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Lack of Involvement of Ataxia Telangiectasia Mutated (ATM) in Regulation of Nuclear Factor-B (NF-B) in Human Diploid Fibroblasts¹

Lineberger Comprehensive Cancer Center [B. P. A., A. S. B.], Department of Biology and Curriculum in Genetics and Molecular Biology [A. S. B.], University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, and National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 [R. E. S., R. S. P.]

It has been suggested that the cellular response to exposure to ionizing radiation involves activation of the transcription factor nuclear factor-B (NF-B) and that this response is defective in cells from individuals with ataxia telangiectasia (AT). In one study, it was found that SV40 large T-transformed cells derived from a patient null for the AT mutated (ATM) gene exhibited constitutive activation of NF-B and that in those cells, inhibition of NF-B by expression of a modified form of IB led to correction of the radiosensitivity associated with the AT phenotype [M. Jung et al., Science (Washington DC), 268: 1691–1621, 1995]. From those data, it was suggested that NF-B played a role in the AT phenotype. We show here that normal diploid cells derived from AT patients do not exhibit constitutive activation of NF-B. Furthermore, we provide data that the transformation process associated with SV40 large T antigen expression in AT-/- cells leads to aberrant cellular responses. Our studies highlight the importance of using diploid, nontransformed AT-/- cells for in vitro studies relevant to the AT phenotype whenever possible.

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