Abstract
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-PK cs gene is the scid gene, we isolated the mouse DNA-PK cs gene and investigated its chromosomal locus by fluorescence in situ hybridization (FISH). Consequently, it became clear that the mouse DNA-PK cs 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-PK cs is the scid gene.
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Received: 22 March 1996
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Hamatani, K., Matsuda, Y., Araki, R. et al. Cloning and chromosomal mapping of the mouse DNA-dependent protein kinase gene. Immunogenetics 45, 1–5 (1996). https://doi.org/10.1007/s002510050159
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DOI: https://doi.org/10.1007/s002510050159