Strain Name:

C.129S4-Traf1tm1Tsi/TsiPryhJ

Stock Number:

008074

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Availability:

Cryopreserved - Ready for recovery

Common Names: BALB/c TRAF1;     BALB/c-TRAF1;    
These TRAF1 mutant mice may be useful in studying negative regulation of tumor necrosis factor (TNF) signaling, NF-kB and AP-1 signaling, T cell receptor (TCR)-induced proliferation of T cells, Th2 responses, TRAF1/Bim function in CD8 memory T cell survival, allergic airway diseases and Rheumatoid arthritis, as well as the role of TRAF1 activation in the pathogenesis of lymphomas. Of note, TRAF1 mutant mice are available on either a BALB/c congenic (Stock No. 008074) or C57BL/6 congenic (Stock No. 008076) background.

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 C.129S4-Traf1tm1Tsi/J    (Changed: 17-DEC-08 )
Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
GenerationF?pN1
Generation Definitions
 
Donating Investigator Gloria Pryhuber,   University of Rochester

Description
Mice homozygous for the TRAF1 mutant allele (TRAF1-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that elicit enhanced Th2 responses in vivo. BALB/c-TRAF1-/- T cells exhibit elevated nuclear expression of NFAT-interacting protein (NIP45) and also induce significantly more intense pulmonary inflammation and higher airway hyper-responsiveness in OVA allergic inflammation models. Pulmonary leukocyte recruitment is attenuated following inhalation of lipopolysaccharide in BALB/c-TRAF1-/- mice.

Homozygous mice on a C57BL/6 congenic background (B6-TRAF1-/-) have abnormal memory T cell survival and impaired influenza virus CD8 T cell responses. Activated B6-TRAF1-/- T cells accumulate increased levels of proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bims. The donating investigator reports that B6-TRAF1 mutant mice may be difficult to breed and gain more weight than BALB/c-TRAF1 mutant mice. TRAF1 strains may be useful in studying negative regulation of tumor necrosis factor (TNF) signaling, NF-kB and AP-1 signaling, T cell receptor (TCR)-induced proliferation of T cells, Th2 responses, TRAF1/Bim function in CD8 memory T cell survival, allergic airway diseases and Rheumatoid arthritis, as well as the role of TRAF1 activation in the pathogenesis of lymphomas.

Of note, TRAF1 mutant mice are available on either a BALB/c congenic (Stock No. 008074) or C57BL/6 congenic (Stock No. 008076) background.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
The targeted mutation was generated in the laboratory of Dr. Erdyni Tsitsikov (Immune Disease Institute (formerly CBRI), Boston, Massachusetts). The targeting vector was designed to replace exons 2-5 (beginning at the first coding exon) with a neomycin resistance gene. This construct was electroporated into 129S4/SvJae-derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts and the resulting chimeric males were bred with BALB/c females. Heterozygotes were then backcrossed to BALB/cAnNCrl inbred mice for many generations. In 2002, mutant mice were sent to Dr. Gloria Pryhuber (University of Rochester School of Medicine and Dentistry) and rederived using BALB/c inbred mice (most likely BALB/cJ). The resulting mice were made homozygous and then found to be less sensitive to intratracheal treatment of TNF&alpha than reported for the original Traf1-mutant mice from Tsitsikov's lab. Therefore, these mutant mice were subsequently bred to wildtype siblings for approximately 5 generations and then made homozygous. The resulting Traf1-deficient homozygous mice were found to be more sensitive to intratracheal treatment of TNF&alpha (like the original Traf1-mutant mice from Tsitsikov's lab). Homozygous mice were then sent to The Jackson Laboratory. Upon arrival, mice were bred to BALB/cJ inbred mice (Stock No. 000651) for at least one generation to establish the current colony.

Control Information

  Control
   001026 BALB/cByJ (approximate)
   000651 BALB/cJ (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Traf1tm1Tsi allele
008076   B6.129S4-Traf1tm1Tsi/J
View Strains carrying   Traf1tm1Tsi     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Traf1tm1Tsi/Traf1tm1Tsi

        involves: 129S4/SvJae * C57BL/6
  • immune system phenotype
  • *normal* immune system phenotype
    • homozygotes display normal T and B lymphocyte development, with no differences in thymus or spleen size relative to wild-type controls   (MGI Ref ID J:72327)
    • in culture, mutant splenic B cells show normal proliferation to anti-IgM and anti-CD40 stimulation as well as normal activation of NF-kappaB and AP-1 following CD40 ligation   (MGI Ref ID J:72327)
    • homozygotes display normal antibody responses to T-dependent antigens (ovalbumin) and type 1 and type 2 T-independent antigens (TNP-LPS and TNP-Ficoll, respectively)   (MGI Ref ID J:72327)
    • abnormal lymph node cell ratio
      • homozygotes exhibit an increased T/B cell ratio in inguinal lymph nodes relative to wild-type controls   (MGI Ref ID J:72327)
      • however, the CD4/CD8 ratio remains normal   (MGI Ref ID J:72327)
    • increased T cell proliferation
      • in culture, mutant splenic T cells show higher proliferation to immobilized anti-CD3 mAb than wild-type T cells; however, no differences in annexin V staining, expression of CD25 (IL-2R-alpha) or intracellular IL-2 protein content are observed   (MGI Ref ID J:72327)
      • increased T cell proliferation persists following stimulation with submitogenic concentrations of anti-CD3 mAb and increasing concentrations of CD28 mAb or of recombinant IL-2   (MGI Ref ID J:72327)
      • following prestimulation with anti-CD3 mAb, activated mutant, but not wild-type, T cells, respond to TNF by proliferation, as determined by [3H]-thymidine incorporation   (MGI Ref ID J:72327)
      • proliferation of activated mutant T cells to TNF is abrogated by antagonistic mAb to TNF receptor superfamily, member 1b (TNFR2, p75) but not by antagonistic mAb to TNF receptor superfamily, member 1a (TNFR1, p55)   (MGI Ref ID J:72327)
      • however, following injection of staphylococcal enterotoxin B (SEB), homozygotes display normal superantigen-induced clonal expansion and deletion of peripheral Vbeta8-bearing T cells, as determined by changes in lymph node Vbeta8+ and Vbeta6+ subsets, BrdU incorporation of Vbeta8-bearing T cells, and apoptosis of CD4+ and CD8+ populations by annexin V-FITC staining   (MGI Ref ID J:72327)
      • activated mutant, but not wild-type, T cells respond to TNF by activation of the NF-kappaB and AP-1 signaling pathways   (MGI Ref ID J:72327)
    • increased lymphocyte cell number
      • homozygotes show a significant increase of total lymphocyte number in inguinal lymph nodes relative to wild-type controls   (MGI Ref ID J:72327)
  • hematopoietic system phenotype
  • increased T cell proliferation
    • in culture, mutant splenic T cells show higher proliferation to immobilized anti-CD3 mAb than wild-type T cells; however, no differences in annexin V staining, expression of CD25 (IL-2R-alpha) or intracellular IL-2 protein content are observed   (MGI Ref ID J:72327)
    • increased T cell proliferation persists following stimulation with submitogenic concentrations of anti-CD3 mAb and increasing concentrations of CD28 mAb or of recombinant IL-2   (MGI Ref ID J:72327)
    • following prestimulation with anti-CD3 mAb, activated mutant, but not wild-type, T cells, respond to TNF by proliferation, as determined by [3H]-thymidine incorporation   (MGI Ref ID J:72327)
    • proliferation of activated mutant T cells to TNF is abrogated by antagonistic mAb to TNF receptor superfamily, member 1b (TNFR2, p75) but not by antagonistic mAb to TNF receptor superfamily, member 1a (TNFR1, p55)   (MGI Ref ID J:72327)
    • however, following injection of staphylococcal enterotoxin B (SEB), homozygotes display normal superantigen-induced clonal expansion and deletion of peripheral Vbeta8-bearing T cells, as determined by changes in lymph node Vbeta8+ and Vbeta6+ subsets, BrdU incorporation of Vbeta8-bearing T cells, and apoptosis of CD4+ and CD8+ populations by annexin V-FITC staining   (MGI Ref ID J:72327)
    • activated mutant, but not wild-type, T cells respond to TNF by activation of the NF-kappaB and AP-1 signaling pathways   (MGI Ref ID J:72327)
  • increased lymphocyte cell number
    • homozygotes show a significant increase of total lymphocyte number in inguinal lymph nodes relative to wild-type controls   (MGI Ref ID J:72327)
  • cellular phenotype
  • increased sensitivity to induced cell death
    • homozygotes display increased sensitivity to TNF-induced skin necrosis relative to wild-type controls   (MGI Ref ID J:72327)
    • following subcutaneous injection of a suboptimal TNF dose (1.5 ug/day for 5 days), homozygotes display significantly more skin ulcerations and hemorrhages than wild-type controls, with complete loss of the epidermis and extensive cellular damage in dermis and hypodermis, including vacuolization and disintegration   (MGI Ref ID J:72327)
View Research Applications

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

Apoptosis Research
Endogenous Regulators

Cancer Research
Genes Regulating Growth and Proliferation
Growth Factors/Receptors/Cytokines

Cell Biology Research
Genes Regulating Growth and Proliferation
Signal Transduction
Transcriptional Regulation

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
Growth Factors/Receptors/Cytokines
Immunodeficiency
      T cell deficiency
Intracellular Signaling Molecules
Lymphoid Tissue Defects
T Cell Receptor Signaling Defects

Internal/Organ Research
Lymphoid Tissue Defects
      T cell deficiency

Research Tools
Apoptosis Research
Cancer Research
      T cell deficiency
      genes regulating lymphoma development
      production of B and T cells, antibodies, and hybridomas
      production of T cells and hybridoma
Cell Biology Research
Genetics Research
      Mutagenesis and Transgenesis
      Mutagenesis and Transgenesis: transcriptional activation
Immunology, Inflammation and Autoimmunity Research
      T Cell Receptor Deficiency
      T cell deficiency
      production of B cells, antibodies T cell lines, and hybridomas
      production of T cell lines and hybridomas

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Traf1tm1Tsi
Allele Name targeted mutation 1, Erdyni Y Tsitsikov
Allele Type Targeted (Null/Knockout)
Common Name(s) TRAF1-;
Mutation Made By Erdyni Tsitsikov,   Immune Disease Institute (formerly CBRI)
Strain of Origin129S4/SvJae
ES Cell Line NameJ1
ES Cell Line Strain129S4/SvJae
Gene Symbol and Name Traf1, TNF receptor-associated factor 1
Chromosome 2
Gene Common Name(s) 4732496E14Rik; EBI6; MGC:10353; RIKEN cDNA 4732496E14 gene;
Molecular Note The gene was disrupted by replacement of exons 2-5 with a neomycin resistance cassette. Homozygous mutant animals did not express protein product as determined by Western blot analysis of stimulated splenocytes using polyclonal antibodies directed against the C-terminus of the protein. [MGI Ref ID J:72327]

Genotyping

Genotyping Information

Genotyping Protocols

Traf1tm1Tsi, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Bryce PJ; Oyoshi MK; Kawamoto S; Oettgen HC; Tsitsikov EN. 2006. TRAF1 regulates Th2 differentiation, allergic inflammation and nuclear localization of the Th2 transcription factor, NIP45. Int Immunol 18(1):101-11. [PubMed: 16352630]  [MGI Ref ID J:104165]

Oyoshi MK; Barthel R; Tsitsikov EN. 2007. TRAF1 regulates recruitment of lymphocytes and, to a lesser extent, neutrophils, myeloid dendritic cells and monocytes to the lung airways following lipopolysaccharide inhalation. Immunology 120(3):303-14. [PubMed: 17328785]  [MGI Ref ID J:122710]

Pryhuber GS; Huyck HL; Roper JM; Cornejo J; O'reilly MA; Pierce RH; Tsitsikov EN. 2005. Acute Tumor Necrosis Factor-{alpha}-Induced Liver Injury in the Absence of Tumor Necrosis Factor Receptor-Associated Factor 1 Gene Expression. Am J Pathol 166(6):1637-45. [PubMed: 15920149]  [MGI Ref ID J:98818]

Sabbagh L; Srokowski CC; Pulle G; Snell LM; Sedgmen BJ; Liu Y; Tsitsikov EN; Watts TH. 2006. A critical role for TNF receptor-associated factor 1 and Bim down-regulation in CD8 memory T cell survival. Proc Natl Acad Sci U S A 103(49):18703-8. [PubMed: 17116875]  [MGI Ref ID J:118166]

Tsitsikov EN; Laouini D; Dunn IF; Sannikova TY; Davidson L; Alt FW; Geha RS. 2001. Traf1 is a negative regulator of tnf signaling. enhanced tnf signaling in traf1-deficient mice. Immunity 15(4):647-57. [PubMed: 11672546]  [MGI Ref ID J:72327]

Zhang B; Wang Z; Li T; Tsitsikov EN; Ding HF. 2007. NF-kappaB2 mutation targets TRAF1 to induce lymphomagenesis. Blood 110(2):743-51. [PubMed: 17405906]  [MGI Ref ID J:123872]

Additional References

Traf1tm1Tsi related

Lai Y; Di Nardo A; Nakatsuji T; Leichtle A; Yang Y; Cogen AL; Wu ZR; Hooper LV; Schmidt RR; von Aulock S; Radek KA; Huang CM; Ryan AF; Gallo RL. 2009. Commensal bacteria regulate Toll-like receptor 3-dependent inflammation after skin injury. Nat Med 15(12):1377-82. [PubMed: 19966777]  [MGI Ref ID J:155874]

McPherson AJ; Snell LM; Mak TW; Watts TH. 2012. Opposing roles for TRAF1 in the alternative versus classical NF-kappaB pathway in T cells. J Biol Chem 287(27):23010-9. [PubMed: 22570473]  [MGI Ref ID J:188379]

Missiou A; Kostlin N; Varo N; Rudolf P; Aichele P; Ernst S; Munkel C; Walter C; Stachon P; Sommer B; Pfeifer D; Zirlik K; MacFarlane L; Wolf D; Tsitsikov E; Bode C; Libby P; Zirlik A. 2010. Tumor necrosis factor receptor-associated factor 1 (TRAF1) deficiency attenuates atherosclerosis in mice by impairing monocyte recruitment to the vessel wall. Circulation 121(18):2033-44. [PubMed: 20421522]  [MGI Ref ID J:172624]

Oussa NA; Soumounou Y; Sabbagh L. 2013. TRAF1 phosphorylation on Serine 139 modulates NF-kappaB activity downstream of 4-1BB in T cells. Biochem Biophys Res Commun 432(1):129-34. [PubMed: 23376065]  [MGI Ref ID J:198056]

Oyoshi MK; Bryce P; Goya S; Pichavant M; Umetsu DT; Oettgen HC; Tsitsikov EN. 2008. TNF receptor-associated factor 1 expressed in resident lung cells is required for the development of allergic lung inflammation. J Immunol 180(3):1878-85. [PubMed: 18209085]  [MGI Ref ID J:131500]

Sabbagh L; Andreeva D; Laramee GD; Oussa NA; Lew D; Bisson N; Soumounou Y; Pawson T; Watts TH. 2013. Leukocyte-specific protein 1 links TNF receptor-associated factor 1 to survival signaling downstream of 4-1BB in T cells. J Leukoc Biol 93(5):713-21. [PubMed: 23446150]  [MGI Ref ID J:200793]

Sabbagh L; Pulle G; Liu Y; Tsitsikov EN; Watts TH. 2008. ERK-dependent Bim modulation downstream of the 4-1BB-TRAF1 signaling axis is a critical mediator of CD8 T cell survival in vivo. J Immunol 180(12):8093-101. [PubMed: 18523273]  [MGI Ref ID J:137236]

Snell LM; McPherson AJ; Lin GH; Sakaguchi S; Pandolfi PP; Riccardi C; Watts TH. 2010. CD8 T cell-intrinsic GITR is required for T cell clonal expansion and mouse survival following severe influenza infection. J Immunol 185(12):7223-34. [PubMed: 21076066]  [MGI Ref ID J:167467]

Wang C; McPherson AJ; Jones RB; Kawamura KS; Lin GH; Lang PA; Ambagala T; Pellegrini M; Calzascia T; Aidarus N; Elford AR; Yue FY; Kremmer E; Kovacs CM; Benko E; Tremblay C; Routy JP; Bernard NF; Ostrowski MA; Ohashi PS; Watts TH. 2012. Loss of the signaling adaptor TRAF1 causes CD8+ T cell dysregulation during human and murine chronic infection. J Exp Med 209(1):77-91. [PubMed: 22184633]  [MGI Ref ID J:181722]

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, these mice may be bred as homozygotes.

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* $2140.00
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* $2782.00
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
   001026 BALB/cByJ (approximate)
   000651 BALB/cJ (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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