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