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.
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.
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C1D 不直接参与紫外线损伤 DNA 的修复，但通过调节人类细胞系中的基因表达来保护细胞免受氧化应激。
作者：
Tomita T;Ieguchi K;Takita M;Tsukahara F;Yamada M;Egly JM;Maru Y.
一种小的核蛋白，C1 D，在各种细胞过程中发挥作用，转录调节，基因组稳定性监测，DNA修复和RNA加工，所有这些都是维持宿主生命周期所必需的。在先前的报告中，C1 D直接与XPB相互作用，XPB是核苷酸切除修复复合物的一种组分，C1 D敲低降低了UV照射后27-1细胞（CHO衍生细胞）的细胞存活率。为了找出C1 D在UV损伤细胞中的作用，我们使用具有siRNA或shRNA的人类细胞系来敲低C1 D。C1 D敲除降低了UV照射后LU 99和786-O的细胞存活率，尽管C1 D敲除不影响核苷酸切除修复的效率。免疫染色数据支持C1 D不直接参与UV损伤细胞的DNA修复过程。然而，H2 O2处理降低了LU 99和786-O细胞的细胞活力。我们还发现，C1 D敲低上调LU 99细胞中DDIT 3的表达，下调786-O细胞中APEX 1的表达，表明C1 D作为共阻遏物/激活物发挥作用。该数据解释了UV照射后细胞存活率的降低。
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, H2O2treatment 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.