Radiotherapy is one of the most common countermeasures for treating a wide range of
tumors. However, the radioresistance of cancer cells is still a major limitation for …

DNA double stranded breaks (DSBs) are the most cytoxic DNA lesion as the inability to
properly repair them can lead to genomic instability and tumorigenesis. The prominent DSB …

Efficient repair of DNA double-strand breaks (DSBs) requires a coordinated DNA Damage
Response (DDR), which includes phosphorylation of histone H2Ax, forming γH2Ax. This …

Nonhomologous end-joining (NHEJ) is a major DNA double-strand break repair pathway
that is conserved in eukaryotes. In vertebrates, NHEJ further acquires end-processing …

DNA damage, especially DNA double strand breaks (DSBs) and replication stress, activates
a complex post-translational network termed DNA damage response (DDR). Our review …

The DNA damage response (DDR) is an organized network of multiple interwoven
components evolved to repair damaged DNA and maintain genome fidelity. Conceptually …

The DNA-dependent protein kinase (DNA-PK), which comprises the KU heterodimer and a
catalytic subunit (DNA-PKcs), is a classical non-homologous end-joining (cNHEJ) factor. KU …

Non-homologous end joining (NHEJ) is the major pathway for the repair of ionizing radiation
induced DNA double strand breaks in human cells. Here, we discuss current insights into …

Using data generated with cells exposed to ionizing-radiation (IR) in G2-phase of the cell
cycle, we describe dose-dependent interactions between ATM, ATR and DNA-PKcs …

Ataxia-telangiectasia mutated (ATM) drives the DNA damage response via modulation of
multiple signal transduction and DNA repair pathways. Previously, ATM activity was …