催化亚单位
细胞生物学
DNA
核酸酶
DNA修复
生物
DNA连接酶
非同源性末端接合
蛋白质亚单位
分子生物学
蛋白激酶A
激酶
化学
遗传学
基因
作者
Go Watanabe,Michael R. Lieber
标识
DOI:10.1016/j.jmb.2022.167858
摘要
Pathologic chromosome breaks occur in human dividing cells ∼10 times per day, and physiologic breaks occur in each lymphoid cell many additional times per day. Nonhomologous DNA end joining (NHEJ) is the major pathway for the repair of all of these double-strand breaks (DSBs) during most of the cell cycle. Nearly all broken DNA ends require trimming before they can be suitable for joining by ligation. Artemis is the major nuclease for this purpose. Artemis is tightly regulated by one of the largest protein kinases, which tethers Artemis to its surface. This kinase is called DNA-dependent protein kinase catalytic subunit (or DNA-PKcs) because it is only active when it encounters a broken DNA end. With this activation, DNA-PKcs permits the Artemis catalytic domain to enter a large cavity in the center of DNA-PKcs. Given this remarkably tight supervision of Artemis by DNA-PKcs, it is an appropriate time to ask what we know about the Artemis:DNA-PKcs complex, as we integrate recent structural information with the biochemistry of the complex and how this relates to other NHEJ proteins and to V(D)J recombination in the immune system.
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