Smider V, Rathmell W K, Lieber M R, Chu G
Department of Medicine, Stanford University Medical Center, CA 94305.
Science. 1994 Oct 14;266(5183):288-91. doi: 10.1126/science.7939667.
Three genetic complementation groups of rodent cells are defective for both repair of x-ray-induced double-strand breaks and V(D)J recombination. Cells from one group lack a DNA end-binding activity that is biochemically and antigenically similar to the Ku autoantigen. Transfection of complementary DNA (cDNA) that encoded the 86-kilodalton subunit of Ku rescued these mutant cells for DNA end-binding activity, x-ray resistance, and V(D)J recombination activity. These results establish a role for Ku in DNA repair and recombination. Furthermore, as a component of a DNA-dependent protein kinase, Ku may initiate a signaling pathway induced by DNA damage.
啮齿动物细胞的三个基因互补组在X射线诱导的双链断裂修复和V(D)J重组方面均存在缺陷。其中一组细胞缺乏一种DNA末端结合活性，这种活性在生化和抗原性上与Ku自身抗原相似。编码Ku 86千道尔顿亚基的互补DNA（cDNA）转染可使这些突变细胞恢复DNA末端结合活性、X射线抗性和V(D)J重组活性。这些结果确立了Ku在DNA修复和重组中的作用。此外，作为DNA依赖性蛋白激酶的一个组成部分，Ku可能启动由DNA损伤诱导的信号通路。
