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 |
This allele interacts with the STS/A allele at Rapop2 to increase radiation-induced apoptosis.
Mapping and Phenotype information for this QTL, its variants and associated markersJ:24435Susceptibility to cell death (apoptosis) varies significantly between the inbred strains BALB/cHeA (resistant) and STS/A (susceptible), therefore recombinant congenic strains derived from these inbreds will be informative for identifying chromosome regions contributing to the cell death phenotype. Analysis of the strain distribution patterns of 20 recombinant congenic strains derived from the BALB/cHeA and STS/A progenitors suggests that loci on proximal Chr 16 segregated with the apoptosis phenotype. In an F2 cross involving recombinant congenic strain CcS-7 with progenitor inbred BALB/cHeA a highly significant association was found in the region of mouse Chromosome 16 including the D16Mit32, D16Mit81, and D16Mit34 loci. The symbol assigned for the phenotype is Rapop1 and can be considered a quantitative trait. J:47265Authors analyzed linkage of radiation-induced apoptosis susceptibility in colon using 180 (CcS-7 x BALB/c)F2 animals. The CcS-7 strain is more susceptible to colonic apoptosis (but less susceptible to thymic apoptosis) than the BALB/c strain. Linkage of the phenotype to marker D16Mit32 on mouse Chromosome 16 was found. This marker is included in the region defining the Rapop1 QTL responsible for apoptosis susceptibility in the thymus. It is not clear whether the colonic susceptibility gene is the same or near the thymic susceptibility gene. |
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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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