在用紫外线对细胞进行预处理后，正常和缺乏修复能力的人成纤维细胞中SV40诱导的转化和T抗原产生增强。
SV40-induced transformation and T-antigen production is enhanced in normal and repair-deficient human fibroblasts after pretreatment of cells with UV light.
作者信息
Hagedorn R, Thielmann H W, Fischer H, Schroeder C H
出版信息
J Cancer Res Clin Oncol. 1983;106(2):93-6. doi: 10.1007/BF00395385.
Human fibroblasts irradiated with UV light were infected with simian virus 40 and tested either for transformation or T-antigen production. At UV doses that allowed approximately 5-10% of the irradiated cells to survive, the number of surviving transformed colonies increased. This result was confirmed by testing for T-antigen 96 h post infection by means of indirect immunofluorescence. Since these results were obtained for a normal cell line as well as for two UV excision repair-deficient ones (XP groups A and D), it was concluded that excision repair functions cannot play a decisive role in the events leading to increased transformation and T-antigen production. It is proposed that the relative increase of transformation and T-antigen production is the expression of host functions which are induced by DNA damage threatening cell survival.
用紫外线照射的人成纤维细胞感染了猴病毒40，并进行了转化或T抗原产生的检测。在紫外线剂量允许约5-10%的照射细胞存活的情况下，存活的转化集落数量增加。通过间接免疫荧光在感染后96小时检测T抗原，证实了这一结果。由于这些结果是在一个正常细胞系以及两个紫外线切除修复缺陷细胞系（XP A组和D组）中获得的，因此得出结论，切除修复功能在导致转化增加和T抗原产生的事件中不能起决定性作用。有人提出，转化和T抗原产生的相对增加是由威胁细胞存活的DNA损伤诱导的宿主功能的表达。
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