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Open AccessJournal ArticleDOI

Macrophages are sensitive to anthrax lethal toxin through an acid-dependent process.

A M Friedlander
- 05 Jun 1986 - 
- Vol. 261, Iss: 16, pp 7123-7126
TLDR
It is suggested that anthrax lethal toxin requires passage through an acidic endocytic vesicle in order to exert its toxic effect within the cytosol.
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This article is published in Journal of Biological Chemistry.The article was published on 1986-06-05 and is currently open access. It has received 540 citations till now. The article focuses on the topics: Anthrax toxin & Endocytic vesicle.

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Citations
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Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death

TL;DR: The discovery of caspase-11/4/5 function in sensing intracellular lipopolysaccharide expands the spectrum of pyroptosis mediators and also reveals that pyroPTosis is not cell type specific.
Journal ArticleDOI

Proteolytic Inactivation of MAP-Kinase-Kinase by Anthrax Lethal Factor

TL;DR: It is shown that LF is a protease that cleaves the amino terminus of mitogen-activated protein kinase kinases 1 and 2 and that this cleavage inactivates MAPKK1 and inhibits the MAPK signal transduction pathway.
Journal ArticleDOI

Intracellular NOD-like Receptors in Host Defense and Disease

TL;DR: The recent understanding in NLRs is discussed, which indicates that two NLRs sense the cytosolic presence of the peptidoglycan fragments meso-DAP and muramyl dipeptide, respectively, and drive the activation of mitogen-activated protein kinase and the transcription factor NF-kappaB.
Journal ArticleDOI

Identification of the cellular receptor for anthrax toxin.

TL;DR: The cloning of the human PA receptor is described using a genetic complementation approach and a soluble version of this domain can protect cells from the action of the toxin.
Journal ArticleDOI

Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin.

TL;DR: It is shown that an extremely polymorphic gene in this locus, Nalp1b, is the primary mediator of mousemacrophage susceptibility to LeTx, and that LeTx-induced macrophage death requires caspase-1, which is activated in susceptible, but not resistant, macrophages after intoxication.
References
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Journal ArticleDOI

Anthrax toxin edema factor: a bacterial adenylate cyclase that increases cyclic AMP concentrations of eukaryotic cells.

TL;DR: It is shown here that EF is an adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1] produced by Bacillus anthracis in an inactive form and nearly equals that of the most active known cyclase.
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On the entry of Semliki Forest virus into BHK-21 cells.

TL;DR: The results suggest that the penetration of the viral genome into the cytosol takes place intracellularly through fusion between the limiting membrane of intrACEllular vacuoles and the membrane of viruses contained within them.
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Effect of weak bases on the intralysosomal pH in mouse peritoneal macrophages.

B Poole, +1 more
TL;DR: The spectral characteristics of dextran, labeled with fluorescein, depend upon pH, and the results of these studies are interpreted in terms of energy-dependent lysosomal acidification and leakage of protons out of theLysosomes in the form of protonated weak bases.
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Diphtheria toxin entry into cells is facilitated by low pH.

TL;DR: The data suggest that, at low pH, diphtheria toxin penetrates directly through the surface membrane of the cell, and the rate of protein synthesis in the cells decreased much faster than when the normal pH was maintained.
Journal ArticleDOI

The entry of diphtheria toxin into the mammalian cell cytoplasm: evidence for lysosomal involvement

TL;DR: Exposing the toxin to an acidic environment, such as that found within lysosomes, is an important step in the penetration of diphtheria toxin into the cytoplasm.
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