Literature summary for 3.2.2.22 extracted from

Landoni, V.I.; de Campos-Nebel, M.; Schierloh, P.; Calatayud, C.; Fernandez, G.C.; Ramos, M.V.; Rearte, B.; Palermo, M.S.; Isturiz, M.A.
Shiga toxin 1-induced inflammatory response in lipopolysaccharide-sensitized astrocytes is mediated by endogenous tumor necrosis factor alpha (2010), Infect. Immun., 78, 1193-1201.

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Activating Compound

Activating Compound	Comment	Organism	Structure
additional information	inflammatory mediators such as bacterial lipopolysaccharide and polymorphonuclear neutrophils contribute to hemolytic-uremic syndrome pathophysiology by potentiating Stx effects in human astrocytes. Inhibition of NF-kappaB or blockade of TNF-alpha activity abrogates effects mediated by Stx1 in lipopolysaccharide-sensitized astrocytes	Escherichia coli

Organism

Organism	UniProt	Comment	Textmining
Escherichia coli	-	Shiga-toxin producing strains	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
additional information	Stx1 binding and internalization in L929 human host cells, and cytotoxicity, overview	Escherichia coli	-

Synonyms

Synonyms	Comment	Organism
Shiga toxin 1	-	Escherichia coli
Stx type 1	-	Escherichia coli
Stx1	-	Escherichia coli

General Information

General Information	Comment	Organism
malfunction	hemolytic-uremic syndrome is generally caused by Shiga toxin-producing Escherichia coli. Endothelial dysfunction mediated by Stx is a central aspect in hemolytic-uremic syndrome development. Inflammatory mediators such as bacterial lipopolysaccharide and polymorphonuclear neutrophils contribute to HUS pathophysiology by potentiating Stx effects, pathology, overview	Escherichia coli

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Release 2023.1 (January 2023)