Nature Communications (Feb 2019)
Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner
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.