DNA double-strand breaks (DSBs) are cytotoxic lesions that threaten genome integrity and
cell viability. Typically, cells repair DSBs by either nonhomologous end joining (NHEJ) or …

Exposure to environmental mutagens but also cell-endogenous processes can create DNA
double-strand breaks (DSBs) in a cell's genome. DSBs need to be repaired accurately and …

DNA double-strand breaks (DSBs) can be repaired by several pathways. In eukaryotes, DSB
repair pathway choice occurs at the level of DNA end resection and is controlled by the cell …

In Saccharomyces cerevisiae (S. cerevisiae), Mre11-Rad50-Xrs2 (MRX)-Sae2 nuclease
activity is required for the resection of DNA breaks with secondary structures or protein …

Our understanding of the DNA damage responses of human cells to radiation has increased
remarkably over the recent years although some notable signaling events remain to be …

CtIP initiates DNA end resection and mediates homologous recombination (HR) repair.
However, the underlying mechanisms of CtIP regulation and how the control of its regulation …

BMI-1 is an essential regulator of transcriptional silencing during development. Recently, the
role of BMI-1 in the DNA damage response has gained much attention, but the exact …

DNA double-strand breaks (DSBs) are a significant threat to cell viability due to the induction
of genome instability and the potential loss of genetic information. One of the key players for …

Telomeres protect chromosome ends from unscheduled DNA repair, including from the
MRN (MRE11, RAD50, NBS1) complex, which processes double-stranded DNA breaks …

Heterochromatin is a conserved feature of eukaryotic chromosomes, with central roles in
gene expression regulation and maintenance of genome stability. How heterochromatin …