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Kwon, Hyug Moo
Immunometabolism and Cancer Lab.
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PARP1-mediated PARylation of TonEBP prevents R-loop-associated DNA damage

Author(s)
Ye, Byeong JinKang, Hyun JeLee-Kwon, WhaseonKwon, Hyug MooChoi, Soo Youn
Issued Date
2021-08
DOI
10.1016/j.dnarep.2021.103132
URI
https://scholarworks.unist.ac.kr/handle/201301/53489
Fulltext
https://www.sciencedirect.com/science/article/pii/S1568786421000884?via%3Dihub
Citation
DNA REPAIR, v.104, pp.103132
Abstract
Lack of coordination between the DNA replication and transcription machineries can increase the frequency of transcription-replication conflicts, leading ultimately to DNA damage and genomic instability. A major source of these conflicts is the formation of R-loops, which consist of a transcriptionally generated RNA-DNA hybrid and the displaced single-stranded DNA. R-loops play important physiological roles and have been implicated in human diseases. Although these structures have been extensively studied, many aspects of R-loop biology and Rloop-mediated genome instability remain unclear. We found that in cancer cells, tonicity-responsive enhancerbinding protein (TonEBP, also called NFAT5) interacted with PARP1 and localized to R-loops in response to DNAdamaging agent camptothecin (CPT), which is associated with R-loop formation. PARP1-mediated PARylation was required for recruitment of TonEBP to the sites of R-loop-associated DNA damage. Loss of TonEBP increased levels of R-loop accumulation and DNA damage, and promoted cell death in response to CPT. These findings suggest that TonEBP mediates resistance to CPT-induced cell death by preventing R-loop accumulation in cancer cells.
Publisher
ELSEVIER
ISSN
1568-7864
Keyword (Author)
NFAT5PARylationCamptothecinDNA damage responseDNA repairGenome instabilityCancer cell
Keyword
TRANSCRIPTIONGENOMEREPLICATIONPATHWAYSTHREATSREPAIR

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