Strain Name:

B6;129S-Tnftm1Gkl/J

Stock Number:

003008

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Mice homozygous for the Tnftm1Gkl targeted mutation completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice develop significantly less benign and malignant tumors than treated wildtype mice when treated to induce skin carcinogenesis. Male 28 week old mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Fasting plasma glucose and insulin levels, and the insulin response to an oral glucose load were significantly decreased in obese TNF deficient mice compared to obese wildtype controls. These results indicate TNF plays a role in lipid and glucose metabolism but is not sufficient to completely eliminate hyperglycemia and hyperinsulinemia in this induced obesity model.

Description

Strain Information

Former Names B6;129S6-Tnftm1Gkl/J    (Changed: 03-OCT-07 )
Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Specieslaboratory mouse
GenerationN2F2 (14-AUG-14)
Generation Definitions
 
Donating InvestigatorDr. George Kollias,   Biomedical Sciences Research Centre Alexander Fleming

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Related Genotype: a/a

Description
Mice homozygous for the Tnftm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obesity. However, fasting plasma glucose and insulin levels, and the insulin response to an oral glucose load were significantly decreased in obese TNF deficient mice compared to obese wildtype controls. These results indicate TNF plays a role in lipid and glucose metabolism but is not sufficient to completely eliminate hyperglycemia and hyperinsulinemia in this induced obesity model.

Development
The targeting vector was constructed by replacing with an MC1neopA cassette (Stratagene) the 438-bp Narl-BglII fragment containing 40 bp of the 5' UTR, all the coding region, including the ATG translation initiation codon, of the first exon and part of the first intron of the muTNFa gene. The construct was electroporated into 129S/SvEv-Gpi1c-derived CCE embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice before being intercrossed to produce homozygotes.

Control Information

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

Related Strains

Strains carrying   Tnftm1Gkl allele
005540   B6.129S-Tnftm1Gkl/J
007082   CByJ.129S(B6)-Tnftm1Gkl/J
View Strains carrying   Tnftm1Gkl     (2 strains)

Strains carrying other alleles of Tnf
005108   B6.129P2-Ltb/Tnf/Ltatm1Dvk/J
025956   B6.Cg-Tg(Tek-Tnf*)5382Mcla/J
005112   STOCK Ltb/Tnftm1.1Dvk/J
View Strains carrying other alleles of Tnf     (3 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Asthma, Susceptibility to   (TNF)
Malaria, Susceptibility to   (TNF)
Migraine with or without Aura, Susceptibility to, 1   (TNF)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tnftm1Gkl/Tnftm1Gkl

        involves: 129S/SvEv * C57BL/6
  • growth/size/body phenotype
  • decreased body weight
    • at 28 weeks, mutant animals weigh less   (MGI Ref ID J:42579)
  • decreased percent body fat   (MGI Ref ID J:42579)
  • adipose tissue phenotype
  • abnormal fat pad morphology   (MGI Ref ID J:42579)
  • decreased percent body fat   (MGI Ref ID J:42579)
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis   (MGI Ref ID J:42579)
    • decreased circulating glucose level
      • decreased fasting plasma glucose concentrations at 28 weeks of age   (MGI Ref ID J:42579)
    • decreased circulating insulin level
      • decreased plasma insulin concentrations at 28 weeks of age   (MGI Ref ID J:42579)
  • abnormal lipid homeostasis   (MGI Ref ID J:42579)
    • decreased circulating triglyceride level
      • decreased plasma triglyceride concentrations at 28 weeks of age   (MGI Ref ID J:42579)
  • decreased circulating leptin level
    • decreased plasma leptin concentrations at 28 weeks of age   (MGI Ref ID J:42579)
  • decreased incidence of tumors by chemical induction
    • DMBA and TPA-treated mice exhibit papillomas that develop with a greater latency than in similarly treated wild-type mice DMBA and TPA-treated mice exhibit papillomas that develop with a greater latency than in similarly treated wild-type mice however, malignant progression of tumors is normal   (MGI Ref ID J:56068)
    • however, malignant progression of tumors is normal   (MGI Ref ID J:56068)
  • immune system phenotype
  • *normal* immune system phenotype
    • mutant spleen cells isolated 49 days after myelin oligodendrocyte glycoprotein (MOG) display lack of autoimmune T cell responses (proliferation) to MOG peptide, similar to wild type spleen cells mutant spleen cells isolated 49 days after myelin oligodendrocyte glycoprotein (MOG) display lack of autoimmune T cell responses (proliferation) to MOG peptide, similar to wild-type spleen cells   (MGI Ref ID J:114740)
    • abnormal Peyer's patch morphology
      • the typical subepithelial dome areas fail to form   (MGI Ref ID J:40970)
      • abnormal Peyer's patch follicle morphology
        • B cells are present but no organized follicles are seen and organized follicular dendritic cell networks are absent   (MGI Ref ID J:40970)
      • decreased Peyer's patch number
        • average of 2 - 4 per mouse compared to 6 - 8 in wild-type mice   (MGI Ref ID J:40970)
    • abnormal inflammatory response
      • when treated with D-gal (a hepatotoxin) at 20 mg/animal and doses of lipopolysaccharide (LPS) up to 100ug/25g body weight, mutants are completely resistant to LPS-induced death, but wild-type mice all die at 100-fold lower LPS doses   (MGI Ref ID J:114740)
      • decreased inflammatory response
        • in the skin following treatment with TPA compared with similarly treated wild-type mice   (MGI Ref ID J:56068)
        • decreased susceptibility to type IV hypersensitivity reaction
          • impaired contact hypersensitivity response   (MGI Ref ID J:47673)
    • abnormal lymph node B cell domain morphology
      • B cell follicles and follicular dendritic cell network formation are impaired in mesenteric and peripheral lymph nodes; however, B cells are present and B and T cell areas are segregated   (MGI Ref ID J:40970)
    • abnormal lymphocyte physiology
      • after intraperitoneal injection of SRBC, mutants exhibit severely impaired SRBC-specific IgG1 antibody responses   (MGI Ref ID J:114740)
    • abnormal macrophage physiology
      • LPS-stimulated thioglycollate-elicited peritoneal macrophages (TEPMs) cannot induce thymocyte proliferation, but stimulated TEPMs in wild-type and Tnf homozygotes induce thymocyte proliferation with equal efficiency   (MGI Ref ID J:114740)
    • abnormal mesenteric lymph node morphology
      • mesenteric lymph nodes (MLN) lack organized B cell follicles but occasionally have GC-like regions that are centered in B cell areas   (MGI Ref ID J:114740)
    • abnormal spleen follicular dendritic cell network
      • organized follicular dendritic cell networks are absent   (MGI Ref ID J:42579)
    • abnormal spleen primary B follicle morphology
      • absence of splenic primary B cell follicles   (MGI Ref ID J:47673)
    • absent follicular dendritic cells
      • organized follicular dendritic cell networks are absent   (MGI Ref ID J:40970)
    • absent spleen germinal center
      • inability to form organized germinal centers   (MGI Ref ID J:47673)
      • after immunization with sheep red blood cells (SRBCs), mutants fail to form organized germinal centers   (MGI Ref ID J:114740)
    • decreased susceptibility to experimental autoimmune encephalomyelitis
      • 16 days post-immunization with pertussis toxin, mutants begin to show clinical signs of experimental allergic encephalomyelitis (EAE) which progresses to chronic non-remitting disease compared to wild-type mice which show signs of EAE at 12 days post-injectiona and peak EAE occurs at ~15 days, with gradual remission and results in only a mild deficit   (MGI Ref ID J:114740)
    • increased susceptibility to bacterial infection
      • susceptibility to death from Listeria monocytogenes infection   (MGI Ref ID J:47673)
      • with challenge at high doses (10000 cfu) of Listeria monocytogenes (LM), mutants show high sensitivity with maximal lethality at 6 days post-infection, compared to wild-type; mutants are highly sensitive when challenged with a physiological dose of LM (100 cfu) compared to wild-type   (MGI Ref ID J:114740)
  • hematopoietic system phenotype
  • abnormal lymphocyte physiology
    • after intraperitoneal injection of SRBC, mutants exhibit severely impaired SRBC-specific IgG1 antibody responses   (MGI Ref ID J:114740)
  • abnormal macrophage physiology
    • LPS-stimulated thioglycollate-elicited peritoneal macrophages (TEPMs) cannot induce thymocyte proliferation, but stimulated TEPMs in wild-type and Tnf homozygotes induce thymocyte proliferation with equal efficiency   (MGI Ref ID J:114740)
  • abnormal spleen follicular dendritic cell network
    • organized follicular dendritic cell networks are absent   (MGI Ref ID J:42579)
  • abnormal spleen primary B follicle morphology
    • absence of splenic primary B cell follicles   (MGI Ref ID J:47673)
  • absent spleen germinal center
    • inability to form organized germinal centers   (MGI Ref ID J:47673)
    • after immunization with sheep red blood cells (SRBCs), mutants fail to form organized germinal centers   (MGI Ref ID J:114740)
  • tumorigenesis
  • decreased incidence of tumors by chemical induction
    • DMBA and TPA-treated mice exhibit papillomas that develop with a greater latency than in similarly treated wild-type mice DMBA and TPA-treated mice exhibit papillomas that develop with a greater latency than in similarly treated wild-type mice however, malignant progression of tumors is normal   (MGI Ref ID J:56068)
    • however, malignant progression of tumors is normal   (MGI Ref ID J:56068)
  • craniofacial phenotype
  • abnormal alveolar process morphology
    • modest alveolar bone loss at 30 weeks   (MGI Ref ID J:147935)
  • skeleton phenotype
  • abnormal alveolar process morphology
    • modest alveolar bone loss at 30 weeks   (MGI Ref ID J:147935)
  • abnormal trabecular bone morphology
    • 32% increase in trabecular bone volume   (MGI Ref ID J:135519)
  • increased bone mineral density
    • significantly increased   (MGI Ref ID J:135519)
  • increased osteoblast cell number   (MGI Ref ID J:135519)
  • integument phenotype
  • decreased keratinocyte proliferation
    • following DMBA and TPA treatment compared with similarly treated wild-type mice   (MGI Ref ID J:56068)
  • cellular phenotype
  • decreased keratinocyte proliferation
    • following DMBA and TPA treatment compared with similarly treated wild-type mice   (MGI Ref ID J:56068)

Tnftm1Gkl/Tnftm1Gkl

        either: B6.129-Tnftm1Gkl or (involves: 129/Sv * C57BL/6)
  • immune system phenotype
  • decreased Peyer's patch number
    • Peyer's patches are fewer in number   (MGI Ref ID J:97783)
  • decreased susceptibility to bacterial infection
    • homozygotes are protected from LPS/D-Gal induced shock   (MGI Ref ID J:97783)
  • increased leukocyte cell number
    • a modest increase in peripheral white cell count is seen compared to wild-type mice   (MGI Ref ID J:97783)
    • increased lymphocyte cell number
      • lymphocyte numbers are increased compared to Tnftm1.2Sned homozygotes   (MGI Ref ID J:97783)
    • increased neutrophil cell number
      • neutrophil numbers are increased compared to Tnftm1.2Sned homozygotes   (MGI Ref ID J:97783)
  • increased susceptibility to parasitic infection
    • homozygotes show increased sensitivity to systemic and alimentary L. monocytogenes infection   (MGI Ref ID J:97783)
  • small Peyer's patches   (MGI Ref ID J:97783)
  • hematopoietic system phenotype
  • increased leukocyte cell number
    • a modest increase in peripheral white cell count is seen compared to wild-type mice   (MGI Ref ID J:97783)
    • increased lymphocyte cell number
      • lymphocyte numbers are increased compared to Tnftm1.2Sned homozygotes   (MGI Ref ID J:97783)
    • increased neutrophil cell number
      • neutrophil numbers are increased compared to Tnftm1.2Sned homozygotes   (MGI Ref ID J:97783)

Tnftm1Gkl/Tnftm1Gkl

        involves: 129S/SvEv * C57BL/6J
  • immune system phenotype
  • abnormal Peyer's patch morphology
    • Peyer's patches have a flattened appearance   (MGI Ref ID J:124642)
    • abnormal Peyer's patch follicle morphology
      • B cells fail to segregate from T cell areas   (MGI Ref ID J:124642)
      • abnormal Peyer's patch T cell area morphology
        • T cells fail to segregate from B cells   (MGI Ref ID J:124642)
      • abnormal Peyer's patch germinal center morphology
        • upon immunization with a T cell dependent antigen, germinal centers fail to develop   (MGI Ref ID J:124642)
    • decreased Peyer's patch number
      • the mean number of Peyer's patches in mutant mice is 5 compared to 7 in wild-type mice   (MGI Ref ID J:124642)
  • abnormal metallophilic macrophage morphology
    • there are almost no metallophillic macrophages present in the marginal zone   (MGI Ref ID J:124642)
  • abnormal spleen follicular dendritic cell network
    • upon immunization with a T cell dependent antigen, there is a no formation of a follicular dendritic cell network   (MGI Ref ID J:124642)
  • abnormal spleen marginal sinus morphology
    • marginal sinus lining cells expressing mucosal addressin cell adhesion molecules are not present when immunized with a T cell antigen   (MGI Ref ID J:124642)
  • abnormal spleen primary B follicle morphology
    • B cells fail to form a defined primary follicle instead forming a ring-like structure that is partially mixed with the T cell region   (MGI Ref ID J:124642)
  • absent spleen germinal center
    • upon immunization with T cell dependent antigen, germinal centers fail to develop   (MGI Ref ID J:124642)
  • increased susceptibility to bacterial infection
    • 7 days after a sublethal dose of Listeria monocytogenes, no mice survive compared to 60% survival of wild-type mice   (MGI Ref ID J:124642)
  • hematopoietic system phenotype
  • abnormal metallophilic macrophage morphology
    • there are almost no metallophillic macrophages present in the marginal zone   (MGI Ref ID J:124642)
  • abnormal spleen follicular dendritic cell network
    • upon immunization with a T cell dependent antigen, there is a no formation of a follicular dendritic cell network   (MGI Ref ID J:124642)
  • abnormal spleen marginal sinus morphology
    • marginal sinus lining cells expressing mucosal addressin cell adhesion molecules are not present when immunized with a T cell antigen   (MGI Ref ID J:124642)
  • abnormal spleen primary B follicle morphology
    • B cells fail to form a defined primary follicle instead forming a ring-like structure that is partially mixed with the T cell region   (MGI Ref ID J:124642)
  • absent spleen germinal center
    • upon immunization with T cell dependent antigen, germinal centers fail to develop   (MGI Ref ID J:124642)

Tnftm1Gkl/Tnftm1Gkl

        B6;129S-Tnftm1Gkl/J
  • reproductive system phenotype
  • abnormal spermatogenesis
    • male homozygotes show a significant delay in the onset of spermatogenesis, likely due to decreased testicular testosterone levels   (MGI Ref ID J:143457)
    • at P26, the most advanced germ cells in mutant testes remain as late pachytene spermatocytes, instead of developing into haploid round spermatids as in wild-type testes   (MGI Ref ID J:143457)
    • at P33, only early elongated spermatids are noted in mutant testes, whereas late elongated spermatids are seen in wild-type testes   (MGI Ref ID J:143457)
    • abnormal spermiation
      • at P37, no sperm are yet detected in mutant epididymides   (MGI Ref ID J:143457)
      • at P56, spermatozoa are detected at the luminal edge of seminiferous epithelia in both wild-type and mutant testes; however, the lumen is only dilated in wild-type tubules indicating active release of sperm   (MGI Ref ID J:143457)
    • oligozoospermia
      • at 12 weeks of age, male homozygotes show a ~53% reduction in epididymal sperm count relative to wild-type controls   (MGI Ref ID J:143457)
      • in mutant males, the number of sperm per testis weight is only ~68% that of wild-type controls   (MGI Ref ID J:143457)
  • abnormal testis physiology
    • after puberty (P30 to adulthood), mRNA levels of key steroidogenesis-related genes are significantly lower in mutant testes than in wild-type testes   (MGI Ref ID J:143457)
    • abnormal testes secretion
      • after puberty, male homozygotes display significantly lower testicular testosterone levels than wild-type males, as a result of higher anti-Mullerian hormone levels in mutant testes   (MGI Ref ID J:143457)
  • decreased testis weight
    • at 12 weeks of age, male homozygotes show a ~30% reduction in average testis weight relative to wild-type controls   (MGI Ref ID J:143457)
  • endocrine/exocrine gland phenotype
  • abnormal testis physiology
    • after puberty (P30 to adulthood), mRNA levels of key steroidogenesis-related genes are significantly lower in mutant testes than in wild-type testes   (MGI Ref ID J:143457)
    • abnormal testes secretion
      • after puberty, male homozygotes display significantly lower testicular testosterone levels than wild-type males, as a result of higher anti-Mullerian hormone levels in mutant testes   (MGI Ref ID J:143457)
  • decreased testis weight
    • at 12 weeks of age, male homozygotes show a ~30% reduction in average testis weight relative to wild-type controls   (MGI Ref ID J:143457)

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

Tnftm1Gkl/Tnftm1Gkl

        involves: 129S/SvEv
  • immune system phenotype
  • abnormal chemokine secretion
    • induction of MCP-1 was reduced in spleens of mutants infected with Listeria monocytogenes   (MGI Ref ID J:95684)
  • decreased circulating tumor necrosis factor level
    • serum TNF levels were reduced in mutants injected with LPS and could not be detected on day 2 of Listeria monocytogenes infection   (MGI Ref ID J:95684)
  • decreased susceptibility to autoimmune disorder
    • increased resistance to liver injury after ConA-induced autoimmune hepatitis, with only infiltrating cells but no liver necrosis detected   (MGI Ref ID J:95684)
  • decreased susceptibility to endotoxin shock
    • protected from S. aureus enterotoxin B induced toxic shock   (MGI Ref ID J:95684)
  • increased susceptibility to bacterial infection
    • loss of resistance against Listeria monocytogenes infection   (MGI Ref ID J:95684)
  • homeostasis/metabolism phenotype
  • decreased circulating tumor necrosis factor level
    • serum TNF levels were reduced in mutants injected with LPS and could not be detected on day 2 of Listeria monocytogenes infection   (MGI Ref ID J:95684)

Tnftm1Gkl/Tnftm1Gkl

        C.129S-Tnftm1Gkl
  • tumorigenesis
  • decreased incidence of tumors by chemical induction
    • DMBA and TPA-treated mice exhibit papillomas than in similarly treated wild-type mice   (MGI Ref ID J:56068)
  • homeostasis/metabolism phenotype
  • decreased incidence of tumors by chemical induction
    • DMBA and TPA-treated mice exhibit papillomas than in similarly treated wild-type mice   (MGI Ref ID J:56068)
View Research Applications

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

Tnftm1Gkl related

Apoptosis Research
Extracellular Modulators

Cancer Research
Growth Factors/Receptors/Cytokines
Increased Tumor Incidence
      Skin Cancers
      Skin Cancers: Resistant

Cardiovascular Research
Hypotriglyceridemia

Diabetes and Obesity Research
Obesity Without Diabetes
      induced

Endocrine Deficiency Research
Spleen Defects

Hematological Research
Immunological Defects

Immunology, Inflammation and Autoimmunity Research
Growth Factors/Receptors/Cytokines
Immunodeficiency
Inflammation
T Cell Receptor Signaling Defects

Internal/Organ Research
Spleen Defects

Neurobiology Research
Neurodegeneration

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tnftm1Gkl
Allele Name targeted mutation 1, George Kollias
Allele Type Targeted (Null/Knockout)
Common Name(s) TNF-; TNFKO; TNFalpha KO; TNFalpha-; Tnf-alpha-; Tnf0; Tnfa-;
Mutation Made ByDr. George Kollias,   Biomedical Sciences Research Centre Alexander Fleming
Strain of Origin129S/SvEv-Gpi1
ES Cell Line NameCCE/EK.CCE
ES Cell Line Strain129S/SvEv-Gpi1
Gene Symbol and Name Tnf, tumor necrosis factor
Chromosome 17
Gene Common Name(s) DIF; RATTNF; TNF alpha; TNF-alpha; TNFA; TNFSF2; TNFalpha; Tnfa; Tnfsf1a; tumor necrosis factor, alpha; tumor necrosis factor-alpha;
General Note Phenotypic Similarity to Human Syndrome: Inflammatory Bowel Disease when compound heterozygote with Tnftm2Gkl (J:54056).
Molecular Note Replacement of 40 bp of the 5' UTR, all the coding region, including the ATG translation initiation codon, of the first exon and part of the first intron with MC1neopA cassette. Northern blot analysis of LPS stimulated macrophages confirmed disruption ofTnf mRNA expression. [MGI Ref ID J:47673]

Genotyping

Genotyping Information

Genotyping Protocols

Tnftm1Gkl, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Pasparakis M; Alexopoulou L; Episkopou V; Kollias G. 1996. Immune and inflammatory responses in TNF alpha-deficient mice: a critical requirement for TNF alpha in the formation of primary B cell follicles, follicular dendritic cell networks and germinal centers, and in the maturation of the humoral immune response [see comments] J Exp Med 184(4):1397-411. [PubMed: 8879212]  [MGI Ref ID J:47673]

Additional References

Alexopoulou L; Pasparakis M; Kollias G. 1997. A murine transmembrane tumor necrosis factor (TNF) transgene induces arthritis by cooperative p55/p75 TNF receptor signaling. Eur J Immunol 27(10):2588-92. [PubMed: 9368614]  [MGI Ref ID J:43603]

Bitsaktsis C; Huntington J; Winslow G. 2004. Production of IFN-gamma by CD4 T cells is essential for resolving ehrlichia infection. J Immunol 172(11):6894-901. [PubMed: 15153508]  [MGI Ref ID J:90518]

Kassiotis G; Bauer J; Akassoglou K; Lassmann H; Kollias G; Probert L. 1999. A tumor necrosis factor-induced model of human primary demyelinating diseases develops in immunodeficient mice. Eur J Immunol 29(3):912-7. [PubMed: 10092095]  [MGI Ref ID J:53471]

Kassiotis G; Pasparakis M; Kollias G; Probert L. 1999. TNF accelerates the onset but does not alter the incidence and severity of myelin basic protein-induced experimental autoimmune encephalomyelitis. Eur J Immunol 29(3):774-80. [PubMed: 10092079]  [MGI Ref ID J:53472]

Moore RJ; Owens DM; Stamp G; Arnott C; Burke F; East N; Holdsworth H; Turner L; Rollins B; Pasparakis M; Kollias G; Balkwill F. 1999. Mice deficient in tumor necrosis factor-alpha are resistant to skin carcinogenesis. Nat Med 5(7):828-831. [PubMed: 10395330]  [MGI Ref ID J:56068]

Neurath MF; Fuss I; Pasparakis M; Alexopoulou L; Haralambous S ; Meyer zum Buschenfelde KH ; Strober W ; Kollias G. 1997. Predominant pathogenic role of tumor necrosis factor in experimental colitis in mice. Eur J Immunol 27(7):1743-50. [PubMed: 9247586]  [MGI Ref ID J:41489]

Ventre J; Doebber T; Wu M; MacNaul K; Stevens K; Pasparakis M ; Kollias G ; Moller DE. 1997. Targeted disruption of the tumor necrosis factor-alpha gene: metabolic consequences in obese and nonobese mice. Diabetes 46(9):1526-31. [PubMed: 9287059]  [MGI Ref ID J:42579]

Tnftm1Gkl related

Abdullah Z; Geiger S; Nino-Castro A; Bottcher JP; Muraliv E; Gaidt M; Schildberg FA; Riethausen K; Flossdorf J; Krebs W; Chakraborty T; Kurts C; Schultze JL; Knolle PA; Klotz L. 2012. Lack of PPARgamma in myeloid cells confers resistance to Listeria monocytogenes infection. PLoS One 7(5):e37349. [PubMed: 22629382]  [MGI Ref ID J:196535]

Abe K; Yarovinsky FO; Murakami T; Shakhov AN; Tumanov AV; Ito D; Drutskaya LN; Pfeffer K; Kuprash DV; Komschlies KL; Nedospasov SA. 2003. Distinct contributions of TNF and LT cytokines to the development of dendritic cells in vitro and their recruitment in vivo. Blood 101(4):1477-83. [PubMed: 12560241]  [MGI Ref ID J:115537]

Acharyya S; Villalta SA; Bakkar N; Bupha-Intr T; Janssen PM; Carathers M; Li ZW; Beg AA; Ghosh S; Sahenk Z; Weinstein M; Gardner KL; Rafael-Fortney JA; Karin M; Tidball JG; Baldwin AS; Guttridge DC. 2007. Interplay of IKK/NF-kappaB signaling in macrophages and myofibers promotes muscle degeneration in Duchenne muscular dystrophy. J Clin Invest 117(4):889-901. [PubMed: 17380205]  [MGI Ref ID J:121279]

Akassoglou K; Bauer J; Kassiotis G; Pasparakis M; Lassmann H; Kollias G; Probert L. 1998. Oligodendrocyte apoptosis and primary demyelination induced by local TNF/p55TNF receptor signaling in the central nervous system of transgenic mice: models for multiple sclerosis with primary oligodendrogliopathy. Am J Pathol 153(3):801-13. [PubMed: 9736029]  [MGI Ref ID J:106592]

Akassoglou K; Douni E; Bauer J; Lassmann H; Kollias G; Probert L. 2003. Exclusive tumor necrosis factor (TNF) signaling by the p75TNF receptor triggers inflammatory ischemia in the CNS of transgenic mice. Proc Natl Acad Sci U S A 100(2):709-14. [PubMed: 12522266]  [MGI Ref ID J:135049]

Alayan J; Ivanovski S; Farah CS. 2007. Alveolar bone loss in T helper 1/T helper 2 cytokine-deficient mice. J Periodontal Res 42(2):97-103. [PubMed: 17305866]  [MGI Ref ID J:147935]

Alexopoulou L; Kranidioti K; Xanthoulea S; Denis M; Kotanidou A; Douni E; Blackshear PJ; Kontoyiannis DL; Kollias G. 2006. Transmembrane TNF protects mutant mice against intracellular bacterial infections, chronic inflammation and autoimmunity. Eur J Immunol 36(10):2768-80. [PubMed: 16983719]  [MGI Ref ID J:114740]

Alexopoulou L; Pasparakis M; Kollias G. 1997. A murine transmembrane tumor necrosis factor (TNF) transgene induces arthritis by cooperative p55/p75 TNF receptor signaling. Eur J Immunol 27(10):2588-92. [PubMed: 9368614]  [MGI Ref ID J:43603]

Anderson AL; Sporici R; Lambris J; Larosa D; Levinson AI. 2006. Pathogenesis of B-cell superantigen-induced immune complex-mediated inflammation. Infect Immun 74(2):1196-203. [PubMed: 16428769]  [MGI Ref ID J:104987]

Ando T; Matsumoto K; Namiranian S; Yamashita H; Glatthorn H; Kimura M; Dolan BR; Lee JJ; Galli SJ; Kawakami Y; Jamora C; Kawakami T. 2013. Mast Cells Are Required for Full Expression of Allergen/SEB-Induced Skin Inflammation. J Invest Dermatol 133(12):2695-705. [PubMed: 23752044]  [MGI Ref ID J:202870]

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Wuthrich M; Filutowicz HI; Warner T; Klein BS. 2002. Requisite elements in vaccine immunity to Blastomyces dermatitidis: plasticity uncovers vaccine potential in immune-deficient hosts. J Immunol 169(12):6969-76. [PubMed: 12471131]  [MGI Ref ID J:118419]

Xanthoulea S; Pasparakis M; Kousteni S; Brakebusch C; Wallach D; Bauer J; Lassmann H; Kollias G. 2004. Tumor necrosis factor (TNF) receptor shedding controls thresholds of innate immune activation that balance opposing TNF functions in infectious and inflammatory diseases. J Exp Med 200(3):367-76. [PubMed: 15289505]  [MGI Ref ID J:92470]

Xiao N; Yin M; Zhang L; Qu X; Du H; Sun X; Mao L; Ren G; Zhang C; Geng Y; An L; Pan J. 2009. Tumor necrosis factor-alpha deficiency retards early fatty-streak lesion by influencing the expression of inflammatory factors in apoE-null mice. Mol Genet Metab 96(4):239-44. [PubMed: 19157944]  [MGI Ref ID J:146902]

Xiong W; MacTaggart J; Knispel R; Worth J; Persidsky Y; Baxter BT. 2009. Blocking TNF-alpha attenuates aneurysm formation in a murine model. J Immunol 183(4):2741-6. [PubMed: 19620291]  [MGI Ref ID J:151559]

Xu J; Chakrabarti AK; Tan JL; Ge L; Gambotto A; Vujanovic NL. 2007. Essential role of the TNF-TNFR2 cognate interaction in mouse dendritic cell-natural killer cell crosstalk. Blood 109(8):3333-41. [PubMed: 17164346]  [MGI Ref ID J:145343]

Xu L; Yoon H; Zhao MQ; Liu J; Ramana CV; Enelow RI. 2004. Cutting edge: pulmonary immunopathology mediated by antigen-specific expression of TNF-alpha by antiviral CD8+ T cells. J Immunol 173(2):721-5. [PubMed: 15240656]  [MGI Ref ID J:91920]

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Yamakawa I; Kojima H; Terashima T; Katagi M; Oi J; Urabe H; Sanada M; Kawai H; Chan L; Yasuda H; Maegawa H; Kimura H. 2011. Inactivation of TNF-alpha ameliorates diabetic neuropathy in mice. Am J Physiol Endocrinol Metab 301(5):E844-52. [PubMed: 21810933]  [MGI Ref ID J:182178]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX30

Colony Maintenance

Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $181.40Female or MaleHomozygous for Tnftm1Gkl  
4 weeks $181.40Female or MaleHomozygous for Tnftm1Gkl  
5 weeks $181.40Female or MaleHomozygous for Tnftm1Gkl  
6 weeks $186.85Female or MaleHomozygous for Tnftm1Gkl  
7 weeks $192.30Female or MaleHomozygous for Tnftm1Gkl  
8 weeks $197.75Female or MaleHomozygous for Tnftm1Gkl  
9 weeks $203.20Female or MaleHomozygous for Tnftm1Gkl  
10 weeks $208.65Female or MaleHomozygous for Tnftm1Gkl  
11 weeks $214.10Female or MaleHomozygous for Tnftm1Gkl  
12 weeks $219.55Female or MaleHomozygous for Tnftm1Gkl  
Price per Pair (US dollars $)Pair Genotype
$373.70Homozygous for Tnftm1Gkl x Homozygous for Tnftm1Gkl  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $235.90Female or MaleHomozygous for Tnftm1Gkl  
4 weeks $235.90Female or MaleHomozygous for Tnftm1Gkl  
5 weeks $235.90Female or MaleHomozygous for Tnftm1Gkl  
6 weeks $243.00Female or MaleHomozygous for Tnftm1Gkl  
7 weeks $250.00Female or MaleHomozygous for Tnftm1Gkl  
8 weeks $257.10Female or MaleHomozygous for Tnftm1Gkl  
9 weeks $264.20Female or MaleHomozygous for Tnftm1Gkl  
10 weeks $271.30Female or MaleHomozygous for Tnftm1Gkl  
11 weeks $278.40Female or MaleHomozygous for Tnftm1Gkl  
12 weeks $285.50Female or MaleHomozygous for Tnftm1Gkl  
Price per Pair (US dollars $)Pair Genotype
$485.90Homozygous for Tnftm1Gkl x Homozygous for Tnftm1Gkl  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Control Information

  Control
   101045 B6129SF2/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
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

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.


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