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1
Activation of apurinic/apyrimidinic endonuclease in human cells by reactive oxygen species and its correlation with their adaptive response to genotoxicity of free radicals.活性氧对人细胞中脱嘌呤/脱嘧啶内切核酸酶的激活作用及其与细胞对自由基遗传毒性适应性反应的相关性。
Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5061-6. doi: 10.1073/pnas.95.9.5061.
2
Requirement for human AP endonuclease 1 for repair of 3'-blocking damage at DNA single-strand breaks induced by reactive oxygen species.人类脱嘌呤嘧啶内切核酸酶1对活性氧诱导的DNA单链断裂处3'端阻断损伤修复的需求。
Carcinogenesis. 2000 Jul;21(7):1329-34.
3
Expression of yeast but not human apurinic/apyrimidinic endonuclease renders Chinese hamster cells more resistant to DNA damaging agents.酵母而非人类无嘌呤/无嘧啶内切核酸酶的表达使中国仓鼠细胞对DNA损伤剂更具抗性。
Mutat Res. 1997 Mar 12;383(2):155-65. doi: 10.1016/s0921-8777(96)00055-9.
4
Repair of apurinic/apyrimidinic sites by UV damage endonuclease; a repair protein for UV and oxidative damage.紫外线损伤内切核酸酶修复无嘌呤/无嘧啶位点；一种针对紫外线和氧化损伤的修复蛋白。
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5
Activation of APE/Ref-1 redox activity is mediated by reactive oxygen species and PKC phosphorylation.APE/Ref-1氧化还原活性的激活由活性氧和蛋白激酶C磷酸化介导。
Nucleic Acids Res. 2001 Jul 15;29(14):3116-22. doi: 10.1093/nar/29.14.3116.
6
Deletion analysis of human AP-endonuclease: minimum sequence required for the endonuclease activity.人类脱嘌呤嘧啶内切核酸酶的缺失分析：内切核酸酶活性所需的最小序列
Carcinogenesis. 1998 Mar;19(3):525-7. doi: 10.1093/carcin/19.3.525.
7
Apurinic endonuclease (Ref-1) is induced in mammalian cells by oxidative stress and involved in clastogenic adaptation.脱嘌呤内切酶（Ref-1）在哺乳动物细胞中由氧化应激诱导产生，并参与致断裂适应过程。
Cancer Res. 1998 Oct 1;58(19):4410-6.
8
Phosphorylation of the DNA repair protein APE/REF-1 by CKII affects redox regulation of AP-1.CKII对DNA修复蛋白APE/REF-1的磷酸化作用影响AP-1的氧化还原调节。
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9
Early decrease in apurinic/apyrimidinic endonuclease is followed by DNA fragmentation after cold injury-induced brain trauma in mice.小鼠冷损伤诱导的脑外伤后，脱嘌呤/脱嘧啶内切酶早期减少之后会出现DNA片段化。
Neuroscience. 1999;93(4):1465-73. doi: 10.1016/s0306-4522(99)00231-6.
10
Creation of a fully functional human chimeric DNA repair protein. Combining O6-methylguanine DNA methyltransferase (MGMT) and AP endonuclease (APE/redox effector factor 1 (Ref 1)) DNA repair proteins.创建一种功能齐全的人类嵌合DNA修复蛋白。将O6-甲基鸟嘌呤DNA甲基转移酶（MGMT）和AP核酸内切酶（APE/氧化还原效应因子1（Ref 1））DNA修复蛋白相结合。
J Biol Chem. 1998 Jan 9;273(2):756-62. doi: 10.1074/jbc.273.2.756.

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Live-cell imaging of human apurinic/apyrimidinic endonuclease 1 in the nucleus and nucleolus using a chaperone@DNA probe.利用伴侣蛋白@DNA 探针在细胞核和核仁中对人嘌呤/嘧啶内切核酸酶 1 进行活细胞成像。
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The Role of DNA Damage in Neural Plasticity in Physiology and Neurodegeneration.DNA损伤在生理和神经退行性变中神经可塑性中的作用。
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本文引用的文献

1
Deletion analysis of human AP-endonuclease: minimum sequence required for the endonuclease activity.人类脱嘌呤嘧啶内切核酸酶的缺失分析：内切核酸酶活性所需的最小序列
Carcinogenesis. 1998 Mar;19(3):525-7. doi: 10.1093/carcin/19.3.525.
2
The apurinic/apyrimidinic endonuclease (APE/ref-1) DNA repair enzyme is elevated in premalignant and malignant cervical cancer.脱嘌呤/脱嘧啶内切核酸酶（APE/ref-1）这种DNA修复酶在癌前和恶性宫颈癌中水平升高。
Anticancer Res. 1997 Sep-Oct;17(5B):3713-19.
3
The DNA repair activity of human redox/repair protein APE/Ref-1 is inactivated by phosphorylation.人类氧化还原/修复蛋白APE/Ref-1的DNA修复活性可因磷酸化作用而失活。
Cancer Res. 1997 Dec 15;57(24):5457-9.
4
Complexities of DNA base excision repair in mammalian cells.哺乳动物细胞中DNA碱基切除修复的复杂性
Mol Cells. 1997 Jun 30;7(3):305-12.
5
Molecular cloning and functional expression of a human cDNA encoding the antimutator enzyme 8-hydroxyguanine-DNA glycosylase.编码抗突变酶8-羟基鸟嘌呤-DNA糖基化酶的人cDNA的分子克隆与功能表达
Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):8016-20. doi: 10.1073/pnas.94.15.8016.
6
Cloning and characterization of hOGG1, a human homolog of the OGG1 gene of Saccharomyces cerevisiae.酿酒酵母OGG1基因的人类同源物hOGG1的克隆与特性分析
Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):8010-5. doi: 10.1073/pnas.94.15.8010.
7
Cloning and characterization of a mammalian 8-oxoguanine DNA glycosylase.一种哺乳动物8-氧代鸟嘌呤DNA糖基化酶的克隆与特性分析
Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7429-34. doi: 10.1073/pnas.94.14.7429.
8
A mammalian DNA repair enzyme that excises oxidatively damaged guanines maps to a locus frequently lost in lung cancer.一种切除氧化损伤鸟嘌呤的哺乳动物DNA修复酶定位于肺癌中经常缺失的一个基因座。
Curr Biol. 1997 Jun 1;7(6):397-407. doi: 10.1016/s0960-9822(06)00187-4.
9
3'-phosphodiesterase activity of human apurinic/apyrimidinic endonuclease at DNA double-strand break ends.人脱嘌呤/脱嘧啶内切核酸酶在DNA双链断裂末端的3'-磷酸二酯酶活性。
Nucleic Acids Res. 1997 Jun 15;25(12):2495-500. doi: 10.1093/nar/25.12.2495.
10
Failure of HPV E6 to rapidly degrade p53 in human HeLa x PNET cell hybrids.人HeLa x PNET细胞杂交体中HPV E6未能快速降解p53。
Oncogene. 1997 Apr 10;14(14):1669-78. doi: 10.1038/sj.onc.1201001.

活性氧对人细胞中脱嘌呤/脱嘧啶内切核酸酶的激活作用及其与细胞对自由基遗传毒性适应性反应的相关性。

Activation of apurinic/apyrimidinic endonuclease in human cells by reactive oxygen species and its correlation with their adaptive response to genotoxicity of free radicals.

作者信息

Ramana C V, Boldogh I, Izumi T, Mitra S

机构信息

Sealy Center for Molecular Science and Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, TX 77555, USA.

出版信息

Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5061-6. doi: 10.1073/pnas.95.9.5061.

DOI:10.1073/pnas.95.9.5061
PMID:9560228
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC20213/
Abstract

Apurinic/apyrimidinic (AP) endonuclease (APE; EC 4.2.99.18) plays a central role in repair of DNA damage due to reactive oxygen species (ROS) because its DNA 3'-phosphoesterase activity removes 3' blocking groups in DNA that are generated by DNA glycosylase/AP-lyases during removal of oxidized bases and by direct ROS reaction with DNA. The major human APE (APE-1) gene is activated selectively by sublethal levels of a variety of ROS and ROS generators, including ionizing radiation, but not by other genotoxicants-e.g., UV light and alkylating agents. Increased expression of APE mRNA and protein was observed both in the HeLa S3 tumor line and in WI 38 primary fibroblasts, and it was accompanied by translocation of the endonuclease to the nucleus. ROS-treated cells showed a significant increase in resistance to the cytotoxicity of such ROS generators as H2O2 and bleomycin, but not to UV light. This "adaptive response" appears to result from enhanced repair of cytotoxic DNA lesions due to an increased activity of APE-1, which may be limiting in the base excision repair process for ROS-induced toxic lesions.

摘要

脱嘌呤/脱嘧啶（AP）核酸内切酶（APE；EC 4.2.99.18）在因活性氧（ROS）导致的DNA损伤修复中起核心作用，因为其DNA 3'-磷酸二酯酶活性可去除DNA中的3'阻断基团，这些基团是由DNA糖基化酶/AP裂解酶在去除氧化碱基过程中以及ROS与DNA直接反应产生的。人类主要的APE（APE-1）基因可被多种ROS及ROS生成剂的亚致死水平选择性激活，包括电离辐射，但不被其他基因毒性剂激活，如紫外线和烷基化剂。在HeLa S3肿瘤细胞系和WI 38原代成纤维细胞中均观察到APE mRNA和蛋白质表达增加，且伴随着核酸内切酶向细胞核的转位。经ROS处理的细胞对H2O2和博来霉素等ROS生成剂的细胞毒性的抗性显著增加，但对紫外线不增加。这种“适应性反应”似乎是由于APE-1活性增加导致细胞毒性DNA损伤的修复增强所致，而APE-1在ROS诱导的毒性损伤的碱基切除修复过程中可能是受限的。