50-4. [PubMed: 23760478]  [MGI Ref ID J:204560]

Jankovic M; Feldhahn N; Oliveira TY; Silva IT; Kieffer-Kwon KR; Yamane A; Resch W; Klein I; Robbiani DF; Casellas R; Nussenzweig MC. 2013. 53BP1 alters the landscape of DNA rearrangements and suppresses AID-induced B cell lymphoma. Mol Cell 49(4):623-31. [PubMed: 23290917]  [MGI Ref ID J:195088]

Liu X; Jiang W; Dubois RL; Yamamoto K; Wolner Z; Zha S. 2012. Overlapping functions between XLF repair protein and 53BP1 DNA damage response factor in end joining and lymphocyte development. Proc Natl Acad Sci U S A 109(10):3903-8. [PubMed: 22355127]  [MGI Ref ID J:182138]

Martinez P; Ferrara-Romeo I; Flores JM; Blasco MA. 2014. Essential role for the TRF2 telomere protein in adult skin homeostasis. Aging Cell :. [PubMed: 24725274]  [MGI Ref ID J:210514]

Martinez P; Flores JM; Blasco MA. 2012. 53BP1 deficiency combined with telomere dysfunction activates ATR-dependent DNA damage response. J Cell Biol 197(2):283-300. [PubMed: 22508511]  [MGI Ref ID J:185038]

Minter-Dykhouse K; Ward I; Huen MS; Chen J; Lou Z. 2008. Distinct versus overlapping functions of MDC1 and 53BP1 in DNA damage response and tumorigenesis. J Cell Biol 181(5):727-35. [PubMed: 18504301]  [MGI Ref ID J:137023]

Orsburn B; Escudero B; Prakash M; Gesheva S; Liu G; Huso DL; Franco S. 2010. Differential requirement for H2AX and 53BP1 in organismal development and genome maintenance in the absence of poly(ADP)ribosyl polymerase 1. Mol Cell Biol 30(10):2341-52. [PubMed: 20231360]  [MGI Ref ID J:162591]

Ramiro AR; Jankovic M; Callen E; Difilippantonio S; Chen HT; McBride KM; Eisenreich TR; Chen J; Dickins RA; Lowe SW; Nussenzweig A; Nussenzweig MC. 2006. Role of genomic instability and p53 in AID-induced c-myc-Igh translocations. Nature 440(7080):105-9. [PubMed: 16400328]  [MGI Ref ID J:106450]

Reina-San-Martin B; Chen J; Nussenzweig A; Nussenzweig MC. 2007. Enhanced intra-switch region recombination during immunoglobulin class switch recombination in 53BP1(-/-) B cells. Eur J Immunol 37(1):235-9. [PubMed: 17183606]  [MGI Ref ID J:117038]

Rybanska-Spaeder I; Reynolds TL; Chou J; Prakash M; Jefferson T; Huso DL; Desiderio S; Franco S. 2013. 53BP1 is limiting for NHEJ repair in ATM-deficient model systems that are subjected to oncogenic stress or radiation. Mol Cancer Res 11(10):1223-34. [PubMed: 23858098]  [MGI Ref ID J:205436]

Schotta G; Sengupta R; Kubicek S; Malin S; Kauer M; Callen E; Celeste A; Pagani M; Opravil S; De La Rosa-Velazquez IA; Espejo A; Bedford MT; Nussenzweig A; Busslinger M; Jenuwein T. 2008. A chromatin-wide transition to H4K20 monomethylation impairs genome integrity and programmed DNA rearrangements in the mouse. Genes Dev 22(15):2048-61. [PubMed: 18676810]  [MGI Ref ID J:139510]

Sfeir A; de Lange T. 2012. Removal of shelterin reveals the telomere end-protection problem. Science 336(6081):593-7. [PubMed: 22556254]  [MGI Ref ID J:184522]

Sin HS; Barski A; Zhang F; Kartashov AV; Nussenzweig A; Chen J; Andreassen PR; Namekawa SH. 2012. RNF8 regulates active epigenetic modifications and escape gene activation from inactive sex chromosomes in post-meiotic spermatids. Genes Dev 26(24):2737-48. [PubMed: 23249736]  [MGI Ref ID J:192008]

Squatrito M; Vanoli F; Schultz N; Jasin M; Holland EC. 2012. 53BP1 is a haploinsufficient tumor suppressor and protects cells from radiation response in glioma. Cancer Res 72(20):5250-60. [PubMed: 22915756]  [MGI Ref ID J:191806]

Ward IM; Difilippantonio S; Minn K; Mueller MD; Molina JR; Yu X; Frisk CS; Ried T; Nussenzweig A; Chen J. 2005. 53BP1 cooperates with p53 and functions as a haploinsufficient tumor suppressor in mice. Mol Cell Biol 25(22):10079-86. [PubMed: 16260621]  [MGI Ref ID J:102355]

Ward IM; Reina-San-Martin B; Olaru A; Minn K; Tamada K; Lau JS; Cascalho M; Chen L; Nussenzweig A; Livak F; Nussenzweig MC; Chen J. 2004. 53BP1 is required for class switch recombination. J Cell Biol 165(4):459-64. [PubMed: 15159415]  [MGI Ref ID J:91130]

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, homozygous mice are bred together. Homozygotes have an increased frequency (approximately 8%) of thymic tumors between 4-7 months of age.

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* $2525.00
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 willfulfill 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* $3283.00
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 willfulfill 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
   101043 B6129SF1/J (approximate)
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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.
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