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本文引用的文献

1
Use of mixed infections with Salmonella strains to study virulence genes and their interactions in vivo.利用沙门氏菌菌株的混合感染来研究体内毒力基因及其相互作用。
Microbes Infect. 2001 Nov-Dec;3(14-15):1345-52. doi: 10.1016/s1286-4579(01)01496-4.
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Complete genome sequence of Salmonella enterica serovar Typhimurium LT2.肠炎沙门氏菌鼠伤寒血清型LT2全基因组序列
Nature. 2001 Oct 25;413(6858):852-6. doi: 10.1038/35101614.
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Characterization of the Escherichia coli sigma E regulon.大肠杆菌σE调控子的表征
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The SurA periplasmic PPIase lacking its parvulin domains functions in vivo and has chaperone activity.缺少小泛素相关修饰蛋白结构域的SurA周质肽脯氨酰顺反异构酶在体内发挥作用并具有伴侣活性。
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Chaperone function of FkpA, a heat shock prolyl isomerase, in the periplasm of Escherichia coli.热休克脯氨酰异构酶FkpA在大肠杆菌周质中的伴侣功能。
Mol Microbiol. 2001 Jan;39(1):199-210. doi: 10.1046/j.1365-2958.2001.02250.x.
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Salmonella enterica serovar typhimurium surA mutants are attenuated and effective live oral vaccines.肠炎沙门氏菌鼠伤寒血清型surA突变体是减毒且有效的口服活疫苗。
Infect Immun. 2000 Mar;68(3):1109-15. doi: 10.1128/IAI.68.3.1109-1115.2000.
7
A temperature-dependent switch from chaperone to protease in a widely conserved heat shock protein.一种广泛保守的热休克蛋白中从伴侣蛋白到蛋白酶的温度依赖性转变。
Cell. 1999 Apr 30;97(3):339-47. doi: 10.1016/s0092-8674(00)80743-6.
8
The alternative sigma factor, sigmaE, is critically important for the virulence of Salmonella typhimurium.替代σ因子σE对鼠伤寒沙门氏菌的毒力至关重要。
Infect Immun. 1999 Apr;67(4):1560-8. doi: 10.1128/IAI.67.4.1560-1568.1999.
9
The sigma(E) and the Cpx signal transduction systems control the synthesis of periplasmic protein-folding enzymes in Escherichia coli.σ(E) 和Cpx信号转导系统控制大肠杆菌周质蛋白折叠酶的合成。
Genes Dev. 1997 May 1;11(9):1183-93. doi: 10.1101/gad.11.9.1183.
10
Decreased intracellular survival of an fkpA mutant of Salmonella typhimurium Copenhagen.鼠伤寒沙门氏菌哥本哈根fkpA突变体的细胞内存活能力降低。
Infect Immun. 1997 Feb;65(2):806-10. doi: 10.1128/iai.65.2.806-810.1997.

周质肽基脯氨酰异构酶在鼠伤寒沙门氏菌毒力中的作用。

Role of periplasmic peptidylprolyl isomerases in Salmonella enterica serovar Typhimurium virulence.

作者信息

Humphreys Sue, Rowley Gary, Stevenson Andrew, Kenyon William J, Spector Michael P, Roberts Mark

机构信息

Molecular Bacteriology Group, Institute of Comparative Medicine, Department of Veterinary Pathology, Glasgow University Veterinary School, Glasgow G61 1QH, United Kingdom.

出版信息

Infect Immun. 2003 Sep;71(9):5386-8. doi: 10.1128/IAI.71.9.5386-5388.2003.

DOI:10.1128/IAI.71.9.5386-5388.2003
PMID:12933889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC187313/
Abstract

FkpA is a peptidylprolyl isomerase whose expression is regulated by the alternative sigma factor, sigma factor E (sigma(E)). In contrast to the results of a previous report, inactivation of fkpA was found to have only a minor effect on the ability of Salmonella enterica serovar Typhimurium to invade and survive within epithelial and macrophage cell lines and cause infection in mice. However, an effect of the fkpA mutation on serovar Typhimurium virulence was seen if the mutation was combined with mutations in surA or htrA, two other sigma(E)-regulated genes, which encode proteins involved in protein folding and/or degradation in the periplasm.

摘要

FkpA是一种肽基脯氨酰异构酶,其表达受替代σ因子E(σE)调控。与之前一份报告的结果相反,研究发现fkpA的失活对鼠伤寒沙门氏菌侵袭上皮细胞系和巨噬细胞系并在其中存活以及在小鼠体内引发感染的能力仅有轻微影响。然而,如果fkpA突变与surA或htrA(另外两个受σE调控的基因)的突变相结合,就会观察到fkpA突变对鼠伤寒沙门氏菌毒力的影响,surA和htrA编码参与周质中蛋白质折叠和/或降解的蛋白质。