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Please use this identifier to cite or link to this item: http://hdl.handle.net/10564/3342

Title: Lysines 3241 and 3260 of DNA-PKcs are important for genomic stability and radioresistance.
Other Titles: DNA-PKcsのリジン3241と3260はゲノムの安定性と放射線抵抗性に重要である
Authors: Mori, Eiichiro
Davis, Anthony J.
Hasegawa, Masatoshi
Chen, David J.
Keywords: DNA double-strand breaks
Non-homologous end-joining
Acetylation
DNA-PKcs
Issue Date: 19-Aug-2016
Publisher: Elsevier
Citation: Biochemical and biophysical research communications Vol.477 No.2 p.235-240 (2016 Aug)
Abstract: DNA-dependent protein kinase (DNA-PK) is a serine/threonine kinase that plays an essential role in the repair of DNA double-strand breaks (DSBs) in the non-homologous end-joining (NHEJ) pathway. The DNA-PK holoenzyme consists of a catalytic subunit (DNA-PKcs) and DNA-binding subunit (Ku70/80, Ku). Ku is a molecular sensor for double-stranded DNA and once bound to DSB ends it recruits DNA-PKcs to the DSB site. Subsequently, DNA-PKcs is activated and heavily phosphorylated, with these phosphorylations modulating DNA-PKcs. Although phosphorylation of DNA-PKcs is well studied, other post-translational modifications of DNA-PKcs are not. In this study, we aimed to determine if acetylation of DNA-PKcs regulates DNA-PKcs-dependent DSB repair. We report that DNA-PKcs is acetylated in vivo and identified two putative acetylation sites, lysine residues 3241 and 3260. Mutating these sites to block potential acetylation results in increased radiosensitive, a slight decrease in DSB repair capacity as assessed by γH2AX resolution, and increased chromosomal aberrations, especially quadriradial chromosomes. Together, our results provide evidence that acetylation potentially regulates DNA-PKcs.
Description: 博士(医学)・甲第670号・平成29年6月28日
Copyright © 2016 Elsevier Inc. All rights reserved.
URI: http://hdl.handle.net/10564/3342
ISSN: 0006291X
Academic Degrees and number: 24601A670
Degree-granting date: 2017-06-28
Degree name: 博士(医学)
Degree-granting institutions: 奈良県立医科大学
Appears in Collections:2017年度

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