Boubnov N V, Hall K T, Wills Z, Lee S E, He D M, Benjamin D M, Pulaski C R, Band H, Reeves W, Hendrickson E A
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.
Proc Natl Acad Sci U S A. 1995 Jan 31;92(3):890-4. doi: 10.1073/pnas.92.3.890.
Two ionizing radiation-sensitive (IRs) and DNA double-strand break (DSB) mutants, sxi-3 and sxi-2, were shown to be severely deficient in a DNA end binding activity, similar to a previously described activity of the Ku autoantigen, correlating with the xrs (XRCC5) mutations. Cell fusions with xrs-6, another IRs, DSB repair-deficient cell line, defined these sxi mutants in the XRCC5 group. sxi-3 cells have low expression levels of the p86Ku mRNA. Introduction of the Ku p86 gene, but not the p70 Ku gene, complemented the IRs, DNA end binding, and variable (diversity) joining [V(D)J] recombination signal and coding junction deficiencies of sxi-3. Thus, the p86 Ku gene product is essential for DSB repair and V(D)J recombination.
两个对电离辐射敏感（IRs）且存在DNA双链断裂（DSB）的突变体sxi - 3和sxi - 2，被证明在DNA末端结合活性方面严重缺陷，这类似于先前描述的Ku自身抗原的活性，与xrs（XRCC5）突变相关。与另一个IRs、DSB修复缺陷细胞系xrs - 6的细胞融合，将这些sxi突变体归为XRCC5组。sxi - 3细胞中p86Ku mRNA的表达水平较低。导入Ku p86基因而非p70 Ku基因，可弥补sxi - 3的IRs、DNA末端结合以及可变（多样）连接[V(D)J]重组信号和编码连接缺陷。因此，p86 Ku基因产物对于DSB修复和V(D)J重组至关重要。
