DNA damage response (DDR) pathway prevents high level endogenous and environmental
DNA damage being replicated and passed on to the next generation of cells via an …

The chemical treatment of cancer started with the realization that DNA damaging agents
such as mustard gas present notable antitumoural properties. Consequently, early drug …

DNA replication begins with the assembly of pre-replication complexes (pre-RCs) at
thousands of DNA replication origins during the G1 phase of the cell cycle. At the G1–S …

The cell cycle checkpoint proteins ataxia-telangiectasia-mutated-and-Rad3-related kinase
(ATR) and its major downstream effector checkpoint kinase 1 (CHK1) prevent the entry of …

Mammalian development, adult tissue homeostasis and the avoidance of severe diseases
including cancer require a properly orchestrated cell cycle, as well as error-free genome …

The interplay between replication stress and the S phase checkpoint is a key determinant of
genome maintenance, and has a major impact on human diseases, notably, tumour …

The ATR-Chk1 pathway is critical for DNA damage responses and cell-cycle progression.
Chk1 inhibition is more deleterious to cycling cells than ATR inhibition, raising questions …

DNA damage is a key factor both in the evolution and treatment of cancer. Genomic
instability is a common feature of cancer cells, fuelling accumulation of oncogenic mutations …

The evolutionally conserved DNA damage response (DDR) and cell cycle checkpoints
preserve genome integrity. Central to these genome surveillance pathways is a protein …

SLFN11 sensitizes cancer cells to a broad range of DNA-targeted therapies. Here we show
that, in response to replication stress induced by camptothecin, SLFN11 tightly binds …