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Activation of SoxR by overproduction of desulfoferrodoxin: multiple ways to induce the soxRS regulon.通过过量生产脱硫铁氧化还原蛋白激活SoxR：诱导soxRS调控子的多种方式。
J Bacteriol. 2000 Mar;182(6):1761-3. doi: 10.1128/JB.182.6.1761-1763.2000.
2
The soxRS response of Escherichia coli can be induced in the absence of oxidative stress and oxygen by modulation of NADPH content.大肠杆菌的 SoxRS 应答可以通过调节 NADPH 含量在没有氧化应激和氧气的情况下被诱导。
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Sensing and protecting against superoxide stress in Escherichia coli--how many ways are there to trigger soxRS response?大肠杆菌中超氧化物应激的感知与防护——引发soxRS应答有多少种方式？
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The SoxRS response of Escherichia coli is directly activated by redox-cycling drugs rather than by superoxide.大肠杆菌 SoxRS 反应直接受氧化还原循环药物激活，而非超氧化物激活。
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Hydrogen peroxide activates the SoxRS regulon in vivo.过氧化氢在体内激活SoxRS调节子。
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Molecular characterization of the soxRS genes of Escherichia coli: two genes control a superoxide stress regulon.大肠杆菌soxRS基因的分子特征：两个基因控制一个超氧化物应激调节子。
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Transcription Factors That Defend Bacteria Against Reactive Oxygen Species.保护细菌抵御活性氧的转录因子。
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Escherichia coli avoids high dissolved oxygen stress by activation of SoxRS and manganese-superoxide dismutase.大肠杆菌通过 SoxRS 和锰超氧化物歧化酶的激活来避免高溶解氧应激。
Microb Cell Fact. 2013 Mar 12;12:23. doi: 10.1186/1475-2859-12-23.
3
Does UVB radiation induce SoxS gene expression in Escherichia coli cells?紫外线B辐射会诱导大肠杆菌细胞中SoxS基因的表达吗？
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The flavoenzyme ferredoxin (flavodoxin)-NADP(H) reductase modulates NADP(H) homeostasis during the soxRS response of Escherichia coli.黄素酶铁氧化还原蛋白（黄素氧还蛋白）-NADP(H)还原酶在大肠杆菌的soxRS应答过程中调节NADP(H)的稳态。
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Hydrogen peroxide activates the SoxRS regulon in vivo.过氧化氢在体内激活SoxRS调节子。
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本文引用的文献

1
Reaction of the desulfoferrodoxin from Desulfoarculus baarsii with superoxide anion. Evidence for a superoxide reductase activity.巴氏脱硫弧菌脱硫铁氧化还原蛋白与超氧阴离子的反应。超氧化物还原酶活性的证据。
J Biol Chem. 2000 Jan 7;275(1):115-21. doi: 10.1074/jbc.275.1.115.
2
Isolation of reductase for SoxR that governs an oxidative response regulon from Escherichia coli.从大肠杆菌中分离出调控氧化应激反应调节子的SoxR还原酶。
FEBS Lett. 1999 May 28;451(3):227-30. doi: 10.1016/s0014-5793(99)00565-7.
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Induction of the soxRS regulon of Escherichia coli by superoxide.
J Biol Chem. 1999 Apr 2;274(14):9479-81. doi: 10.1074/jbc.274.14.9479.
4
Balance between endogenous superoxide stress and antioxidant defenses.内源性超氧化物应激与抗氧化防御之间的平衡。
J Bacteriol. 1998 Mar;180(6):1402-10. doi: 10.1128/JB.180.6.1402-1410.1998.
5
Redox signal transduction via iron-sulfur clusters in the SoxR transcription activator.通过SoxR转录激活因子中的铁硫簇进行的氧化还原信号转导。
Trends Biochem Sci. 1997 Jun;22(6):207-10. doi: 10.1016/s0968-0004(97)01068-2.
6
Regulation of the soxRS oxidative stress regulon. Reversible oxidation of the Fe-S centers of SoxR in vivo.soxRS氧化应激调节子的调控。体内SoxR的铁硫中心的可逆氧化。
J Biol Chem. 1997 Feb 21;272(8):5082-6. doi: 10.1074/jbc.272.8.5082.
7
Redox signal transduction: mutations shifting [2Fe-2S] centers of the SoxR sensor-regulator to the oxidized form.氧化还原信号转导：突变导致SoxR传感调节蛋白的[2Fe-2S]中心转变为氧化形式。
Cell. 1997 Jan 10;88(1):121-9. doi: 10.1016/s0092-8674(00)81864-4.
8
The redox state of the [2Fe-2S] clusters in SoxR protein regulates its activity as a transcription factor.SoxR蛋白中[2Fe-2S]簇的氧化还原状态调节其作为转录因子的活性。
J Biol Chem. 1996 Dec 27;271(52):33173-5. doi: 10.1074/jbc.271.52.33173.
9
Redox signaling and gene control in the Escherichia coli soxRS oxidative stress regulon--a review.大肠杆菌soxRS氧化应激调节子中的氧化还原信号传导与基因调控——综述
Gene. 1996 Nov 7;179(1):53-7. doi: 10.1016/s0378-1119(96)00329-0.
10
Overproduction of the rbo gene product from Desulfovibrio species suppresses all deleterious effects of lack of superoxide dismutase in Escherichia coli.来自脱硫弧菌属物种的rbo基因产物的过量产生抑制了大肠杆菌中缺乏超氧化物歧化酶的所有有害影响。
J Bacteriol. 1996 Dec;178(23):6736-42. doi: 10.1128/jb.178.23.6736-6742.1996.

通过过量生产脱硫铁氧化还原蛋白激活SoxR：诱导soxRS调控子的多种方式。

Activation of SoxR by overproduction of desulfoferrodoxin: multiple ways to induce the soxRS regulon.

作者信息

Gaudu P, Dubrac S, Touati D

机构信息

Institut Jacques Monod, CNRS-Universités Paris 6 et Paris 7, 75251 Paris Cedex 05, France.

出版信息

J Bacteriol. 2000 Mar;182(6):1761-3. doi: 10.1128/JB.182.6.1761-1763.2000.

DOI:10.1128/JB.182.6.1761-1763.2000
PMID:10692385
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC94477/
Abstract

The soxRS response, which protects cells against superoxide toxicity, is triggered by the oxidation of SoxR, a transcription factor. Superoxide excess and NADPH depletion induce the regulon. Unexpectedly, we found that the overproduction of desulfoferrodoxin, a superoxide reductase from sulfate-reducing bacteria, also induced this response. We suggest that desulfoferrodoxin interferes with the reducing pathway that keeps SoxR in its inactive form.

摘要

soxRS应答可保护细胞免受超氧化物毒性的影响，它由转录因子SoxR的氧化所触发。超氧化物过量和NADPH耗竭会诱导这一调控子。出乎意料的是，我们发现脱硫铁氧化还原蛋白（一种来自硫酸盐还原菌的超氧化物还原酶）的过量表达也会诱导这种应答。我们认为脱硫铁氧化还原蛋白干扰了使SoxR保持无活性形式的还原途径。