试图将辐射抗性转移到共济失调毛细血管扩张细胞系。

Kroc Foundation series Pub Date : 1985-01-01
M H Green, J E Lowe, M R James, C F Arlett
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引用次数: 0

摘要

来自共济失调毛细血管扩张症(AT)的成纤维细胞对电离辐射的致死效应高度敏感。将正常人类细胞的基因组DNA与pSV2质粒上的选择性细菌标记物gpt一起转染到sv40转化的AT系AT5BIVA中。一个抗辐射的克隆(67)在重复的伽玛辐照循环后,从90000个克隆群体中恢复。在没有辐射进一步选择的情况下,抗辐射能力的正常水平至少维持了11个月。根据同工酶分析,抗性克隆不是污染物,携带一个gpt基因拷贝,其DNA合成在辐射后受到抑制,其程度介于AT和正常细胞之间。目前尚不清楚克隆67是一个真正的转化还是作为亲本AT系突变的结果而产生的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
An attempt to transfer radiation resistance to an ataxia-telangiectasia cell line.

Fibroblasts from ataxia-telangiectasia (AT) are hypersensitive to the lethal effects of ionizing radiation. Genomic DNA from normal human cells was transfected together with the selectable bacterial marker, gpt, on plasmid pSV2 into an SV40-transformed AT line, AT5BIVA. One radiation resistant clone (67) was recovered following repeated cycles of gamma-irradiation from a population of 90,000 clones. The normal level of radiation resistance has been maintained for at least 11 months in the absence of further selection by radiation. The resistant clone is not a contaminant as determined by isoenzyme analysis, carries one copy of the gpt gene, and its DNA synthesis is inhibited after radiation to an extent intermediate between that of AT and normal cells. It is not yet established whether clone 67 is a bona fide transformant or arose as a consequence of mutation of the parent AT line.

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