NFKB2/p52 transgenic mice express an N terminal truncation of the NFKB2 protein in lymphocytes. Mice exhibit inflammation in the lungs, salivary glands and kidneys, and immune complex glomerulonephritis. These mice may be useful for studies involving NFKB2 signaling pathways and autoimmunity.
Han-Fei Ding, Georgia Health Sciences University
Genetic Background | Generation |
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Allele Type |
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Transgenic (Inserted expressed sequence, Humanized sequence) |
NFKB2/p52 transgenic mice express an N terminal truncation of the NFKB2 protein in lymphocytes. Approximately 76% of 6-12 month old hemizygous mice develop inflammation in the lungs, salivary glands and kidneys. Both spleen and lymph nodes sizes are increased. Inflammation is characterized by an infiltration of lymphocytes (in particular, activated B cells and CD4+ T cells) and macrophages. Serum from transgenic mice contains an 8.2 fold increase in anti-dsDNA autoantibodies as compared to wild-type. Approximately half of the mice develop immune complex glomerulonephritis. Autoimmune disease in these mice appears to be a function of p52 down-regulation of the pro-apoptotic protein BIM leading to defects in apoptosis of autoreactive lymphocytes. These mice may be useful for studies involving NFKB2 signaling pathways and autoimmunity.
The transgenic construct contains the coding sequence for human NFKB2 p52 under the direction of an H2-Kb promoter and an immunoglobulin mu chain enhancer. The p52 truncation mutant codes for the N-terminal 442 amino acids of NFKB2. The construct was microinjected into (C57BL/6J and SJL/J)F2 fertilized eggs. Founder line 452 was established and crossed to the C57BL/6J inbred strain for 10 generations. Transgene expression is directed to lymphocytes.
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. 2 markers on Chromosomes 3 and 19 were found to be segregating for SJL, and one marker on Chromosome 2 was derived from an unknown source. This suggesting an incomplete backcross.
Expressed Gene | NFKB2, nuclear factor kappa B subunit 2, human |
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Site of Expression |
Allele Name | transgene insertion 452, Han-Fei Ding |
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Allele Type | Transgenic (Inserted expressed sequence, Humanized sequence) |
Allele Synonym(s) | NF-kB2 p52_452 |
Gene Symbol and Name | Tg(H2-Kb-NFKB2*)452Hfdg, transgene insertion 452, Han-Fei Ding |
Gene Synonym(s) | |
Promoter | H2-K, histocompatibility 2, K region, mouse, laboratory |
Expressed Gene | NFKB2, nuclear factor kappa B subunit 2, human |
Strain of Origin | (C57BL/6J x SJL/J)F2 |
Chromosome | UN |
Molecular Note | A transgenic construct containing the coding sequence for human NFKB p52 using a H2-Kb promoter and an immunoglobulin mu chain enhancer. Lines 434 and 452 were generated. |
Mutations Made By | Han-Fei Ding, Georgia Health Sciences University |
While maintaining a live colony, these mice are bred as hemizygote male crossed to C57BL/6J female. The donating investigator has not tried to make this strain homozygous.
When using the STOCK Tg(H2-Kb-NFKB2*)452Hfdg/Mmjax mouse strain in a publication, please cite the originating article(s) and include MMRRC stock #36111 in your Materials and Methods section.
Facility Barrier Level Descriptions
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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