Phenotypic correction of ataxia-telangiectasia cellular defect by exogenously introduced human or mouse subchromosomal fragments.

Abstract excerpt

A human-mouse hybrid containing a human 11q22-23 fragment including the ATM locus was used to examine its capability to correct the cellular defect of ataxia-telangiectasia (A-T). Examination of 21 A-T-derived hybrids indicated that the acquired radioresistance was observed in the clones where the 11q22-23 fragment was transferred intact, but not in those where donor-derived 11q segment was lost. In one...

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