Literature summary for 3.4.24.83 extracted from

Xu, L.; Fang, H.; Frucht, D.M.
Anthrax lethal toxin increases superoxide production in murine neutrophils via differential effects on MAPK signaling pathways (2008), J. Immunol., 180, 4139-4147.

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Application

Application	Comment	Organism
molecular biology	anthrax lethal toxin treatment of neutrophils disrupts signaling to downstream MAPK targets in response to TLR stimulation. Following anthrax lethal toxin treatment, ERK family and p38 phosphorylation are nearly completely blocked, but signaling to JNK family members persists in vitro and ex vivo. In contrast to previous reports involving human neutrophils, anthrax lethal toxin treatment of murine neutrophils increases their production of superoxide in response to PMA or TLR stimulation in vitro or ex vivo. Although this enhanced superoxide production correlates with effects due to the lethal toxin-induced blockade of ERK signaling, it requires JNK signaling that remains largely intact despite the activity of anthrax lethal toxin	Bacillus anthracis

Organism

Organism	UniProt	Comment	Textmining
Bacillus anthracis	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
additional information	anthrax lethal toxin binds and enters murine neutrophils	Bacillus anthracis	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
mitogen-activated protein kinase kinase + H2O	anthrax lethal toxin cleaves mitogen-activated protein kinase kinase/MEK/MAPKK 1-4 and 6, but not mitogen-activated protein kinase kinase 5 and 7 in murine neutrophils	Bacillus anthracis	?	-	?

Synonyms

Synonyms	Comment	Organism
anthrax lethal toxin	-	Bacillus anthracis

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Release 2023.1 (January 2023)