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用8-甲氧基补骨脂素加近紫外线辐射处理的着色性干皮病E互补组细胞中的正常DNA断裂率。

Normal rate of DNA breakage in xeroderma pigmentosum complementation group E cells treated with 8-methoxypsoralen plus near-ultraviolet radiation.

作者信息

Bredberg A, Söderhäll S

出版信息

Biochim Biophys Acta. 1985 Mar 20;824(3):268-71. doi: 10.1016/0167-4781(85)90058-2.

DOI:10.1016/0167-4781(85)90058-2
PMID:3970936
Abstract

Treatment of normal and xeroderma pigmentosum complementation group E skin fibroblasts with 8-methoxypsoralen plus repeated doses of near-ultraviolet radiation elicited a marked increase in DNA strand breakage during a subsequent incubation. No such induction of breaks was noted with cells from xeroderma pigmentosum groups A and D. The results suggest that the gene product which is deficient in xeroderma pigmentosum group E cells is involved in a critical step of DNA repair of far-ultraviolet photoproducts but not so in the repair of psoralen cross-links.

摘要

用8-甲氧基补骨脂素加重复剂量的近紫外线辐射处理正常皮肤成纤维细胞和着色性干皮病E互补组皮肤成纤维细胞,在随后的培养过程中会引起DNA链断裂显著增加。而着色性干皮病A组和D组细胞未观察到这种断裂诱导现象。结果表明,着色性干皮病E组细胞中缺乏的基因产物参与了远紫外线光产物DNA修复的关键步骤,但在补骨脂素交联修复中并非如此。

相似文献

1
Normal rate of DNA breakage in xeroderma pigmentosum complementation group E cells treated with 8-methoxypsoralen plus near-ultraviolet radiation.用8-甲氧基补骨脂素加近紫外线辐射处理的着色性干皮病E互补组细胞中的正常DNA断裂率。
Biochim Biophys Acta. 1985 Mar 20;824(3):268-71. doi: 10.1016/0167-4781(85)90058-2.
2
Induction and repair of psoralen cross-links in DNA of normal human and xeroderma pigmentosum fibroblasts.补骨脂素在正常人及着色性干皮病成纤维细胞DNA中交联的诱导与修复
Mutat Res. 1982 Mar;93(1):221-34. doi: 10.1016/0027-5107(82)90137-3.
3
DNA synthesis in normal and xeroderma pigmentosum fibroblasts following treatment with 8-methoxypsoralen and long wave ultraviolet light.用8-甲氧基补骨脂素和长波紫外线处理后正常及着色性干皮病成纤维细胞中的DNA合成
Biochim Biophys Acta. 1972 Mar 24;262(3):247-55. doi: 10.1016/0005-2787(72)90260-2.
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Repair of ultraviolet radiation damage in xeroderma pigmentosum cells belonging to complementation group F.属于互补组F的着色性干皮病细胞中紫外线辐射损伤的修复
Mutat Res. 1981 Feb;80(2):381-8. doi: 10.1016/0027-5107(81)90110-x.
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Chromatin-associated DNA endonucleases from xeroderma pigmentosum cells are defective in interaction with damaged nucleosomal DNA.来自着色性干皮病细胞的染色质相关DNA内切核酸酶在与受损核小体DNA的相互作用中存在缺陷。
Mutat Res. 1990 Mar;235(2):65-80. doi: 10.1016/0921-8777(90)90059-e.
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Reactivation of psoralen-reacted plasmid DNA in Fanconi anemia, xeroderma pigmentosum, and normal human fibroblast cells.补骨脂素反应性质粒DNA在范可尼贫血、着色性干皮病和正常人成纤维细胞中的再激活
Somat Cell Mol Genet. 1991 May;17(3):229-38. doi: 10.1007/BF01232819.
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Clinical, cellular, and molecular features of an Israeli xeroderma pigmentosum family with a frameshift mutation in the XPC gene: sun protection prolongs life.一个XPC基因发生移码突变的以色列着色性干皮病家族的临床、细胞和分子特征:防晒可延长寿命。
J Invest Dermatol. 2000 Dec;115(6):974-80. doi: 10.1046/j.1523-1747.2000.00190.x.
8
DNA repair in human cells containing photoadducts of 8-methoxypsoralen or angelicin.含有8-甲氧基补骨脂素或当归素光加合物的人类细胞中的DNA修复
Cancer Res. 1980 Mar;40(3):696-702.
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Sedimentation of DNA from human fibroblasts irradiated with ultraviolet light: possible detection of excision breaks in normal and repair-deficient xeroderma pigmentosum cells.紫外线照射后人成纤维细胞中DNA的沉降:正常及色素性干皮病修复缺陷细胞中切除断裂的可能检测
Radiat Res. 1974 Feb;57(2):207-27.
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Single-strand breaks in DNA during repair of UV-induced damage in normal human and xeroderma pigmentosum cells as determined by alkaline DNA unwinding and hydroxylapatite chromatography: effects of hydroxyurea, 5-fluorodeoxyuridine and 1-beta-D-arabinofuranosylcytosine on the kinetics of repair.通过碱性DNA解旋和羟基磷灰石层析法测定正常人及着色性干皮病细胞中紫外线诱导损伤修复过程中DNA的单链断裂:羟基脲、5-氟脱氧尿苷和1-β-D-阿拉伯呋喃糖基胞嘧啶对修复动力学的影响
Mutat Res. 1979 Feb;59(2):257-71. doi: 10.1016/0027-5107(79)90164-7.

引用本文的文献

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Crit Rev Biochem Mol Biol. 2010 Feb;45(1):23-49. doi: 10.3109/10409230903501819.
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Repair of laser-localized DNA interstrand cross-links in G1 phase mammalian cells.G1期哺乳动物细胞中激光定位的DNA链间交联的修复
J Biol Chem. 2009 Oct 9;284(41):27908-27917. doi: 10.1074/jbc.M109.029025. Epub 2009 Aug 14.
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Initiation of DNA interstrand cross-link repair in humans: the nucleotide excision repair system makes dual incisions 5' to the cross-linked base and removes a 22- to 28-nucleotide-long damage-free strand.
人类DNA链间交联修复的起始:核苷酸切除修复系统在交联碱基的5'端进行双重切口,并切除一条22至28个核苷酸长的无损伤链。
Mol Cell Biol. 1997 Dec;17(12):6822-30. doi: 10.1128/MCB.17.12.6822.