Protein kinase and phosphatase signaling in Mycobacterium tuberculosis physiology and pathogenesis

Biochim Biophys Acta. 2010 Mar;1804(3):620-7. doi: 10.1016/j.bbapap.2009.09.008. Epub 2009 Sep 18.

Abstract

Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB), evades the antimicrobial defenses of the host and survives within the infected individual through a complex set of strategies. These include active prevention of host cellular killing processes as well as overwhelming adaptive gene expression. In the past decade, we have gained an increased understanding of how mycobacteria not only have the ability to adapt to a changing host environment but also actively interfere with the signaling machinery within the host cell to counteract or inhibit parts of the killing apparatus employed by the macrophage. Mtb is able to sense its environment via a set of phospho-signaling proteins which mediate its response and interaction with the host in a coordinated manner. In this review, we summarize the current knowledge about selected Mtb serine, threonine, and tyrosine kinase and phosphatase signaling proteins, focusing on the protein kinases, PknG and PtkA, and the protein phosphatase, PtpA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Bacterial Proteins / metabolism*
  • Mycobacterium tuberculosis / enzymology*
  • Mycobacterium tuberculosis / pathogenicity*
  • Phosphoprotein Phosphatases / metabolism*
  • Protein Kinases / metabolism*
  • Tuberculosis / enzymology*

Substances

  • Bacterial Proteins
  • Protein Kinases
  • Phosphoprotein Phosphatases