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共济失调毛细血管扩张症淋巴母细胞样细胞中的DNA修复合成

DNA-repair synthesis in ataxia telangiectasis lymphoblastoid cells.

作者信息

Ford M D, Houldsworth J, Lavin M F

出版信息

Mutat Res. 1981 Dec;84(2):419-27. doi: 10.1016/0027-5107(81)90209-8.

DOI:10.1016/0027-5107(81)90209-8
PMID:6278301
Abstract

The ability of a number of Epstein-Barr virus-transformed lymphoblastoid cells from ataxia telangiectasis (AT) patients to repair gamma-radiation damage to DNA was determined. All of these AT cells were previously shown to be hypersensitive to gamma-radiation. Two methods were used to determine DNA-repair synthesis: isopycnic gradient analysis and a method employing hydroxyurea to inhibit semiconservative DNA synthesis. Control, AT heterozygote and AT homozygote cells were demonstrated to have similar capacities for repair of radiation damage to DNA. In addition at high radiation doses (10-40 krad) the extent of inhibition of DNA synthesis was similar in the different cell types.

摘要

测定了一些来自共济失调毛细血管扩张症(AT)患者的爱泼斯坦-巴尔病毒转化的淋巴母细胞修复γ射线对DNA损伤的能力。所有这些AT细胞先前已被证明对γ射线高度敏感。使用了两种方法来测定DNA修复合成:等密度梯度分析和一种采用羟基脲抑制半保留DNA合成的方法。已证明对照细胞、AT杂合子细胞和AT纯合子细胞修复DNA辐射损伤的能力相似。此外,在高辐射剂量(10 - 40千拉德)下,不同细胞类型中DNA合成的抑制程度相似。

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1
DNA-repair synthesis in ataxia telangiectasis lymphoblastoid cells.共济失调毛细血管扩张症淋巴母细胞样细胞中的DNA修复合成
Mutat Res. 1981 Dec;84(2):419-27. doi: 10.1016/0027-5107(81)90209-8.
2
Ionizing radiation and DNA-chain elongation in ataxia telangiectasia lymphoblastoid cells.共济失调毛细血管扩张症淋巴母细胞样细胞中的电离辐射与DNA链延长
Mutat Res. 1986 Mar;165(2):117-22. doi: 10.1016/0167-8817(86)90067-2.
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Caffeine does not potentiate gamma-radiation induced DNA damage in ataxia telangiectasia lymphoblastoid cells.
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Gamma-irradiation induces mutation in ataxia-telangiectasia lymphoblastoid cells.
Gan. 1984 Dec;75(12):1040-3.
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Transformation and repair replication in lymphocytes from ataxia telangiectasia.共济失调毛细血管扩张症患者淋巴细胞中的转化与修复复制
Proc Soc Exp Biol Med. 1983 Apr;172(4):524-34. doi: 10.3181/00379727-172-41598.
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Induction of p53 protein by gamma radiation in lymphocyte lines from breast cancer and ataxia telangiectasia patients.γ射线对乳腺癌和共济失调毛细血管扩张症患者淋巴细胞系中p53蛋白的诱导作用。
Br J Cancer. 1995 Nov;72(5):1096-101. doi: 10.1038/bjc.1995.471.
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Elevated frequency of p53-independent apoptosis after irradiation increases levels of DNA breaks in ataxia telangiectasia lymphoblasts.共济失调毛细血管扩张症淋巴母细胞受照射后,p53非依赖型凋亡频率升高,导致DNA断裂水平增加。
Int J Radiat Biol. 1997 Sep;72(3):257-69. doi: 10.1080/095530097143257.
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Differential expression of Epstein-Barr virus (EBV) genes BBRF3, BILF1, and BMRF2 in EBV-transformed lymphoblastoid lines from ataxia-telangiectasia patients.共济失调毛细血管扩张症患者的EB病毒(EBV)转化淋巴母细胞系中EBV基因BBRF3、BILF1和BMRF2的差异表达
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High sensitivity but normal DNA-repair activity after UV irradiation in Epstein--Barr virus-transformed lymphoblastoid cell lines from Chediak--Higashi syndrome.来自切-东综合征患者的爱泼斯坦-巴尔病毒转化淋巴母细胞系在紫外线照射后具有高敏感性但DNA修复活性正常。
Mutat Res. 1980 Aug;72(1):143-50. doi: 10.1016/0027-5107(80)90230-4.
10
Increased initial levels of chromosome damage and heterogeneous chromosome repair in ataxia telangiectasia heterozygote cells.共济失调毛细血管扩张症杂合子细胞中染色体损伤初始水平增加及染色体修复异质性
Mutat Res. 1994 Oct 1;310(1):1-13. doi: 10.1016/0027-5107(94)90004-3.

引用本文的文献

1
Study of chromatin structure in ataxia-telangiectasia cells.共济失调毛细血管扩张症细胞中染色质结构的研究。
Mol Biol Rep. 1986;11(3):143-7. doi: 10.1007/BF00419734.
2
Ataxia-telangiectasia: an inherited disorder of ionizing-radiation sensitivity in man. Progress in the elucidation of the underlying biochemical defect.共济失调毛细血管扩张症:一种人类遗传性电离辐射敏感障碍。潜在生化缺陷阐释的进展。
Hum Genet. 1987 Mar;75(3):197-208. doi: 10.1007/BF00281059.