First Author | Hamatani K | Year | 1996 |
Journal | Immunogenetics | Volume | 45 |
Issue | 1 | Pages | 1-5 |
PubMed ID | 8881030 | Mgi Jnum | J:37619 |
Mgi Id | MGI:85008 | Doi | 10.1007/s002510050159 |
Citation | Hamatani K, et al. (1996) Cloning and chromosomal mapping of the mouse DNA-dependent protein kinase gene. Immunogenetics 45(1):1-5 |
abstractText | Severe combined immune deficiency (scid) mice are assumed to have two types of abnormalities: one is high radiosensitivity and the other is abnormal recombination in immunoglobulin and T-cell receptor genes. The human chromosome 8 q1.1 region has an ability to complement the scid aberrations. Moreover, the localization of the subunit DNA-dependent protein kinase [DNA-PKcs] participating in DNA double-strand break repair in the same locus was clarified. In scid mouse cells, the number of DNA-PKcs products and extent of DNA-PK activity remarkably decrease. These observations gave rise to the assumption that DNA-PKcs is the scid factor itself. In order to determine whether the DNA-PKcs gene is the scid gene, we isolated the mouse DNA-PKcs gene and investigated its chromosomal locus by fluorescence in situ hybridization (FISH). Consequently, it became clear that the mouse DNA-PKcs gene existed in the centromeric region of mouse chromosome 16, determined by cross-genetic study, as a scid locus. This finding strongly suggests that mouse DNA-PKcs is the scid gene. |