Fork restart: unloading FANCD2 to travel ahead

被引:0
|
作者
Iyer, Divya R. [1 ]
D'Andrea, Alan D. [1 ,2 ,3 ]
机构
[1] Harvard Med Sch, Dana Farber Canc Inst, Dept Radiat Oncol, Div Radiat & Genome Stabil, Boston, MA 02215 USA
[2] Harvard Med Sch, Dana Farber Canc Inst, Ctr DNA Damage & Repair, Boston, MA 02215 USA
[3] Harvard Med Sch, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA
基金
美国国家卫生研究院;
关键词
PCNA;
D O I
10.1016/j.molcel.2023.09.027
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In this issue of Molecular Cell, Brunner et al.1 reveal that eliminating FANCD2 from stalled forks via FBXL12-mediated degradation enables cells to tolerate oncogene-induced replication stress, making FBXL12 a promising target for cancer treatment.
引用
收藏
页码:3590 / 3592
页数:3
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