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Mapping Data
Experiment
  • Experiment
    TEXT-QTL
  • Chromosome
    17
  • Reference
    J:6920 Maruyama N, et al., Genetic studies of autoimmunity in New Zealand mice. IV. Contribution of NZB and NZW genes to the spontaneous occurrence of retroviral gp70 immune complexes in (NZB X NZW)F1 hybrid and the correlation to renal disease. J Immunol. 1983 Feb;130(2):740-6
  • ID
    MGI:3620204
Genes
GeneAlleleAssay TypeDescription
Agp1 visible phenotype
Agp2 visible phenotype
H2 reported elsewhere
Notes
  • Experiment
    Inbred strain NZB spontaneously develops autoantibodies and glomerulonephritis similar to human lupus nephritis, whereas inbred strain NZW does not. Analysis of 123 (NZB x NZW)F1 x NZW and 113 (NZB x NZW)F1 x NZB female backcross animals reveal 2 dominant H2- linked loci associated with anti-gp70 immune complex formation. Agp1 (anti gp70 immune complex 1) is derived from the NZB genetic background whereas Agp2 (anti gp70 immune complex 2) is derived from the NZW genetic background. Loose linkage between Agp1 and H2 is estimated at 25.2 cM. The location of Agp2 is estimated to be approximately 31 cM from H2. Agp2 may act to intensify formation of gp70 immune complexes in concert with Agp1. A separate unlinked and yet unidentified locus affecting the magnitude of gp70 immune complex formation was hypothesized to exist.

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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory