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通过缺失编码热休克σ因子的rpoH基因使大肠杆菌细胞对氧化应激敏感。

Sensitization of Escherichia coli cells to oxidative stress by deletion of the rpoH gene, which encodes the heat shock sigma factor.

作者信息

Kogoma T, Yura T

机构信息

Institute for Virus Research, Kyoto University, Japan.

出版信息

J Bacteriol. 1992 Jan;174(2):630-2. doi: 10.1128/jb.174.2.630-632.1992.

DOI:10.1128/jb.174.2.630-632.1992
PMID:1729253
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC205760/
Abstract

A deletion in the rpoH gene greatly increased the sensitivity of Escherichia coli sodA sodB mutants to oxidative stress. The effect of the rpoH deletion on sodA+ sodB+ cells was only marginal. Mutations in heat shock genes singly sensitized sodA sodB double mutant cells to plumbagin. sodA sodB double mutants were neither more sensitive nor more resistant to thermal stress than the wild type.

摘要

rpoH基因的缺失极大地增加了大肠杆菌sodA sodB突变体对氧化应激的敏感性。rpoH基因缺失对sodA+ sodB+细胞的影响很小。热休克基因中的突变单独使sodA sodB双突变体细胞对白花丹醌敏感。sodA sodB双突变体对热应激的敏感性既不高于也不低于野生型。

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本文引用的文献

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AppppA and related adenylylated nucleotides are synthesized as a consequence of oxidation stress.AppppA及相关的腺苷酸化核苷酸是氧化应激的产物。 （注：原文中AppppA多了几个p，推测可能有误，正常应该是pppA之类的，这里按照正确理解翻译，但严格来说原文有误。）
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