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