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修复缺陷型人类细胞系中的脱嘌呤DNA内切酶活性

Apurinic DNA endonuclease activities in repair-deficient human cell lines.

作者信息

Moses R E, Beaudet A L

出版信息

Nucleic Acids Res. 1978 Feb;5(2):463-73. doi: 10.1093/nar/5.2.463.

DOI:10.1093/nar/5.2.463
PMID:634794
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC341995/
Abstract

Several autosomal recessive diseases are associated with apparent DNA repair defects in cell culture. It seemed likely that a defect in excision repair reported for ataxia telangiectasia cells might reflect a lack of apurinic endonuclease activity. We report here normal levels of apurinic endonuclease activity in extracts of cell lines derived from patients with ataxia telangiectasia, xeroderma pigmentosum (complementation group D), Cockayne dwarfism, Fanconi anemia and Bloom syndrome.

摘要

几种常染色体隐性疾病与细胞培养中明显的DNA修复缺陷相关。共济失调毛细血管扩张症细胞中报道的切除修复缺陷似乎可能反映了脱嘌呤内切酶活性的缺乏。我们在此报告，来自共济失调毛细血管扩张症、着色性干皮病（互补组D）、科凯恩侏儒症、范可尼贫血和布卢姆综合征患者的细胞系提取物中，脱嘌呤内切酶活性水平正常。

相似文献

1
Apurinic DNA endonuclease activities in repair-deficient human cell lines.修复缺陷型人类细胞系中的脱嘌呤DNA内切酶活性
Nucleic Acids Res. 1978 Feb;5(2):463-73. doi: 10.1093/nar/5.2.463.
2
An altered apurinic DNA endonuclease activity in group A and group D xeroderma pigmentosum fibroblasts.A组和D组着色性干皮病成纤维细胞中脱嘌呤DNA内切酶活性改变。
Proc Natl Acad Sci U S A. 1976 Apr;73(4):1169-73. doi: 10.1073/pnas.73.4.1169.
3
Human uracil DNA N-glycosidase: studies in normal and repair defective cultured fibroblasts.人尿嘧啶DNA N-糖苷酶：对正常及修复缺陷型培养成纤维细胞的研究
Nucleic Acids Res. 1978 Jan;5(1):117-25. doi: 10.1093/nar/5.1.117.
4
Apurinic/apyrimidinic endonucleases in repair of pyrimidine dimers and other lesions in DNA.脱嘌呤/脱嘧啶内切核酸酶在DNA嘧啶二聚体及其他损伤修复中的作用
Proc Natl Acad Sci U S A. 1980 Aug;77(8):4602-6. doi: 10.1073/pnas.77.8.4602.
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DNA polymerases alpha beta and gamma in inherited diseases affecting DNA repair.影响DNA修复的遗传性疾病中的DNA聚合酶α、β和γ
Nucleic Acids Res. 1978 Jun;5(6):2189-96. doi: 10.1093/nar/5.6.2189.
6
Xeroderma pigmentosum fibroblasts of the D group lack an apurinic DNA endonuclease species with a low apparent Km.D组着色性干皮病成纤维细胞缺乏一种表观Km值较低的无嘌呤DNA内切酶。
Nucleic Acids Res. 1978 Mar;5(3):951-60. doi: 10.1093/nar/5.3.951.
7
Maintenance of DNA and repair of Apurinic sites.DNA的维持与脱嘌呤位点的修复。
Basic Life Sci. 1975;5A:39-46. doi: 10.1007/978-1-4684-2895-7_6.
8
Human endonuclease activity for DNA apurinic sites.
Nature. 1975 Dec 11;258(5535):544-7. doi: 10.1038/258544a0.
9
DNA repair enzymes in ataxia telangiectasia and Bloom's syndrome fibroblasts.共济失调毛细血管扩张症和布卢姆综合征成纤维细胞中的DNA修复酶
Biochim Biophys Acta. 1977 Dec 14;479(4):497-500. doi: 10.1016/0005-2787(77)90042-9.
10
Unraveling DNA repair in human: molecular mechanisms and consequences of repair defect.解析人类DNA修复：修复缺陷的分子机制及后果
Crit Rev Biochem Mol Biol. 2001;36(3):261-90. doi: 10.1080/20014091074192.

引用本文的文献

1
Genetic and biochemical studies with ataxia telangiectasia. A review.共济失调毛细血管扩张症的遗传学和生物化学研究。综述。
Hum Genet. 1981;59(1):1-9. doi: 10.1007/BF00278846.
2
Isolation and characterization of monoclonal antibodies directed against the DNA repair enzyme uracil DNA glycosylase from human placenta.针对人胎盘DNA修复酶尿嘧啶DNA糖基化酶的单克隆抗体的分离与鉴定
Proc Natl Acad Sci U S A. 1983 Oct;80(19):5822-6. doi: 10.1073/pnas.80.19.5822.
3
Stable low molecular weight DNA in xeroderma pigmentosum cells.着色性干皮病细胞中的稳定低分子量DNA
Proc Natl Acad Sci U S A. 1983 Nov;80(22):6987-91. doi: 10.1073/pnas.80.22.6987.
4
The response of ataxia telangiectasia cells to bleomycin.共济失调毛细血管扩张症细胞对博来霉素的反应。
Nucleic Acids Res. 1979;6(5):1953-60. doi: 10.1093/nar/6.5.1953.

本文引用的文献

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Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
J Biol Chem. 1951 Nov;193(1):265-75.
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The enzymatic release of O6-methylguanine and 3-methyladenine from DNA reacted with the carcinogen N-methyl-N-nitrosourea.与致癌物N-甲基-N-亚硝基脲反应的DNA中O6-甲基鸟嘌呤和3-甲基腺嘌呤的酶促释放。
Proc Natl Acad Sci U S A. 1974 May;71(5):2022-6. doi: 10.1073/pnas.71.5.2022.
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Properties of the endonuclease for depurinated DNA from Escherichia coli.来自大肠杆菌的脱嘌呤DNA的核酸内切酶特性。
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A high susceptibility of Fanconi's anemia to chromosome breakage by DNA cross-linking agents.范科尼贫血对DNA交联剂导致染色体断裂高度敏感。
Cancer Res. 1973 Aug;33(8):1829-36.