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Disease relevance of Anthrax


Psychiatry related information on Anthrax


High impact information on Anthrax

  • Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin [8].
  • The LDL receptor-related protein LRP6 mediates internalization and lethality of anthrax toxin [9].
  • LRP6 acts as a coreceptor with either TEM8 or CMG2, the two previously identified receptors for anthrax toxin [10].
  • Downregulation of LRP6 or coexpression of a truncated LRP6 dominant-negative peptide inhibited cellular uptake of complexes containing the protective antigen (PA) carrier of anthrax toxin moieties and protected targeted cells from death, as did antibodies against epitopes in the LRP6 extracellular domain [9].
  • Structural basis for the activation of anthrax adenylyl cyclase exotoxin by calmodulin [11].

Chemical compound and disease context of Anthrax

  • Treatment with antibiotics, including intravenous ciprofloxacin, rifampin, and clindamycin, and supportive therapy appears to have slowed the progression of inhalational anthrax and has resulted to date in survival [12].
  • PMN isolated in the absence of lipopolysaccharide (LPS) (less than 0.1 ng/ml) released only small amounts of O-2 after FMLP stimulation; pretreatment with anthrax toxin had little effect [1].
  • An important part of this strategy is to screen PE-resistant clones for those that retain sensitivity to both diphtheria toxin and to a fusion protein composed of lethal factor (from anthrax toxin) fused to the adenosine diphosphate-ribosylating domain of PE [13].
  • Adefovir dipivoxil is a clinically approved drug that can block the action of an anthrax toxin [14].
  • Binding of anthrax toxin to its receptor is similar to alpha integrin-ligand interactions [15].
  • In contrast to previous reports involving human neutrophils, anthrax LT treatment of murine neutrophils increases their production of superoxide in response to PMA or TLR stimulation in vitro or ex vivo [16].

Biological context of Anthrax


Anatomical context of Anthrax

  • Anthrax toxins include the lethal factor (LF), a mitogen-activated protein kinase (MAPK)-kinase-specific metalloprotease, which acts in the cell cytosol and plays a major part in anthrax pathogenesis [20].
  • Additionally, interrupting MAPK signaling with LeTx and elevating cAMP with anthrax edema toxin in both melanoma cells and melanocytes lead to dramatic melanin production, perhaps explaining the formation of blackened eschars in cutaneous anthrax [4].
  • We now report that anthrax LT treatment leads to the specific extracellular release of interleukin (IL)-1beta and IL-18 by the murine macrophage cell lines, RAW264.7 and J774A [21].
  • Specifically, anthrax LT inhibits IL-2 production and proliferative responses in CD4+ T cells, thereby blocking functions that are pivotal in the regulation of immune responses [22].
  • A new study has found that polymorphisms in the host gene kif1C, which encodes a kinesin-like motor protein, determine whether mouse macrophages are resistant or sensitive to anthrax lethal toxin [23].

Gene context of Anthrax

  • MEK1 cleaved with the lethal factor of the anthrax toxin can still be activated by its upstream mitotic kinases, and this form is fully active in the Golgi fragmentation process [24].
  • The current model for intoxication is that protective antigen (PA) toxin subunits bind a single group of cell-surface anthrax toxin receptors (ATRs), encoded by the tumor endothelial marker 8 (TEM8) gene [25].
  • These studies distinguish CMG2 as a second anthrax toxin receptor and identify a potent antitoxin that may prove useful for the treatment of anthrax [25].
  • Inhibition of MAPK signaling with either anthrax lethal toxin (LeTx) or small molecule MAPK kinase inhibitors triggers apoptosis in human melanoma cells [4].
  • This repression is noncompetitive and does not affect ligand binding or DNA binding, suggesting that anthrax lethal toxin (LeTx) probably exerts its effects through a cofactor(s) involved in the interaction between GR and the basal transcription machinery [26].

Analytical, diagnostic and therapeutic context of Anthrax


  1. Anthrax toxin blocks priming of neutrophils by lipopolysaccharide and by muramyl dipeptide. Wright, G.G., Mandell, G.L. J. Exp. Med. (1986) [Pubmed]
  2. Capsule synthesis by Bacillus anthracis is required for dissemination in murine inhalation anthrax. Drysdale, M., Heninger, S., Hutt, J., Chen, Y., Lyons, C.R., Koehler, T.M. EMBO J. (2005) [Pubmed]
  3. Potent antitumor activity of a urokinase-activated engineered anthrax toxin. Liu, S., Aaronson, H., Mitola, D.J., Leppla, S.H., Bugge, T.H. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  4. Apoptosis and melanogenesis in human melanoma cells induced by anthrax lethal factor inactivation of mitogen-activated protein kinase kinase. Koo, H.M., VanBrocklin, M., McWilliams, M.J., Leppla, S.H., Duesbery, N.S., Woude, G.F. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  5. EST-based genome-wide gene inactivation identifies ARAP3 as a host protein affecting cellular susceptibility to anthrax toxin. Lu, Q., Wei, W., Kowalski, P.E., Chang, A.C., Cohen, S.N. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  6. Annulling a dangerous liaison: vaccination strategies against AIDS and tuberculosis. Kaufmann, S.H., McMichael, A.J. Nat. Med. (2005) [Pubmed]
  7. Prediction of proprotein convertase cleavage sites. Duckert, P., Brunak, S., Blom, N. Protein Eng. Des. Sel. (2004) [Pubmed]
  8. Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin. Boyden, E.D., Dietrich, W.F. Nat. Genet. (2006) [Pubmed]
  9. The LDL receptor-related protein LRP6 mediates internalization and lethality of anthrax toxin. Wei, W., Lu, Q., Chaudry, G.J., Leppla, S.H., Cohen, S.N. Cell (2006) [Pubmed]
  10. LRP6 holds the key to the entry of anthrax toxin. Bann, J.G., Cegelski, L., Hultgren, S.J. Cell (2006) [Pubmed]
  11. Structural basis for the activation of anthrax adenylyl cyclase exotoxin by calmodulin. Drum, C.L., Yan, S.Z., Bard, J., Shen, Y.Q., Lu, D., Soelaiman, S., Grabarek, Z., Bohm, A., Tang, W.J. Nature (2002) [Pubmed]
  12. Clinical presentation of inhalational anthrax following bioterrorism exposure: report of 2 surviving patients. Mayer, T.A., Bersoff-Matcha, S., Murphy, C., Earls, J., Harper, S., Pauze, D., Nguyen, M., Rosenthal, J., Cerva, D., Druckenbrod, G., Hanfling, D., Fatteh, N., Napoli, A., Nayyar, A., Berman, E.L. JAMA (2001) [Pubmed]
  13. Pseudomonas exotoxin-mediated selection yields cells with altered expression of low-density lipoprotein receptor-related protein. FitzGerald, D.J., Fryling, C.M., Zdanovsky, A., Saelinger, C.B., Kounnas, M., Winkles, J.A., Strickland, D., Leppla, S. J. Cell Biol. (1995) [Pubmed]
  14. Selective inhibition of anthrax edema factor by adefovir, a drug for chronic hepatitis B virus infection. Shen, Y., Zhukovskaya, N.L., Zimmer, M.I., Soelaiman, S., Bergson, P., Wang, C.R., Gibbs, C.S., Tang, W.J. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  15. Binding of anthrax toxin to its receptor is similar to alpha integrin-ligand interactions. Bradley, K.A., Mogridge, J., Jonah, G., Rainey, A., Batty, S., Young, J.A. J. Biol. Chem. (2003) [Pubmed]
  16. Anthrax lethal toxin increases superoxide production in murine neutrophils via differential effects on MAPK signaling pathways. Xu, L., Fang, H., Frucht, D.M. J. Immunol. (2008) [Pubmed]
  17. Bacillus anthracis requires siderophore biosynthesis for growth in macrophages and mouse virulence. Cendrowski, S., MacArthur, W., Hanna, P. Mol. Microbiol. (2004) [Pubmed]
  18. A plasmid-encoded regulator couples the synthesis of toxins and surface structures in Bacillus anthracis. Mignot, T., Mock, M., Fouet, A. Mol. Microbiol. (2003) [Pubmed]
  19. The anthrax toxin activator gene atxA is associated with CO2-enhanced non-toxin gene expression in Bacillus anthracis. Hoffmaster, A.R., Koehler, T.M. Infect. Immun. (1997) [Pubmed]
  20. Stop the killer: how to inhibit the anthrax lethal factor metalloprotease. Montecucco, C., Tonello, F., Zanotti, G. Trends Biochem. Sci. (2004) [Pubmed]
  21. Anthrax lethal toxin rapidly activates caspase-1/ICE and induces extracellular release of interleukin (IL)-1beta and IL-18. Cordoba-Rodriguez, R., Fang, H., Lankford, C.S., Frucht, D.M. J. Biol. Chem. (2004) [Pubmed]
  22. Anthrax lethal toxin blocks MAPK kinase-dependent IL-2 production in CD4+ T cells. Fang, H., Cordoba-Rodriguez, R., Lankford, C.S., Frucht, D.M. J. Immunol. (2005) [Pubmed]
  23. Anthrax: a motor protein determines anthrax susceptibility. Hanna, P.C. Curr. Biol. (2001) [Pubmed]
  24. A specific activation of the mitogen-activated protein kinase kinase 1 (MEK1) is required for Golgi fragmentation during mitosis. Colanzi, A., Deerinck, T.J., Ellisman, M.H., Malhotra, V. J. Cell Biol. (2000) [Pubmed]
  25. Human capillary morphogenesis protein 2 functions as an anthrax toxin receptor. Scobie, H.M., Rainey, G.J., Bradley, K.A., Young, J.A. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  26. Anthrax lethal factor represses glucocorticoid and progesterone receptor activity. Webster, J.I., Tonelli, L.H., Moayeri, M., Simons, S.S., Leppla, S.H., Sternberg, E.M. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  27. Formation and composition of the Bacillus anthracis endospore. Liu, H., Bergman, N.H., Thomason, B., Shallom, S., Hazen, A., Crossno, J., Rasko, D.A., Ravel, J., Read, T.D., Peterson, S.N., Yates, J., Hanna, P.C. J. Bacteriol. (2004) [Pubmed]
  28. Expression of protective antigen in transgenic plants: a step towards edible vaccine against anthrax. Aziz, M.A., Singh, S., Anand Kumar, P., Bhatnagar, R. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  29. Development of an in vitro-based potency assay for anthrax vaccine. Little, S.F., Webster, W.M., Ivins, B.E., Fellows, P.F., Norris, S.L., Andrews, G.P. Vaccine (2004) [Pubmed]
  30. TNF-alpha detection using a flow cytometric assay to determine cellular responses to anthrax vaccine. Shinn, A.H., Bravo, N.C., Maecker, H.T., Smith, J.W. J. Immunol. Methods (2003) [Pubmed]
  31. Site directed mutagenesis of histidine residues in anthrax toxin lethal factor binding domain reduces toxicity. Arora, N. Mol. Cell. Biochem. (1997) [Pubmed]
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