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作 者:Zhiquan Song Ying Xie Zongpei Guo Yang Han Hua Guan Xiaodan Liu Teng Ma Ping-kun Zhou
机构地区:[1]Department of Radiation Toxicology and Oncology,Beijing Key Laboratory for Radiobiology,Beijing Institute of Radiation Medicine,100850 Beijing,People’s Republic of China [2]Department of Preventive Medicine,Medical School of Hunan Normal University,410078 Changsha,People’s Republic of China [3]Institute for Environmental Medicine and Radiation Hygiene,School of Public Health,University of South China,421001 Hengyang,Hunan Province,People’s Republic of China [4]Department of Cellular and Molecular Biology,Beijing Chest Hospital,Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute,101149 Beijing,China
出 处:《Signal Transduction and Targeted Therapy》2019年第1期493-495,共3页信号转导与靶向治疗(英文)
基 金:This work was supported by grants from the National Key Basic Research Program(973 Program)of MOST,China(Grant No.2015CB910601);the National Natural Science Foundation of China(Grant Nos.31370843 and 31500681)to P.K;Zhou and the National Natural Science Foundation,China(Grant Nos.31570853 and 81602799)to T.Ma.
摘 要:Dear Editor,The DNA-dependent protein kinase catalytic subunit(DNA-PKcs)forms a serine/threonine protein kinase complex with the Ku heterodimer(Ku70/Ku80)and plays an important role in the DNA damage response(DDR)and maintenance of genomic stability through nonhomologous end joining(NHEJ),wherein the Ku heterodimer recognizes and binds broken DNA ends,facilitating the recruitment and activation of DNA-PKcs.1 Activated DNA-PKcs phosphorylates and alters the function of factors that mediate NHEJ,including DNA-PKcs itself.2 In addition,DDR-independent roles of DNA-PKcs have been demonstrated.3 Studies further identified DNA-PKcs as a modulator of cancer-associated pathways distinct from DNA repair,including hypoxia,metabolism,the inflammatory response,and transcriptional regulation.
关 键 词:GENOME METABOLISM damage
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