Subversion of MAPK signaling by pathogenic bacteria


https://doi.org/10.4081/mk.2015.5303
Vol. 4 No. 1 (2015)
Submitted: 4 June 2015
Accepted: 1 September 2015
Published: 22 October 2015
MAPK signaling, pathogenic bacteria, host-pathogen interaction, toxins, effectors.
Abstract Views: 3697
PDF: 1062
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Authors

  • Lihi Gur-Arie Department of Microbiology and Molecular Genetics, Institute of Medical Research Israel-Canada, Faculty of Medicine, The Hebrew University of Jerusalem, Israel.
  • Ilan Rosenshine
    ilanr@ekmd.huji.ac.il
    Department of Microbiology and Molecular Genetics, Institute of Medical Research Israel-Canada, Faculty of Medicine, The Hebrew University of Jerusalem, Israel.
Bacterial components are recognized by host pattern recognition receptors that trigger signaling cascades, leading to inflammation and eradication of the bacteria. The main proinflammatory signaling pathway is the MAP kinase (MAPK)/NF-κB interwoven cascades, which result in transcription of pro-inflammatory genes. Many bacteria have evolved to interfere with the immune response through a mechanism that involves delivery of virulent proteins to the host cells. These proteins posttranslationally modify key components in the host signaling cascades. This review will describe bacterial strategies to directly manipulate host MAPK signaling, summarizing recent discoveries in the field.

Supporting Agencies

The Israel Science Foundation funded by The Israel Academy of Science and Humanities

Gur-Arie, L., & Rosenshine, I. (2015). Subversion of MAPK signaling by pathogenic bacteria. MAP Kinase, 4(1). https://doi.org/10.4081/mk.2015.5303

PAGEPress has chosen to apply the Creative Commons Attribution NonCommercial 4.0 International License (CC BY-NC 4.0) to all manuscripts to be published.

Downloads

Download data is not yet available.

Citations

Crossref
Scopus
Google Scholar
Europe PMC