Analysis of a novel back-up repair system for UV-induced DNA damage in human cells.

分析一种新型后备修复系统，用于修复人体细胞中紫外线引起的 DNA 损伤。

基本信息

批准号：
15310036
负责人：
MATSUNAGA Tsukasa
金额：
$ 7.55万
依托单位：
Kanazawa University, Graduate School of Natural Science and Technology
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

项目摘要

We have established a super-sensitive detection method for measuring cyclobutane pyrimidine dimers (CPDs) and (6-4)photoproducts (6-4PPs) induced by biological doses of ultraviolet (UV) light and suggested that human cells might have a novel repair system mainly for 6-4PPs other than nucleotide excision repair which has been thought to be only repair system for those lesions in humans so far. In this study, we have obtained the following findings.1.The removal of 6-4PPs was observed even in the embryonic fibroblasts derived from xpa(-/-) or xpg(-/-) knock-out mice (30-50% after 24 hr). In addition, the removal of CPDs was also detected in those cells with a less efficiency (20-30% after 48 hr).2.HeLa cells stably expressing AlwNI-type mutant XPA did not show any impairment of nucleotide excision repair activity, suggesting that this mutant XPA protein does not have a dominant-negative effect.3.We have further sensitized the detection method for CPDs, enabling us to determine the repair kinetics of CPDs in cells exposed to non-killing doses of Was low as 0.1 J/m^2. Under this condition, we have found that xeroderma pimentosum cells significantly remove CPDs (〜40% after 48hr).4.We could observe some weak enhancement of repair efficiency after UV irradiation of 1 J/m^2 when the human cells had been pie-exposed to 0.2 J/m^2. However, we need more extensive experiments to conclude whether the back-up repair system is under the control of adaptive responses.Taken together with those results, we concluded that mammalian cells have a certain back-up repair system, independent of XPA and XPG, which removes mainly 6-4PP but also CPDs with a less efficiency.

我们已经建立了一种测量环丁烷嘧啶二聚体（CPD）和（6-4pps）诱导的Y生物剂量的紫外线（UV）光的超敏感检测方法核苷酸的分离获得了以下发现。1。即使在源自XPA（ - / - ）敲除小鼠的胚胎纤维中观察到6-4pps的去除（24小时后30-50％）那些具有效率较低的细胞（48小时后20-30％）。稳定表达alwni-type突变体XPA的细胞没有显示出这种突变XPA蛋白没有主导性耐药作用的核苷酸示意性的任何损害。3。在这种联系下，我们已经进一步敏感了CPDS .1 j/m^2。 1 j/m^2构成0.2 j/m^2。系统，独立于XPA和XPG，它们主要删除6 -4pp，但效率较小。

项目成果

期刊论文数量（54）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Sakamoto, A.: "Disruption of the AtREV3 gene causes hypersensitivity to ultraviolet B light and γ-rays in Arabidopsis : implication of the presence of a translesion synthesis mechanism in plants"Plant Cell. 15(9). 2042-2057 (2003)

Sakamoto, A.：“AtREV3 基因的破坏导致拟南芥对紫外线 B 光和 γ 射线过敏：植物中存在跨损伤合成机制”Plant Cell 15(9)。

DOI：
发表时间：
期刊：
影响因子：
0
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Lan, L.: "Functional and physical interactions between ERCC1 and MSH2 for resistance to cis-platinum in mammalian cells"DNA Repair. 3(2). 135-143 (2004)

Lan, L.：“ERCC1 和 MSH2 之间的功能和物理相互作用对哺乳动物细胞中顺铂的抵抗力”DNA 修复。

DOI：
发表时间：
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影响因子：
0
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cDNA cloning of the chicken DDB1 gene encoding the p127 subunit of damaged DNA-binding protein.

编码受损 DNA 结合蛋白 p127 亚基的鸡 DDB1 基因的 cDNA 克隆。

DOI：
发表时间：
2003
期刊：
Gene Genet.Syst. 78(2)
影响因子：
0
作者：
Fu;D.
通讯作者：
D.

Disruption of the AtREV3 gene causes hypersensitivity to ultraviolet B light and γ-rays in Arabidopsis inplication of the presence of a translesion synthesis mechanism in plants.

AtREV3 基因的破坏会导致拟南芥对紫外线 B 光和 γ 射线过敏，这表明植物中存在跨损伤合成机制。

DOI：
发表时间：
2003
期刊：
Plant Cell 15
影响因子：
0
作者：
Sakamoto;A.;Lan;V.T.T.;Hase;Y.;Shikazono;N.;Matsunaga;T.;Tanaka;A.
通讯作者：
A.

Binding of 14-3-3beta but not 14-3-3sigma controls the cytoplasmic localization of CDC25B : binding site preferences of 14-3-3 subtypes and the subcellular localization of CDC25B.

14-3-3beta 但不是 14-3-3sigma 的结合控制 CDC25B 的细胞质定位：14-3-3 亚型的结合位点偏好和 CDC25B 的亚细胞定位。

DOI：
发表时间：
2004
期刊：
J.Cell Sci. 117
影响因子：
0
作者：
Uchida;S.;Kuma;A.;Ohtsubo;M.;Shimura;M.;Hirata;M.;Nakagama;H.;Matsunaga;T.;Ishizaka;Y.;Yamashita K.
通讯作者：
Yamashita K.