Joe C O, Norman J O, Irvin T R, Busbee D L
Biochem Biophys Res Commun. 1985 Apr 30;128(2):754-9. doi: 10.1016/0006-291x(85)90111-1.
A human low-density-lipoprotein (LDL) receptor-deficient diploid fibroblast cell line (GM1915) was determined to be short patch competent (DNA polymerase-beta) and long patch deficient (DNA polymerase-alpha) for DNA excision repair. Analysis of DNA from GM1915 cells or from WI38 control cells, following treatment with a mutagen known to initiate long patch excision repair, showed that GM1915 cells exhibited decreased resynthesis of oligonucleotide segments excised during repair. When cells deficient in DNA polymerase-alpha activity were permeabilized to permit LDL entry, repair synthesis immediately increased. These data suggest that DNA polymerase-alpha is not activated by mutagen treatment in GM1915 cells and that introduction of LDL into the cells results in activation of the enzyme.
已确定一种人类低密度脂蛋白（LDL）受体缺陷的二倍体成纤维细胞系（GM1915）在DNA切除修复方面是短补丁修复能力正常（DNA聚合酶β）而长补丁修复缺陷（DNA聚合酶α）。在用已知可启动长补丁切除修复的诱变剂处理后，对GM1915细胞或WI38对照细胞的DNA进行分析，结果显示GM1915细胞在修复过程中切除的寡核苷酸片段的重新合成减少。当缺乏DNA聚合酶α活性的细胞被通透化以允许LDL进入时，修复合成立即增加。这些数据表明，在GM1915细胞中，诱变剂处理不会激活DNA聚合酶α，而将LDL引入细胞会导致该酶的激活。
