- abnormal skin morphology / IMPC
- increased large unstained cell number / IMPC
- increased grip strength / IMPC
- increased basophil cell number / IMPC
- increased neutrophil cell number / IMPC
- increased eosinophil cell number / IMPC
- increased NK cell number / IMPC
- abnormal cholesterol homeostasis / IMPC
- decreased circulating calcium level / IMPC
- increased lymphocyte cell number / IMPC
- increased effector memory CD8-positive, alpha-beta T cell number / IMPC
- increased circulating aspartate transaminase level / IMPC
- enlarged heart / IMPC
- increased leukocyte cell number / IMPC
- decreased monocyte cell number / IMPC
- abnormal heart morphology / IMPC
- decreased neutrophil cell number / IMPC
B6.129P2(Cg)-Tnfrsf1atm3.1Gkl/Flmg
Status | Available to order |
EMMA ID | EM:07099 |
Citation information | RRID:IMSR_EM:07099 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
International strain name | B6.129P2(Cg)-Tnfrsf1atm3.1Gkl/Flmg |
Alternative name | TNFRFL/FL or p55TNFRFL/FL, B6.129-Tnfrsf1a |
Strain type | Targeted Mutant Strains : Conditional mutation |
Allele/Transgene symbol | Tnfrsf1atm3.1Gkl |
Gene/Transgene symbol | Tnfrsf1a |
Information from provider
Provider | George Kollias |
Provider affiliation | Institute of Immunology, B.S.R.C. Al. Fleming |
Genetic information | Exons 2-5 of Tnfrsf1a gene were flanked by loxP sites so to result in a frameshift mutation upon recombination. Upstream the first loxP site a flipped neo cassette has been inserted and flanking sequences of 3.6 and 2.8 kb 5prime and 3prime. Sequences of the mouse Tnfrsf1a gene were derived by PCR amplification from the respective BAC clone. Exons have been sequenced and the integrity of the sequences confirmed. The targeting vector was introduced in 129/Ola ES cells and positive clones used for the generation of chimaeras. Chimaeric mice have been crossed to C57BL/6J mice and germline offspring used for expansion. The mice have been crossed to FLP deleter mice for neo cassette removal. Then, Tnfrsf1a;flx/flx mice were crossed with Cre deleter mice for the generation of Tnfrsf1a complete ko. The Tnfrsf1a;flx/flx mouse line was expanded and the mice backcrossed to C57BL/6J for at least 6 generations. The deficiency in p55TNFR expression in the ko was confirmed in BMDMs by FACs analysis. |
Phenotypic information | This is a strain that can be used with tissue specific Cre expressing strains to induce Cre-mediated TNFRI ablation. |
Breeding history | Backcrossed in C57BL/6J, more than 10 generations. |
References |
|
Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | B.S.R.C. Alexander Fleming, Vari, Greece |
Animals used for archiving | homozygous males, wild-type females |
Stage of embryos | Morula |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Tumor necrosis factor receptor 1 associated periodic syndrome / Orphanet_32960
IMPC phenotypes (gene matching)
MGI phenotypes (gene matching)
- increased bone mineral density / MGI
- abnormal Peyer's patch morphology / MGI
- abnormal sleep pattern / MGI
- abnormal immune system physiology / MGI
- decreased IgG level / MGI
- liver inflammation / MGI
- lung inflammation / MGI
- decreased inflammatory response / MGI
- increased skin papilloma incidence / MGI
- decreased tumor incidence / MGI
- abnormal respiratory mechanics / MGI
- abnormal airway responsiveness / MGI
- abnormal lymph node B cell domain morphology / MGI
- abnormal spleen germinal center morphology / MGI
- abnormal Peyer's patch follicle morphology / MGI
- decreased susceptibility to bacterial infection / MGI
- increased susceptibility to bacterial infection / MGI
- abnormal macrophage physiology / MGI
- granulomatous inflammation / MGI
- impaired skin barrier function / MGI
- abnormal glutamate-mediated receptor currents / MGI
- decreased circulating alanine transaminase level / MGI
- abnormal cytokine secretion / MGI
- no phenotypic analysis / MGI
- abnormal nervous system physiology / MGI
- abnormal response/metabolism to endogenous compounds / MGI
- increased susceptibility to experimental autoimmune encephalomyelitis / MGI
- decreased susceptibility to experimental autoimmune encephalomyelitis / MGI
- decreased susceptibility to autoimmune diabetes / MGI
- increased susceptibility to parasitic infection / MGI
- increased susceptibility to type I hypersensitivity reaction / MGI
- decreased Peyer's patch number / MGI
- abnormal follicular dendritic cell morphology / MGI
- absent follicular dendritic cells / MGI
- decreased IgG1 level / MGI
- increased circulating tumor necrosis factor level / MGI
- decreased circulating interleukin-6 level / MGI
- decreased circulating interleukin-1 beta level / MGI
- increased interleukin-6 secretion / MGI
- decreased interleukin-6 secretion / MGI
- abnormal chemokine secretion / MGI
- decreased susceptibility to endotoxin shock / MGI
- increased susceptibility to endotoxin shock / MGI
- decreased physiological sensitivity to xenobiotic / MGI
- increased sensitivity to induced cell death / MGI
- increased sensitivity to induced morbidity/mortality / MGI
- decreased sensitivity to induced morbidity/mortality / MGI
- decreased sensitivity to xenobiotic induced morbidity/mortality / MGI
- increased susceptibility to bacterial infection induced morbidity/mortality / MGI
- abnormal neuron proliferation / MGI
- abnormal oval cell physiology / MGI
- tumor regression / MGI
- impaired adaptive thermogenesis / MGI
- decreased susceptibility to dopaminergic neuron neurotoxicity / MGI
- decreased microglial cell number / MGI
- impaired humoral immune response / MGI
- impaired central nervous system regeneration / MGI
Literature references
- Safe TNF-based antitumor therapy following p55TNFR reduction in intestinal epithelium.;Van Hauwermeiren Filip, Armaka Marietta, Karagianni Niki, Kranidioti Ksanthi, Vandenbroucke Roosmarijn E, Loges Sonja, Van Roy Maarten, Staelens Jan, Puimège Leen, Palagani Ajay, Berghe Wim Vanden, Victoratos Panayiotis, Carmeliet Peter, Libert Claude, Kollias George, ;2013;The Journal of clinical investigation;123;2590-603; 23676465
- Tumor necrosis factor alpha receptor 1 deficiency in hepatocytes does not protect from non-alcoholic steatohepatitis, but attenuates insulin resistance in mice.;Bluemel Sena, Wang Yanhan, Lee Suhan, Schnabl Bernd, ;2020;World journal of gastroenterology;26;4933-4944; 32952340
- Autoimmune Valvular Carditis Requires Endothelial Cell TNFR1 Expression.;Faragher Jessica L, Auger Jennifer L, Osinski Victoria, Meier Lee A, Engelson Brianna J, Firulyova Maria M, Gonzalez-Torres Mayra I, Brombacher Frank, Zaitsev Konstantin, Marath Aubyn, Binstadt Bryce A, ;2023;Arteriosclerosis, thrombosis, and vascular biology;43;943-957; 37021574
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