Year: 2007
Type: article
Abstract: In mammalian cells, DNA is often subjected to stresses such as ionizing radiation (IR) that can induce DNA double strand breaks (DSBs). In response to DNA DSBs, mammalian cells activate a rapid phosphorylation signaling cascade through the protein kinases, Ataxia-Telangiectasia Mutated (ATM) and ATM- and Rad3-Related (ATR). Many well-characterized DNA repair factors are phosphorylated by ATM in response to DSBs, and the sequential phosphorylation of some of these factors, including NBS1, delay cell cycle progression (checkpoint arrest) to allow time for DNA damage repair. Results from a new study suggest that phosphorylation of NBS1 is regulated by the acetylation status of the protein, which is modulated by SIRT1 deacetylase.
Source: Cell Cycle
DOI: 10.4161/cc.6.23.5026
Authors: Zhigang Yuan, Edward Seto
Institution: Moffitt Cancer Center
Language: English
Topic: DNA Repair Mechanisms
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W2038077999