Abstract:
: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. However, 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.
journal_name
J Biochemjournal_title
Journal of biochemistryauthors
Tomita T,Ieguchi K,Takita M,Tsukahara F,Yamada M,Egly JM,Maru Ydoi
10.1093/jb/mvy069subject
Has Abstractpub_date
2018-12-01 00:00:00pages
415-426issue
6eissn
0021-924Xissn
1756-2651pii
5079841journal_volume
164pub_type
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pub_type: 杂志文章
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doi:10.1093/oxfordjournals.jbchem.a133910
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journal_title:Journal of biochemistry
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1093/oxfordjournals.jbchem.a132805
更新日期:1980-03-01 00:00:00
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pub_type: 杂志文章
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更新日期:1998-05-01 00:00:00
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更新日期:2012-10-01 00:00:00