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Literature summary for 3.2.2.22 extracted from

  • Jandhyala, D.; Rogers, T.; Kane, A.; Paton, A.; Paton, J.; Thorpe, C.
    Shiga toxin 2 and flagellin from Shiga-toxigenic Escherichia coli superinduce interleukin-8 through synergistic effects on host stress-activated protein kinase activation (2010), Infect. Immun., 78, 2984-2994.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.2.2.22

Organism

Organism UniProt Comment Textmining
Escherichia coli
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-
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Escherichia coli 98NK2 (O113:H21)
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-
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
28S rRNA + H2O
-
 Escherichia coli ?
-
 ?
28S rRNA + H2O
-
 Escherichia coli 98NK2 (O113:H21) ?
-
 ?

Synonyms

Synonyms Comment Organism
ribosome inactivating protein
-
 Escherichia coli
RIP
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 Escherichia coli
Shiga toxin 2
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 Escherichia coli
Stx2
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 Escherichia coli

General Information

General Information Comment Organism
physiological function Shiga toxins (Stx) expressed in the intestinal lumen during infection with Shiga-toxigenic Escherichia coli must translocate across the epithelium and enter the systemic circulation to cause systemic (pathological) effects, including hemolytic uremic syndrome. Even though Stxs are potent protein synthesis inhibitors, both isoforms Stx1 and Stx2 have been shown to upregulate interleukin-8 protein expression in intestinal epithelial cells via the ribotoxic stress response, a signal transduction event resulting from specific damage to the 28S rRNA that causes activation of host stress-activated protein kinases. Stx1 and Stx2 are also capable of inducing MAPK activation in vitro Escherichia coli