EC Number   |
General Information |
Reference |
|---|
   3.4.24.83 | metabolism |
about 30% demetallation is observed at pH values close to those found in late endosomes. A substantial proportion of lethal factor molecules may not be in their zinc-bound state prior to translocation |
733866 |
| 3.4.24.83 | physiological function |
anthrax lethal factor of Bacillus anthracis is a major factor for lethality of anthrax infection |
718744 |
| 3.4.24.83 | physiological function |
anthrax lethal toxin disrupts endothelial, intestinal epithelial, alveolar-endothelial and blood brain barriers of the host |
721083 |
| 3.4.24.83 | physiological function |
anthrax lethal toxin is a virulence factor of Bacilillus anthracis that is a bivalent toxin, containing lethal factor and protective Ag proteins, which causes cytotoxicity and altered macrophage function. Anthrax lethal toxin exposure results in early K+ efflux from macrophages associated with caspase-1 activation and increased interleukin-1beta release |
720157 |
| 3.4.24.83 | physiological function |
high glucose-induced activation of the MAPK extracellular signal-regulated kinase (ERK1/2) and p38 in the ARPE cell line is blocked by the enzyme. High glucose induced ARPE cells over proliferation is inhibited by the enzyme |
753933 |
| 3.4.24.83 | physiological function |
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 |
| 3.4.24.83 | physiological function |
in lethal systemic anthrax, proliferating bacilli secrete large quantities of the toxins lethal factor (LF) and oedema factor (EF), leading to widespread vascular leakage and shock. Coordinated disruption of the Rab11/Sec15 exocyst by anthrax toxins may contribute to toxin-dependent barrier disruption and vascular dysfunction during Bacillus anthracis infection. LF and EF synergistically inhibit Notch signaling and inhibit Rab11/Sec15-dependent recycling |
720541 |
| 3.4.24.83 | physiological function |
in mice treated with Anthrax lethal factor, serum lactate levels are reduced. Lethal factor inhibits the accumulation of hypoxia-inducible factor HIF-1alpha, a subunit of HIF-1, the master regulator directing cellular responses to hypoxia. The toxin has no effect on the transcription or protein turnover of HIF-1LPH, but inhibits HIF-1alpha translation. Lethal factor treatment diminishes phosphorylation of eIF4B, eIF4E, and rpS6, critical components of the intracellular machinery required for HIF-1alpha translation. Lethal factor treatment decreases the survival of hepatocyte cell lines grown in hypoxic conditions, an effect that is overcome by preinduction of HIF-1alpha |
734292 |
| 3.4.24.83 | physiological function |
lethal toxin (LeTx) containing lethal factor is the major virulence factor contributing to anthrax. LeTx-mediated MAPKK inhibition alters endothelial cell function |
721081 |
| 3.4.24.83 | physiological function |
secreted type-IIA phospholipase A2sPLA2-IIA expression is induced via a sequential MAPK-NF-kappaB activation and anthrax lethal toxin inhibits this expression likely by interfering with the transactivation of NF-kappaB in the nucleus. Anthrax lethal toxin inhibits IL-1b-induced p38 phosphorylation as well as sPLA2-IIA promoter activity in CHO cells. Inhibition of sPLA2-IIA promoter activity is mimicked by co-transfection with dominant negative construct of p38 and reversed by the active form of p38-MAPK. Both anthrax lethal toxin and the dominant negative construct of p38 decrease IL-1b-induced NF-kappaB luciferase activity. Neither anthrax lethal toxin nor specific p-38 inhibitor interfere with LPS-induced IkappaBalpha degradation or NF-kappaB nuclear translocation in guinea pig alveolar macrophages. Subcutaneous administration of anthrax lethal toxin to guinea pig before LPS challenge reduces sPLA2-IIA levels in broncho-alveolar lavages and ear |
711159 |
