Collins A
Carcinogenesis. 1985 Jul;6(7):1033-6. doi: 10.1093/carcin/6.7.1033.
U.v. damage to the DNA of HeLa cells induces the polymerisation of ADP-ribose, but only if repair synthesis is inhibited so that incomplete repair sites (i.e., DNA breaks) accumulate to abnormally high levels. 3-Aminobenzamide greatly reduces the ADP-ribose polymerisation response. However, 3-aminobenzamide does not reduce the rate of rejoining of the accumulated breaks when the inhibition of repair synthesis is reversed. Therefore, rejoining of these DNA breaks (in contrast to the rejoining of other kinds of break) appears not to depend on activation of polynucleotide ligase by ADP-ribosylation.
紫外线对海拉细胞DNA的损伤会诱导ADP核糖聚合,但前提是修复合成受到抑制,以至于不完全修复位点(即DNA断裂处)累积到异常高的水平。3-氨基苯甲酰胺能大大降低ADP核糖聚合反应。然而,当修复合成的抑制被解除时,3-氨基苯甲酰胺并不会降低累积断裂处的重新连接速率。因此,这些DNA断裂处的重新连接(与其他类型断裂处的重新连接不同)似乎并不依赖于通过ADP核糖基化激活多核苷酸连接酶。