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在哺乳动物细胞中,视黄酸和二丁酰环磷腺苷对受损DNA识别蛋白的诱导作用,该诱导作用与受损质粒DNA的宿主细胞再激活无关。

Induction, not associated with host-cell re-activation of damaged plasmid DNA, of damaged-DNA-recognition proteins by retinoic acid and dibutyryl cyclic AMP in mammalian cells.

作者信息

Sun N K, Huang S L, Lin-Chao S, Chao C C

机构信息

Department of Biochemistry, Chang Gung Medical College, Taoyuan, Taiwan, Republic of China.

出版信息

Biochem J. 1996 Jan 15;313 ( Pt 2)(Pt 2):441-5. doi: 10.1042/bj3130441.

Abstract

Our previous studies [Chao (1992) Biochem. J. 282, 203-207; C.C.-K. Chao, unpublished work] has suggested a correlation between the levels of constitutive UV-damaged-DNA-recognitionproteins (UVDRP) and cellular DNA repair in different cell types. In the present study, UVDRP were induced in F9 and NIH3T3 cells by 0.1 microM retinoic acid (RA) and 1 mM dibutyryl cyclic AMP (dbcAMP), which is sufficient to induce differentiation in murine F9 stem cells. The induction of UVDRP in F9 and NIH3T3 cells was optimized after 6 and 2 days incubation with RA/dbcAMP respectively. Since NIH3T3 cells were not induced to differentiate by RA/dbcAMP, the upregulation of the UVDRP in mammalian cells would thus seem not to be mediated directly by differentiation. Using a plasmid re-activation assay to estimate DNA repair, we did not find a correlation between DNA repair and UVDRP in RA/dbcAMP-treated cells. The results suggest that UVDRP may have a function other than, or in addition to, its role in DNA repair.

摘要

我们之前的研究[Chao(1992年)《生物化学杂志》282卷,203 - 207页;C.C.-K. Chao,未发表的研究工作]表明,在不同细胞类型中,组成型紫外线损伤DNA识别蛋白(UVDRP)的水平与细胞DNA修复之间存在关联。在本研究中,用0.1微摩尔视黄酸(RA)和1毫摩尔二丁酰环磷腺苷(dbcAMP)诱导F9和NIH3T3细胞中的UVDRP,这足以诱导小鼠F9干细胞分化。F9和NIH3T3细胞分别在与RA/dbcAMP孵育6天和2天后,UVDRP的诱导效果达到最佳。由于NIH3T3细胞不会被RA/dbcAMP诱导分化,因此哺乳动物细胞中UVDRP的上调似乎并非直接由分化介导。使用质粒再激活试验来评估DNA修复,我们未发现经RA/dbcAMP处理的细胞中DNA修复与UVDRP之间存在关联。结果表明,UVDRP可能除了在DNA修复中的作用之外,还具有其他功能,或者除了该作用之外还具有其他功能。

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Reactions of the UVRABC excision nuclease with DNA damaged by diamminedichloroplatinum(II).
Nucleic Acids Res. 1985 Oct 25;13(20):7395-412. doi: 10.1093/nar/13.20.7395.

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