Fujiko Tsukahara    Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine    Position   Professor (Fixed Term)
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	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.
Journal	Formal name：Journal of biochemistry Abbreviation：J Biochem ISSN code：1756-2651/0021-924X
Domestic / Foregin	Foregin
Volume, Issue, Page	164(6),pp.415-426
Author and coauthor	Tomita Takeshi†*, Ieguchi Katsuaki, Takita Morichika, Tsukahara Fujiko, Yamada Masayuki, Egly Jean-Marc, Maru Yoshiro*
Publication date	2018/08
Summary	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
URL for researchmap	https://academic.oup.com/jb/article/164/6/415/5079841