Cellular pathways that repair chromosomal double-strand breaks (DSBs) have pivotal roles
in cell growth, development and cancer. These DSB repair pathways have been the target of …

The protein kinase ataxia-telangiectasia mutated (ATM) is best known for its role as an
apical activator of the DNA damage response in the face of DNA double-strand breaks …

DNA double-strand breaks (DSBs) are cytotoxic lesions that can result in mutagenic events
or cell death if left unrepaired or repaired inappropriately. Cells use two major pathways for …

DNA double-strand breaks (DSBs) are induced by a variety of genotoxic agents, including
ionizing radiation and chemotherapy drugs for treating cancers. The elimination of DSBs …

The maintenance of genome stability depends on the DNA damage response (DDR), which
is a functional network comprising signal transduction, cell cycle regulation and DNA repair …

The faithful maintenance of chromosome continuity in human cells during DNA replication
and repair is critical for preventing the conversion of normal diploid cells to an oncogenic …

A defining characteristic of damage induced in the DNA by ionizing radiation (IR) is its
clustered character that leads to the formation of complex lesions challenging the cellular …

DNA double-strand breaks (DSBs) threaten genome stability throughout life and are linked
to tumorigenesis in humans. To initiate DSB repair by end joining or homologous …

Nonhomologous DNA end joining (NHEJ) is one of the major double-strand break (DSB)
repair pathways in higher eukaryotes. Recently, it has been shown that alternative NHEJ (A …

Repair and integrity of DNA ends at breaks, replication forks and telomeres are essential for
life; yet, paradoxically, these responses are, in many cases, controlled by a single protein …