Lack of WRN results in extensive deletion at nonhomologous joining ends.
Lack of WRN results in extensive deletion at nonhomologous joining ends.
复制标题
DOI：
--
复制
发表时间：
2002-01
期刊：
影响因子：
11.2
通讯作者：
J. Oshima;Shurong Huang;Chongwon Pae;J. Campisi;R. Schiestl
中科院分区：
文献类型：
--
作者：
J. Oshima;Shurong Huang;Chongwon Pae;J. Campisi;R. Schiestl
WRN的丢失导致基因组不稳定的孕激素综合征，Werner综合征。WRN编码一种多功能核蛋白，具有3‘-->；5’外切酶和3‘-->；5’解旋酶活性。带有不相容末端的线形质粒被引入Werner综合征细胞，在非同源连接末端，特别是在3‘突起的单链末端，发生了广泛的缺失。这种广泛的缺失表型得到了野生型WRN的补充。这些结果表明，WRN可以胜过其他参与双链断裂修复或稳定断裂DNA末端的核酸外切酶。
Loss of WRN causes the genomic instability progeroid syndrome, Werner syndrome. WRN encodes a multifunctional nuclear protein with 3'-->5' exonuclease and 3'-->5' helicase activities. Linear plasmids with noncompatible ends introduced to Werner syndrome cells underwent extensive deletions at nonhomologous joining ends, particularly at the 3' protruding single-stranded end. This extensive deletion phenotype was complemented by wild-type WRN. These results suggest that WRN can out-compete other exonucleases that participate in double-strand break repair or stabilize the broken DNA end.