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pubmed-article:7607692pubmed:abstractTextThe V79 hamster cell line irs1 is a repair-deficient mutant hypersensitive to radiation and DNA-reactive chemical agents. Somatic cell hybrids were formed by fusing irs1 cells with human lymphocytes and selecting for complementation in medium containing concentrations of mitomycin C (MMC) that are toxic to irs1. Thirty-eight MMC-resistant hybrids showed extensive segregation of human chromosomes, with 35 of them retaining human chromosome 7, as indicated by molecular marker and cytogenetic analyses. Inter-Alu-PCR products from the DNA of hybrids, when used as fluorescence in situ hybridization probe onto normal human metaphases, indicated that one resistant hybrid was monochromosomal for chromosome 7 and that the three resistant hybrids shown to be negative for chromosome 7 markers have retained portions of chromosome 7, with region 7q36 being the smallest common region. MMC-sensitive subclones of a resistant hybrid lost human chromosome 7. Therefore, the gene complementing the repair defect, XRCC2 (X-ray repair cross complementing), is assigned to human chromosome 7q36.lld:pubmed
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pubmed-article:7607692pubmed:articleTitleAssignment of the XRCC2 human DNA repair gene to chromosome 7q36 by complementation analysis.lld:pubmed
pubmed-article:7607692pubmed:affiliationBiology and Biotechnology Research Program, Lawrence Livermore National Laboratory, California 94551-0808, USA.lld:pubmed
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