In eukaryotic cells, maintenance of genomic stability relies on the coordinated action of a
network of cellular processes, including DNA replication, DNA repair, cell-cycle progression …

Radiotherapy is one of the major cancer treatment strategies. Exposure to penetrating
radiation causes cellular stress, directly or indirectly, due to the generation of reactive …

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 …

Abstract ARID1A, SWI/SNF chromatin remodeling complex subunit, is a recently identified
tumor suppressor that is mutated in a broad spectrum of human cancers. Thus, it is of …

Damage to our genetic material is an ongoing threat to both our ability to faithfully transmit
genetic information to our offspring as well as our own survival. To respond to these threats …

The ataxia-telangiectasia mutated (ATM) protein kinase is a master regulator of the DNA
damage response, and it coordinates checkpoint activation, DNA repair, and metabolic …

DNA double-strand breaks (DSBs) can arise from multiple sources, including exposure to
ionizing radiation. The repair of DSBs involves both posttranslational modification of …

p53 is a nuclear transcription factor with a pro-apoptotic function. Since over 50% of human
cancers carry loss of function mutations in p53 gene, p53 has been considered to be one of …

Cell cycle checkpoints activated by DNA double-strand breaks (DSBs) are essential for the
maintenance of the genomic integrity of proliferating cells. Following DNA damage, cells …

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 …