B6.129S2-Tnfrsf1b^tm1Mwm/J

Stock number: 002620
Product name: TNF-R2^-
Research areas: Apoptosis Research, Cancer Research, Immunology, Inflammation and Autoimmunity Research

Description

This strain is deficient of tumor necrosis factor receptor superfamily, member 1b (Tnfrsf1b), and are consequently resistant to TNF-induced cell death.

Detailed description

Mice homozygous for a Tnfrsf1b^tm1Mwm targeted mutation (formerly Tnfr2^tm1Mwm, p75 deficient) are viable and fertile. Homozygous mutant mice show normal T-cell development and activity, but are resistant to TNF-induced cell death. Subcutaneous injections of TNF into homozygotes elicit much less tissue necrosis.

Development

This strain was developed by using homologous recombination techniques to target the Tnfr2 gene. The inserted construct contained a neomycin resistance gene under the control of the Pgk promoter and was inserted into the second exon of the Tnfr2 gene.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 1 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.

Allele

Symbol: Tnfrsf1b^tm1Mwm
Name: targeted mutation 1, Mark Moore
MGI accession ID: MGI:1857262
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Tnfrsf1b
Marker name: tumor necrosis factor receptor superfamily, member 1b
Chromosome: 4
Strain of origin: 129S2/SvPas
Molecular note: Exon 2, which codes for the signal peptide region, was disrupted by the insertion of a neomycin cassette. To confirm that the gene was correctly targeted, mice were challenged with lipopolysaccharide (LPS) which results in shedding of the Tnfrsf1b extracellular domian in wild-type mice. No soluble Tnfrsf1b was detected in the serum of homozygous mutant animals.