- abnormal response/metabolism to endogenous compounds / MGI
- decreased circulating interleukin-6 level / MGI
- decreased sensitivity to induced morbidity/mortality / MGI
- decreased physiological sensitivity to xenobiotic / MGI
- decreased sensitivity to xenobiotic induced morbidity/mortality / MGI
- abnormal sleep pattern / MGI
- impaired central nervous system regeneration / MGI
- increased sensitivity to induced cell death / MGI
- increased susceptibility to bacterial infection induced morbidity/mortality / MGI
- impaired humoral immune response / MGI
- decreased susceptibility to bacterial infection / MGI
- decreased circulating alanine transaminase level / MGI
- abnormal Peyer's patch morphology / MGI
- abnormal immune system physiology / MGI
- abnormal lymph node B cell domain morphology / MGI
- abnormal Peyer's patch follicle morphology / MGI
- increased susceptibility to bacterial infection / MGI
- decreased susceptibility to experimental autoimmune encephalomyelitis / MGI
- increased susceptibility to parasitic infection / MGI
- increased susceptibility to type I hypersensitivity reaction / MGI
- decreased Peyer's patch number / MGI
- absent follicular dendritic cells / MGI
- decreased IgG1 level / MGI
- decreased interleukin-6 secretion / MGI
STOCK Tnfrsf1atm1Blt Tg(Gfap-TNF*)K21Gkl/Flmg
Status | Available to order |
EMMA ID | EM:08444 |
International strain name | STOCK Tnfrsf1atm1Blt Tg(Gfap-TNF*)K21Gkl/Flmg |
Alternative name | TgK21 [CBA;B6-Tnfrsf1a |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Tnfrsf1atm1Blt, |
Gene/Transgene symbol | Tnfrsf1a |
Information from provider
Provider | George Kollias |
Provider affiliation | Immunology, BSRC Al. Fleming |
Genetic information | The -2663 to +93 region of the murine Gfap promoter, which has been shown to contain cis-regulatory elements required for astrocyte-specific expression, was fused to human TNF genomic sequences containing a deletion mutation of the codons encoding the 1st to the 12th amino acids of the mature 17-kDa TNF protein. This mutant TNF gene has previously been shown to produce a transmembrane TNF protein that remains bioactive against cellular targets in vitro and in vivo. The genomic DNA was then ligated to the 0.77-kb EcoRI-Sal1 fragment containing the 3' UTR and polyadenylation site of the beta-globin gene, which replaces TNF 3' UTR sequences, thought to negatively regulate mRNA stability and translational efficiency. In this transgenic line, exogenous TNF protein production could be demonstrated by positive immunostaining of astrocytes in the spinal cord and brain sections using a polyclonal anti-human TNF antiserum. |
Phenotypic information | Homozygous:n/aHeterozygous:Neurologic disorder manifested by ataxia, seizures, and paralysis and bearing histologic evidence of chronic CNS inflammation and degeneration; 100% phenotypic penetrance. |
References |
|
Homozygous fertile | no |
Homozygous viable | no |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | B.S.R.C. Alexander Fleming, Vari, Greece |
Animals used for archiving | heterozygous CBA x C57BL/6, wild-type (CBA x C57BL/6)F1 |
Stage of embryos | Morula |
Disease and phenotype information
MGI allele-associated human disease models
Orphanet associated rare diseases, based on orthologous gene matching
- Tumor necrosis factor receptor 1 associated periodic syndrome / Orphanet_32960
MGI phenotypes (allele matching)
Literature references
- Astrocyte-specific but not neuron-specific transmembrane TNF triggers inflammation and degeneration in the central nervous system of transgenic mice.;Akassoglou K, Probert L, Kontogeorgos G, Kollias G, ;1997;Journal of immunology (Baltimore, Md. : 1950);158;438-45; 8977220
- 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.;Akassoglou K, Bauer J, Kassiotis G, Pasparakis M, Lassmann H, Kollias G, Probert L, ;1998;The American journal of pathology;153;801-13; 9736029
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