학술논문
Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner
Document Type
article
Author
Source
Nature Communications, Vol 10, Iss 1, Pp 1-14 (2019)
Subject
Language
English
ISSN
2041-1723
Abstract
Oncogene-induced replication stress (RS) promotes cancer development. Here, the authors report that cancer cells adapt to oncogene-induced RS by overexpressing downstream components of ATR-CHK1 pathway, Claspin and Timeless, which have protective role at the replication forks independent of their checkpoint function.