EC Number   |
Application |
Reference |
|---|
   3.4.24.83 | medicine |
administration of lethal factor proteases early in the infection inhibits dissemination of vegetative bacteria to the organs in the first 32 h following infection. Neutralizing antibodies against edema factor also inhibit bacterial dissemination with similar efficacy |
733112 |
| 3.4.24.83 | medicine |
anthrax lethal factor is a specific biomarker of active infection by Bacillus anthracis |
718573 |
| 3.4.24.83 | 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 |
699322 |
| 3.4.24.83 | medicine |
anthrax toxin entry and activity differs among immune cells. Macrophages, dendritic cells, and B cells display higher activity of a of fusion protein of the anthrax toxin lethal factor N-terminal domain LFn, residues 1-254, with beta-lactamase, i.e. LFnBLA, than CD4+ and CD8+ T cells in both spleen cell suspension and the purified samples of individual cell types. Expression of anthrax toxin receptor CMG2 is higher in CD4+ and CD8+ T cells, which is not correlated to the intracellular LFnBLA activity |
713352 |
| 3.4.24.83 | 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 |
700915 |
| 3.4.24.83 | medicine |
blood borne lethal toxin is a novel therapeutic target for combating anthrax |
720419 |
| 3.4.24.83 | molecular biology |
celastrol is identified as an inhibitor of lethal toxin-mediated macrophage lysis and suggests an inhibitory mechanism involving inhibition of the proteasome pathway |
700878 |
| 3.4.24.83 | medicine |
engineered lethal anthrax toxin prevents tumor growth by inhibiting angiogenesis (10 nmol/l engineered protective antigen + 5.5 nmol/l lethal factor) |
700136 |
| 3.4.24.83 | medicine |
human medical countermeasures for anthrax |
669066 |
| 3.4.24.83 | medicine |
in a murine model of intoxication, lethal factor causes the dose-dependent disruption of intestinal epithelial integrity, characterized by mucosal erosion, ulceration, and bleeding. The pathology correlates with a blockade of intestinal crypt cell proliferation, accompanied by marked apoptosis in the villus tips. Treated mice nearly uniformly develop systemic infections with commensal enteric organisms within 72 hours of administration. Intestinal pathology depends upon lethal factor proteolytic activity and is partially attenuated by co-administration of broad spectrum antibiotics |
735046 |
