Overview

Also Known As:TNFα^-

These tumor necrosis factor null knock-out mice may be useful in studies of susceptibility to parasitic and bacterial infection, endotoxin sensitivity and immune response.

Donating Investigator

Dr. George Kollias, Biomedical Sciences Research Centre Alexander Fleming

Genetic overview

Genetic Background	Generation

Tnf^tm1Gkl

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Tnf	tumor necrosis factor

View Genetics

Research Applications

Internal/Organ Research
Neurobiology Research
Cancer Research
Diabetes and Obesity Research
Endocrine Deficiency Research
Hematological Research
Immunology, Inflammation and Autoimmunity Research
Apoptosis Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Mice homozygous for the Tnf^tm1Gkl 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.

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. This is the case for the strain above. 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 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-Gpi1^c-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. The mice were then backcrossed to BALB/cByJ for 5 generations (using a speed congenic protocol) before being made homozygous.

Control Suggestions

001026 BALB/cByJ

Additional Information

Considerations for Choosing Controls

Selected References

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):1397-411PubMed: 8879212 MGI: J:47673

View All References

Genetics

Tnf^tm1Gkl

Allele Symbol: Tnf^tm1Gkl

Allele Name	targeted mutation 1, George Kollias
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	TNF-; Tnf0; Tnf-alpha-; TNFalpha KO; TNFalpha^-; TNFKO
Gene Symbol and Name	Tnf, tumor necrosis factor
Gene Synonym(s)
Strain of Origin	129S/SvEv-Gpi1^c
Chromosome	17
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 of Tnf mRNA expression.
Mutations Made By	Dr. George Kollias, Biomedical Sciences Research Centre Alexander Fleming

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Genotype: Tnf^tm1Gkl related

Internal/Organ Research
- Spleen Defects
Neurobiology Research
- Neurodegeneration
Cancer Research
- Increased Tumor Incidence
  - Skin Cancers: Resistant
  - Skin Cancers
- Growth Factors/Receptors/Cytokines
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
Apoptosis Research
- Extracellular Modulators
Cardiovascular Research
- Hypotriglyceridemia

Apoptosis Research
- Extracellular Modulators

Mammalian Phenotype Terms by Genotype

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

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
involves: 129S/SvEv * C57BL/6

adipose tissue phenotype

abnormal fat pad morphology

decreased percent body fat/body weight

homeostasis/metabolism phenotype

abnormal glucose homeostasis

abnormal lipid homeostasis

decreased circulating glucose level
- decreased fasting plasma glucose concentrations at 28 weeks of age

decreased circulating insulin level
- decreased plasma insulin concentrations at 28 weeks of age

decreased circulating leptin level
- decreased plasma leptin concentrations at 28 weeks of age

decreased circulating triglyceride level
- decreased plasma triglyceride concentrations at 28 weeks of age

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
- Normal - however, malignant progression of tumors is normal
- lignant progression of tumors is normal

immune system phenotype

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

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

abnormal lymphocyte physiology
- after intraperitoneal injection of SRBC, mutants exhibit severely impaired SRBC-specific IgG1 antibody responses

abnormal macrophage physiology
- LPS-stimulated thioglycollate-elicited peritoneal macrophages (TEPMs) cannot induce thymocyte proliferation, but stimulated TEPMs in wild-type and Tnf^tm3Gki homozygotes induce thymocyte proliferation with equal efficiency

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

abnormal Peyer's patch follicle morphology
- B cells are present but no organized follicles are seen and organized follicular dendritic cell networks are absent

abnormal Peyer's patch morphology
- the typical subepithelial dome areas fail to form

abnormal spleen follicular dendritic cell network
- organized follicular dendritic cell networks are absent

abnormal spleen primary B follicle morphology
- absence of splenic primary B cell follicles

absent follicular dendritic cells
- organized follicular dendritic cell networks are absent

absent spleen germinal center
- after immunization with sheep red blood cells (SRBCs), mutants fail to form organized germinal centers
- inability to form organized germinal centers

decreased inflammatory response
- in the skin following treatment with TPA compared with similarly treated wild-type mice

decreased Peyer's patch number
- average of 2 - 4 per mouse compared to 6 - 8 in wild-type mice

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
- ctiona and peak EAE occurs at ~15 days, with gradual remission and results in only a mild deficit

decreased susceptibility to type IV hypersensitivity reaction
- impaired contact hypersensitivity response

increased susceptibility to bacterial infection
- 0 cfu) compared to wild-type
- susceptibility to death from Listeria monocytogenes infection
- 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

cellular phenotype

decreased keratinocyte proliferation
- following DMBA and TPA treatment compared with similarly treated wild-type mice

craniofacial phenotype

alveolar process atrophy
- modest alveolar bone loss at 30 weeks

integument phenotype

decreased keratinocyte proliferation
- following DMBA and TPA treatment compared with similarly treated wild-type mice

mammalian phenotype

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
- Normal - 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

neoplasm

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
- Normal - however, malignant progression of tumors is normal
- lignant progression of tumors is normal

growth/size/body region phenotype

alveolar process atrophy
- modest alveolar bone loss at 30 weeks

decreased body weight
- at 28 weeks, mutant animals weigh less

skeleton phenotype

abnormal trabecular bone morphology
- 32% increase in trabecular bone volume

alveolar process atrophy
- modest alveolar bone loss at 30 weeks

increased bone mineral density
- significantly increased

increased osteoblast cell number

hematopoietic system phenotype

abnormal lymphocyte physiology
- after intraperitoneal injection of SRBC, mutants exhibit severely impaired SRBC-specific IgG1 antibody responses

abnormal macrophage physiology
- LPS-stimulated thioglycollate-elicited peritoneal macrophages (TEPMs) cannot induce thymocyte proliferation, but stimulated TEPMs in wild-type and Tnf^tm3Gki homozygotes induce thymocyte proliferation with equal efficiency

abnormal spleen follicular dendritic cell network
- organized follicular dendritic cell networks are absent

abnormal spleen primary B follicle morphology
- absence of splenic primary B cell follicles

absent spleen germinal center
- after immunization with sheep red blood cells (SRBCs), mutants fail to form organized germinal centers
- inability to form organized germinal centers

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
involves: 129S/SvEv

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

immune system phenotype

abnormal chemokine secretion
- induction of MCP-1 was reduced in spleens of mutants infected with Listeria monocytogenes

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

decreased susceptibility to autoimmune disorder
- increased resistance to liver injury after ConA-induced autoimmune hepatitis, with only infiltrating cells but no liver necrosis detected

decreased susceptibility to endotoxin shock
- protected from S. aureus enterotoxin B induced toxic shock

increased susceptibility to bacterial infection
- loss of resistance against Listeria monocytogenes infection

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
either: B6.129-Tnf or (involves: 129 * C57BL/6)

hematopoietic system phenotype

increased leukocyte cell number
- a modest increase in peripheral white cell count is seen compared to wild-type mice

increased lymphocyte cell number
- lymphocyte numbers are increased compared to Tnf^tm1.2Sned homozygotes

increased neutrophil cell number
- neutrophil numbers are increased compared to Tnf^tm1.2Sned homozygotes

immune system phenotype

decreased Peyer's patch number
- Peyer's patches are fewer in number

decreased susceptibility to bacterial infection
- homozygotes are protected from LPS/D-Gal induced shock

increased leukocyte cell number
- a modest increase in peripheral white cell count is seen compared to wild-type mice

increased lymphocyte cell number
- lymphocyte numbers are increased compared to Tnf^tm1.2Sned homozygotes

increased neutrophil cell number
- neutrophil numbers are increased compared to Tnf^tm1.2Sned homozygotes

increased susceptibility to parasitic infection
- homozygotes show increased sensitivity to systemic and alimentary L. monocytogenes infection

small Peyer's patches

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
involves: 129S/SvEv * C57BL/6J

hematopoietic system phenotype

abnormal metallophilic macrophage morphology
- there are almost no metallophillic macrophages present in the marginal zone

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

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

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

absent spleen germinal center
- upon immunization with T cell dependent antigen, germinal centers fail to develop

immune system phenotype

abnormal metallophilic macrophage morphology
- there are almost no metallophillic macrophages present in the marginal zone

abnormal Peyer's patch follicle morphology
- B cells fail to segregate from T cell areas

abnormal Peyer's patch germinal center morphology
- upon immunization with a T cell dependent antigen, germinal centers fail to develop

abnormal Peyer's patch morphology
- Peyer's patches have a flattened appearance

abnormal Peyer's patch T cell area morphology
- T cells fail to segregate from B cells

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

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

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

absent spleen germinal center
- upon immunization with T cell dependent antigen, germinal centers fail to develop

decreased Peyer's patch number
- the mean number of Peyer's patches in mutant mice is 5 compared to 7 in wild-type mice

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

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
B6;129S-Tnf/J

cellular phenotype

oligozoospermia
- at 12 weeks of age, male homozygotes show a ~53% reduction in epididymal sperm count relative to wild-type controls
- in mutant males, the number of sperm per testis weight is only ~68% that of wild-type controls

endocrine/exocrine gland phenotype

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

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

decreased testis weight
- at 12 weeks of age, male homozygotes show a ~30% reduction in average testis weight relative to wild-type controls

reproductive system phenotype

abnormal spermatogenesis
- 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
- at P33, only early elongated spermatids are noted in mutant testes, whereas late elongated spermatids are seen in wild-type testes
- male homozygotes show a significant delay in the onset of spermatogenesis, likely due to decreased testicular testosterone levels

abnormal spermiation
- at P37, no sperm are yet detected in mutant epididymides
- 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

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

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

decreased testis weight
- at 12 weeks of age, male homozygotes show a ~30% reduction in average testis weight relative to wild-type controls

oligozoospermia
- at 12 weeks of age, male homozygotes show a ~53% reduction in epididymal sperm count relative to wild-type controls
- in mutant males, the number of sperm per testis weight is only ~68% that of wild-type controls

The following phenotype relates to a compound genotype created using this strain

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
C.129S-Tnf

homeostasis/metabolism phenotype

decreased incidence of tumors by chemical induction
- DMBA and TPA-treated mice exhibit papillomas than in similarly treated wild-type mice

neoplasm

decreased incidence of tumors by chemical induction
- DMBA and TPA-treated mice exhibit papillomas than in similarly treated wild-type mice

References

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):1397-411PubMed: 8879212 MGI: J:47673

Additional - Tnf^tm1Gkl related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Tnf
- Standard PCR:Tnf
- Genotyping resources and troubleshooting
Breeding Considerations

When maintaining a live colony, these mice can be bred as homozygotes.
- Additional Breeding and Husbandry Support
Citation
When using the TNFα^- mouse strain in a publication, please cite the originating article(s) and include JAX stock #007082 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

Domestic
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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous for Tnf<tm1Gkl>

Related Products and Services

Frozen Mouse Embryo	CByJ.129S(B6)-Tnf<tm1Gkl>/J	$2595.00
Frozen Mouse Embryo	CByJ.129S(B6)-Tnf<tm1Gkl>/J	$2595.00
Frozen Mouse Embryo	CByJ.129S(B6)-Tnf<tm1Gkl>/J	$3373.50
Frozen Mouse Embryo	CByJ.129S(B6)-Tnf<tm1Gkl>/J	$3373.50

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Also Known As:TNFα-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Tnftm1Gkl

Allele Symbol: Tnftm1Gkl

Disease Terms

Research Areas By Phenotype

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

Genotype: Tnftm1Gkl related

Mammalian Phenotype Terms by Genotype

Genotype: Tnftm1Gkl/Tnftm1Gklinvolves: 129S/SvEv * C57BL/6

adipose tissue phenotype

homeostasis/metabolism phenotype

immune system phenotype

cellular phenotype

craniofacial phenotype

integument phenotype

mammalian phenotype

neoplasm

growth/size/body region phenotype

skeleton phenotype

hematopoietic system phenotype

Genotype: Tnftm1Gkl/Tnftm1Gklinvolves: 129S/SvEv

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Tnftm1Gkl/Tnftm1Gkleither: B6.129-Tnf or (involves: 129 * C57BL/6)

hematopoietic system phenotype

immune system phenotype

Genotype: Tnftm1Gkl/Tnftm1Gklinvolves: 129S/SvEv * C57BL/6J

hematopoietic system phenotype

immune system phenotype

Genotype: Tnftm1Gkl/Tnftm1GklB6;129S-Tnf/J

cellular phenotype

endocrine/exocrine gland phenotype

reproductive system phenotype

Genotype: Tnftm1Gkl/Tnftm1GklC.129S-Tnf

homeostasis/metabolism phenotype

neoplasm

References

Additional - Tnftm1Gkl related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Also Known As:TNFα^-

Tnf^tm1Gkl

Allele Symbol: Tnf^tm1Gkl

Genotype: Tnf^tm1Gkl related

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
involves: 129S/SvEv * C57BL/6

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
involves: 129S/SvEv

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
either: B6.129-Tnf or (involves: 129 * C57BL/6)

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
involves: 129S/SvEv * C57BL/6J

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
B6;129S-Tnf/J

Genotype: Tnf^tm1Gkl/Tnf^tm1Gkl
C.129S-Tnf

Additional - Tnf^tm1Gkl related