Year: 2015
Type: editorial
Abstract: Chromosomal double stranded breaks (DSBs) are regarded as the most cytotoxic form of DNA damage, and occur as a result of normal cellular processes, such as DNA replication, as well as in response to ionizing radiation, and chemotherapeutics. These breaks must be repaired to ensure genomic stability and viability. In vertebrates, nonhomologous end joining (NHEJ) is the main pathway for repair of DSBs, and is active throughout the cell cycle. According to common measures for the rate of occurrence of DSBs in cell culture, an estimated 1012-14 DSBs are repaired in the human body each day [1, 2]. NHEJ is therefore vital for maintaining genomic stability by suppressing gross chromosomal translocations and for offsetting senescence, apoptosis, and the aging process. Deficient NHEJ also often manifests as immune system
Source: Oncotarget
Authors: Dylan A. Reid, Eli Rothenberg
Institution: New York University
Language: English
Topic: DNA Repair Mechanisms
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W2237644450