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.
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。
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