ツカハラ　フジコ   TSUKAHARA Fujiko   塚原　富士子    所属   医学部 医学科（東京女子医科大学病院）    職種   特任教授
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	C1D is not directly involved in the repair of UV-damaged DNA but protects cells from oxidative stress by regulating gene expressions in human cell lines.
掲載誌名	正式名：Journal of biochemistry 略　 称：J Biochem ISSNコード：1756-2651/0021-924X
掲載区分	国外
巻・号・頁	164(6),pp.415-426
著者・共著者	Tomita Takeshi†*, Ieguchi Katsuaki, Takita Morichika, Tsukahara Fujiko, Yamada Masayuki, Egly Jean-Marc, Maru Yoshiro*
発行年月	2018/08
概要	A small nuclear protein, C1D, has roles in various cellular processes, transcription regulation, genome stability surveillance, DNA repair, and RNA processing, all of which are required to maintain the host life cycles. In the previous report, C1D directly interacts with XPB, a component of the nucleotide excision repair complex, and C1D knockdown reduced cell survival of 27-1 cells, CHO derivative cells, after UV irradiation. To find out the role of C1D in UV damaged cells, we used human cell lines with siRNA or shRNA to knockdown C1D. C1D knockdown reduced cell survival rates of LU99 and 786-O after UV irradiation, although C1D knockdown did not affect the efficiency of the nucleotide excision repair. Immunostaining data support that C1D is not directly involved in the DNA repair process in UV damaged cells. On the other hand, H2O2 treatment reduced cell viability in LU99 and 786-O cells. We also found that C1D knockdown upregulated DDIT3 expression in LU99 cells and downregulated APEX1 in 786-O cells, suggesting that C1D functions as a co-repressor/activator. The data accounts for the reduction of cell survival rates upon UV irradiation.
DOI	10.1093/jb/mvy069
PMID	30165670
researchmap用URL	https://academic.oup.com/jb/article/164/6/415/5079841