Application | Comment | Organism |
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molecular biology | Bacillus anthracis represses the immune response, in part by altering chromatin accessibility of IL-8 promoter to NFkappaB in epithelial cells. This epigenetic reprogramming, in addition to previously reported effects of lethal toxin, represents an efficient strategy used by Bacillus anthracis for invading the host | Bacillus anthracis |
Protein Variants | Comment | Organism |
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additional information | intranasal instillationin a mouse model of pulmonary anthrax of a Bacillus anthracis strain RPLC2 bearing inactive lethal toxin (double mutant) lethal toxin stimulates cytokine production (IL-6 and KC, mouse orthologue of IL-8) and polymorphonuclear neutrophils recruitment in lungs. These responses are repressed by a prior instillation of an lethal toxin preparation. In contrast, instillation of a Bacillus anthracis strain expressing active lethal toxin represses lung inflammation. The inhibitory effects of lethal toxin on cytokine production are associated with an alteration of ERK and p38-MAPK phosphorylation, but not JNK phosphorylation. Although NF-kappaB is essential for IL-8 expression, lethal toxin downregulates this expression without interfering with NF-kappaB activation in epithelial cells. Lethal toxin selectively prevents histone H3 phosphorylation at Ser 10 and recruitment of the p65 subunit of NF-kappaB at the IL-8 and KC promoters | Bacillus anthracis |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
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additional information | Bacillus anthracis | prevention of inflammatory response of immune system by preventing interleukin-8 expression: selective blocking of histone H3 phosphorylation at serine 10 and acetylation at lysine 14, H3 normally promotes the accessibility of NF-kappaB (transcription factor for inflammatory gene expression) to target promoters, the histone blocking is mitigated by cleaving mitogen-activated protein kinase kinase, thus preventing the activation of p38-mitogen-activated protein kinase and extracellular signal-regulated kinase | ? | - |
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Organism | UniProt | Comment | Textmining |
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Bacillus anthracis | - |
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Bacillus anthracis | - |
single mutant strain RP9 producing active lethal factor and inactive edema factor, and double-mutant strain RPLC2 producing inactive lethal factor and edema factor, action in mouse model and in human epithelial lung cells | - |
Source Tissue | Comment | Organism | Textmining |
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Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
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additional information | prevention of inflammatory response of immune system by preventing interleukin-8 expression: selective blocking of histone H3 phosphorylation at serine 10 and acetylation at lysine 14, H3 normally promotes the accessibility of NF-kappaB (transcription factor for inflammatory gene expression) to target promoters, the histone blocking is mitigated by cleaving mitogen-activated protein kinase kinase, thus preventing the activation of p38-mitogen-activated protein kinase and extracellular signal-regulated kinase | Bacillus anthracis | ? | - |
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Synonyms | Comment | Organism |
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anthrax lethal toxin | - |
Bacillus anthracis |
anthrax lethal toxin | LT | Bacillus anthracis |