Ataxia Telangiectasia Mutated (ATM) signaling is essential for the repair of a subset of DNA
double-strand breaks (DSBs); however, its precise role is unclear. Here, we show that ≤25…

DNA double-strand breaks (DSBs) represent an important radiation-induced lesion and
impaired DSB repair provides the best available correlation with radiosensitivity. Physical …

Homologous recombination (HR) and non‐homologous end joining (NHEJ) represent
distinct pathways for repairing DNA double‐strand breaks (DSBs). Previous work implicated …

The Artemis nuclease is defective in radiosensitive severe combined immunodeficiency
patients and is required for the repair of a subset of ionising radiation induced DNA double‐…

The phosphatidyl inositol 3‐kinase‐like kinases (PIKKs), ataxia‐telangiectasia mutated (ATM)
and ATM‐ and Rad3‐related (ATR) regulate parallel damage response signalling …

The p53 tumor suppressor protein preserves genome integrity by regulating growth arrest
and apoptosis in response to DNA damage. In response to ionizing radiation (IR), ATM, the …

DNA double-strand breaks (DSBs) trigger ATM (ataxia telangiectasia mutated) signalling
and elicit genomic rearrangements and chromosomal fragmentation if misrepaired or …

DNA non-homologous end-joining (NHEJ) and homologous recombination (HR) represent
the major DNA double strand break (DSB) pathways in mammalian cells, whilst ataxia …

Ionizing radiation induces autophosphorylation of the ataxia‐telangiectasia mutated (ATM)
protein kinase on serine 1981; however, the precise mechanisms that regulate ATM …

KAP-1 poses a substantial barrier to DNA double-strand break (DSB) repair within
heterochromatin that is alleviated by ATM-dependent KAP-1 phosphorylation (pKAP-1). Here we …