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The 2 bp deletion found in A/J and AKR/J strains is associated with susceptibility to allergen-induced bronchial hyperresponsiveness and is a candidate for QTL Abhr2.
early conceptus |
embryo ectoderm |
embryo endoderm |
embryo mesoderm |
embryo mesenchyme |
extraembryonic component |
alimentary system |
auditory system |
branchial arches |
cardiovascular system |
connective tissue |
endocrine system |
exocrine system |
hemolymphoid system |
integumental system |
limbs |
liver and biliary system |
musculoskeletal system |
nervous system |
olfactory system |
reproductive system |
respiratory system |
urinary system |
visual system |
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| Transcription Start Site | Location | Distance from Gene 5'-end |
| Tssr23687 | Chr2:34951443-34951459 (-) | -1 bp |
| Tssr23686 | Chr2:34951433-34951441 (-) | 13 bp |
| Tssr23685 | Chr2:34951415-34951431 (-) | 27 bp |
| Tssr23684 | Chr2:34926009-34926025 (-) | 25,433 bp |
| Tssr23683 | Chr2:34920388-34920393 (-) | 31,059 bp |
| Tssr23682 | Chr2:34903683-34903685 (-) | 47,766 bp |
| QTL | Genetic Location* | Genome Location (GRCm39) | Reference | QTL Note |
| Abhr2 | Chr2, 22.83 cM | J:108211 | Abhr2 (allergen induced bronchial hyperresponsiveness 2) is a previously identified QTL at approximately 30 cM on mouse Chromosome 2. Gene expression microarray analysis of lung RNA extracted from sensitive high-responder strain A/J and resistant low-responder strain C3H/HeJ, as well as low- and high-responding (A/J x C3H/HeJ)F1 x A/J backcross animals. Twenty-one differentially expressed genes were identified one of which, Hc (formerly C5), mapped near Abhr2 at 23.5 cM on chromosome 2. Hc mRNA expression patterns correlated with bronchial hyperresponsive phenotype- A/J and high-responder backcross animals exhibit high Hc expression whereas C3H/HeJ and low-responder backcross animals exhibit low Hc expression. In addition, Hc genotype also correlated with severity of bronchial hyperresponsiveness in backcross animals. Homozygosity for A/J-derived alleles at Hc was associated with high responsiveness while heterozygosity at Hc was associated with low responsiveness. Hc SNP analysis revealed a 2 bp deletion in the sensitive A/J strain resulting in deficient Hc mRNA and protein production. Resistant strain C3H/HeJ does not have this mutation and produces functional Hc mRNA and protein. This SNP was screened in other inbred strains with known bronchial hyperresponsive phenotypes. The 2 bp Hc deletion was observed in sensitive strains AKR/J and A/J, but not in resistant strains C57BL/6J, BALB/cJ, and C3H/HeJ. |
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 03/18/2025 MGI 6.24 |
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