ArticleInfection and immunity1994
Protein synthesis is required for expression of anthrax lethal toxin cytotoxicity.
Article in Infection and immunity, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 45 citations in OpenAlex.
- GeneChip analyses of global transcriptional responses of murine macrophages to the lethal toxin of Bacillus anthracis.Infection and immunity · 2005Article
- Toxin-induced resistance in Bacillus anthracis lethal toxin-treated macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Anthrax lethal factor represses glucocorticoid and progesterone receptor activity.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Purification of anthrax edema factor from Escherichia coli and identification of residues required for binding to anthrax protective antigen.Infection and immunity · 2001Article
- Proteasome activity is required for anthrax lethal toxin to kill macrophages.Infection and immunity · 1999Article
- Expression and purification of the recombinant lethal factor of Bacillus anthracis.Infection and immunity · 1998Article
- Cytotoxic effects of anthrax lethal toxin on macrophage-like cell line J774A.1.Current microbiology · 1996Article
- Pertussis toxin-catalyzed ADP-ribosylation of Gi-2 and Gi-3 in CHO cells is modulated by inhibitors of intracellular trafficking.Infection and immunity · 1996Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anthrax lethal toxin, which is composed of two proteins, i.e., protective antigen and lethal factor, is cytolytic to mouse peritoneal macrophages and the macrophage-like cell line J774A.1. After exposure of cells to lethal toxin, inhibition of protein synthesis occurred only slightly before the onset of cytolysis. Thus, cell death did not appear to be due to inhibition of protein synthesis. However, prior treatment of J774A.1 cells with cycloheximide or puromycin, which inhibited protein synthesis, protected them completely against lethal toxin-induced cytolysis, which suggested that continuous protein synthesis is required for the expression of lethal toxin activity. Inhibition of protein synthesis had no appreciable effect on the binding of protective antigen to the cell surface receptor or on proteolytic cleavage of surface-bound protective antigen. Furthermore, inhibition of protein synthesis did not alter the uptake of toxin, which suggested that protein synthesis is required at a later stage of the intoxication process. The protection provided by inhibition of protein synthesis was effective, even up to 1 h after exposure to anthrax lethal toxin. The increased uptake of calcium observed in cells exposed to lethal toxin did not occur when they were protected by blocking protein synthesis. Identifying the protein(s) synthesized during the intoxication process may help to understand the mechanism of cell death produced by anthrax lethal toxin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.