Shigella flexneri invasion of HeLa cells induces NF-kappa B DNA-binding activity.
Shigella flexneri invasion of HeLa cells induces NF-kappa B DNA-binding activity.
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福氏志贺氏菌入侵 HeLa 细胞可诱导 NF-kappa B DNA 结合活性。
DOI：
10.1128/iai.61.10.4427-4433.1993
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发表时间：
1993
影响因子：
3.1
通讯作者：
Herzog,NK
中科院分区：
文献类型：
--
作者：
Dyer,RB;Collaco,CR;Niesel,DW;Herzog,NK
Although information about the genetic basis and mechanisms of Shigella flexneri cellular invasion is accumulating, little is known about changes in cell signaling and their consequences following bacterium-host cell interactions. A general result of signal transduction is alterations in the levels and/or activities of transcription factors. Alterations in transcription factor binding activities were observed following challenge with S. flexneri. Changes in the DNA-binding activities of cellular transcription factors to AP1, AP2, cyclic AMP response element, CTF1/NF1, NF-kappa B/Rel, OCT1, and SP1 DNA-binding sites were investigated by electrophoretic mobility shift assays. NF-kappa B/Rel DNA-binding activity was enhanced more than 11-fold by cellular invasion; noninvasive S. flexneri strains induced low levels of kappa B DNA binding. Both subunits of the NF-kappa B transcription factor, p50 and p65, but not c-Rel (p85), are components of the kappa B DNA-binding activity. These data suggest that changes in cellular transcription factor binding activity are a consequence of S. flexneri invasion, and these changes could play a role in the initial host response or in the pathogenesis of the disease.
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DOI：
10.1073/pnas.89.13.5976
发表时间：
1992-07-01
影响因子：
11.1
作者：
GINOCCHIO, C;PACE, J;GALAN, JE
通讯作者：
GALAN, JE
介导福氏志贺氏菌感染的宿主细胞早期死亡的代谢事件。
影响因子：
3.8
作者：
P. Sansonetti;J. Mounier
通讯作者：
J. Mounier
影响因子：
64.8
作者：
GALAN, JE;PACE, J;HAYMAN, MJ
通讯作者：
HAYMAN, MJ
福氏志贺氏菌进入 HeLa 细胞所需的质粒基因座的定位，以及编码四种免疫原性多肽的一个基因座的表征。
DOI：
--
发表时间：
1987
期刊：
Journal of General Microbiology
影响因子：
--
作者：
B. Baudry;A. Maurelli;Philippe Clerc;J. Sadoff;P. Sansonetti
通讯作者：
P. Sansonetti
抑制性锚蛋白和激活剂 Rel 蛋白
影响因子：
9.2
作者：
G. Nolan;D. Baltimore
通讯作者：
D. Baltimore