Summary |
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Variant origin |
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Variant description |
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Phenotypes |
View phenotypes and curated references for all genotypes (concatenated display).
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Notes |
Dbacl has a stronger diabetes accelerating effect in females compared to males.
Mapping and Phenotype information for this QTL, its variants and associated markersJ:144964NOD.CD72 congenic mice carry a C57BL/6-derived centromeric interval (24 - 45 cM) containing the CD72 locus on chromosome 4 The interval ranged from D4Mit193 to D4Mit17 and included the Cd72 locus between D4Mit268 and D4Mit17. (The C57BL/6 and NOD parental strains were obtained from Clea Japan and designated C57BL/6Jcl and NOD/ShiJicJcl, respectively.) NOD.CD72 congenic mice were not protected from diabetes but did express more of the disease compared to NOD mice. NOD.CD72 congenic animals develop diabetes starting at 16 weeks of age and display increased incidence compared to the 20-week disease onset displayed in NOD parental animals. In addition, female NOD.CD72 animals have more pronounced diabetes acceleration compared to males. At 10 to 12 weeks of age NOD.CD72 females displayed a significantly higher insulitis incidence compared to NOD females. The authors suggests that the centromeric region of mouse Chromosome 4 in NOD mice includes a gene or cluster of genes that negatively regulates the rapid progression of diabetes. This interval is designated Dbacl (diabetes accelerating locus). Besides Cd72, other plausiblecandidate genes for the Dbacl include Pax5 (20.7 cM) and Unc13b. Previously identified diabetes QTL Idd11 (64.6 cM) and Idd4 (42.6 cM) map near Dbacl. |
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References |
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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 12/10/2024 MGI 6.24 |
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