scispace - formally typeset
Journal ArticleDOI

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

TLDR
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.
Abstract
Anthrax lethal toxin, produced by the bacterium Bacillus anthracis, is the major cause of death in animals infected with anthrax. One component of this toxin, lethal factor (LF), is suspected to be a metalloprotease, but no physiological substrates have been identified. Here it is shown that LF is a protease that cleaves the amino terminus of mitogen-activated protein kinase kinases 1 and 2 (MAPKK1 and MAPKK2) and that this cleavage inactivates MAPKK1 and inhibits the MAPK signal transduction pathway. The identification of a cleavage site for LF may facilitate the development of LF inhibitors.

read more

Citations
More filters
Journal ArticleDOI

Quantum mechanical/molecular mechanical study of anthrax lethal factor catalysis

TL;DR: In this paper, a hybrid quantum mechanical and molecular mechanical study of the catalysis of anthrax lethal factor was carried out and it was shown that the zinc peptidase uses the same general base-general acid mechanism as in thermolysin and carboxypeptidase A, in which a zinc-bound water is activated by Glu687 to nucleophilically attack the scissile carbonyl carbon in the substrate.
Journal ArticleDOI

Implication of pH in the catalytic properties of anthrax lethal factor.

TL;DR: It is presented the first evidence that additional metal ions are required for the LF catalyzed hydrolysis of native substrate, and that the pH alteration causes a significant change of catalytic properties of LF.
Journal ArticleDOI

Combinatory action of VEGFR2 and MAP kinase pathways maintains endothelial-cell integrity

TL;DR: This is the first study to elucidate the pathways controlling maintenance of endothelial Integrity using a chemical genetics approach, indicating that endothelial integrity is controlled by the combined action of the VEGFR2 and MAP kinase pathways.
Journal ArticleDOI

NMR conformational properties of an Anthrax Lethal Factor domain studied by multiple amino acid-selective labeling.

TL;DR: This work presents the successful overexpression of a polypeptide of 233 residues, corresponding to the structured part of the N-terminal domain of Anthrax Lethal Factor, using Escherichia coli expression system.
Journal ArticleDOI

PAK in pathogen-host interactions

TL;DR: Examples of modulation of PAK activity in human cells by both intracellular and extracellular pathogens are presented, focusing on one eukaryotic pathogen, the human malaria parasite Plasmodium falciparum, and two Gram-negative bacteria.
References
More filters
Journal ArticleDOI

A synthetic inhibitor of the mitogen-activated protein kinase cascade.

TL;DR: Results indicate that the MAPK pathway is essential for growth and maintenance of the ras-transformed phenotype and PD 098059 is an invaluable tool that will help elucidate the role of theMAPK cascade in a variety of biological settings.
Journal ArticleDOI

Cyclin is degraded by the ubiquitin pathway

TL;DR: Cyclin degradation is the key step governing exit from mitosis and progress into the next cell cycle, and anaphase may be triggered by the recognition of cyclin by the ubiquitin-conjugating system.
Journal ArticleDOI

Transformation of mammalian cells by constitutively active MAP kinase kinase

TL;DR: It is found that constitutive activation of MAPKK is sufficient to promote cell transformation and is associated with highly tumorigenic in nude mice.
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.
Journal ArticleDOI

Multiple Ras functions can contribute to mammalian cell transformation.

TL;DR: Results indicate that multiple cellular components, including Raf1, are activated by Ha-Ras and contribute to Ha- Ras-induced mammalian cell transformation.
Related Papers (5)