- 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
B6.129S-Tnfrsf1atm1Gkl/Flmg
Status | Available to order |
EMMA ID | EM:11071 |
Citation information | RRID:IMSR_EM:11071 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 | B6.129S-Tnfrsf1atm1Gkl/Flmg |
Alternative name | B6.Cg-Tnfrsf1a |
Strain type | Targeted Mutant Strains : Conditional mutation |
Allele/Transgene symbol | Tnfrsf1atm1Gkl |
Gene/Transgene symbol | Tnfrsf1a |
Information from provider
Provider | George Kollias |
Provider affiliation | BSRC Fleming |
Genetic information | A mutation deleting 15 nucleotides encoding amino acids 202-206 was introduced in exon 6 of mp55TNFR (Tnfrsf1a) gene. The targeting vector contained a 4.6-kb XbaI/SmaI genomic fragment as the left homology arm and a 4-kb Sma/HindIII genomic fragment, containing the mutation, as the right homology arm. A loxP flanked neo selection cassette (L2neo) was introduced into a SmaI site in intron 5 of Tnfrsf1a gene between the two homology arms and a PGK-tk selection marker was introduced at the 3' of targeting vector. Upon cre-mediated recombination, a cell-specific Tnfrsf1a-tm1.1Gkl allele is generated. |
Phenotypic information | Homozygous:No overt phenotype. Homozygous mice are fertile but they are smaller than their littermates and in poor health so we do not mate the homozygous mice. Heterozygous:No overt phenotype |
Breeding history | Homozygous mice and wild-type controls are generated by crossing heterozygous mice. |
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 C57BL/6 males, wild-type C57BL/6 females |
Stage of embryos | 2-cell |
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
- Tumor necrosis factor (TNF) receptor shedding controls thresholds of innate immune activation that balance opposing TNF functions in infectious and inflammatory diseases.;Xanthoulea Sofia, Pasparakis Manolis, Kousteni Stavroula, Brakebusch Cord, Wallach David, Bauer Jan, Lassmann Hans, Kollias George, ;2004;The Journal of experimental medicine;200;367-76; 15289505
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