1: Infect Immun. 1993 Oct;61(10):4427-33. 

Shigella flexneri invasion of HeLa cells induces NF-kappa B DNA-binding
activity.

Dyer RB, Collaco CR, Niesel DW, Herzog NK.

Department of Microbiology, University of Texas Medical Branch, Galveston
77555-0605.

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.

PMID: 8406833 [PubMed - indexed for MEDLINE]


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