ELG1 protein interacts with PCNAs that are localized at stalled replication forks.

We demonstrate that hPif1 specifically recognizes and unwinds DNA structures resembling putative stalled replication forks.

In proliferating cells, PhIP treatment increased the frequency of stalled replication forks and reduced fork speed.

Thus, Nbs1 has a function in ATR signalling in a manner distinct to any role at stalled replication forks.

Thus, cells have developed several pathways and a complex set of proteins to overcome the challenge at stalled replication forks.

Thus, interaction of ATR with a critical protein at stalled replication forks and sites of DNA damage triggers its activation.

To address the second, we disrupted RAD18, a gene involved in translesion DNA synthesis, a mechanism that relieves stalled replication.

Importantly, cells with artificially accelerated p21 degradation display evidence of stalled replication in mid-S phase and sensitivity to replication arrest.

HDR is critical for the error-free repair of DNA double-strand breaks and other lesions, and HDR factors also protect stalled replication forks.

Loss of Pol kappa prevents timely rescue of stalled replication forks, leading to replication-associated genomic instability, and a p53-dependent cell cycle defect.

RFWD3 is necessary for replication fork restart, normal repair kinetics during replication stress, and homologous recombination (HR) at stalled replication forks.

Thus, BRCA2 prevents rather than repairs nucleolytic lesions at stalled replication forks to maintain genomic integrity and hence likely suppresses tumorigenesis through this replication-specific function.

Depletion of Rif1 from egg extracts compromises the activation of Chk1 in response to DSBs but not stalled replication forks.