Laskowski-Arce Michelle A, Orth Kim
Department of Molecular Biology, UT Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390-9148, USA.
Trends Microbiol. 2007 Oct;15(10):437-40. doi: 10.1016/j.tim.2007.09.002. Epub 2007 Oct 24.
Yersinia spp. pathogens use their type III secretion system to translocate effectors that manipulate host signaling pathways during infection. Although molecular targets for five of the six known Yersinia effectors are known, the target for the serine/threonine kinase domain of Yersinia protein kinase A (YpkA) has remained elusive. Recently, Navarro et al. (2007) demonstrated that YpkA phosphorylates Galphaq, and inhibits Galphaq-mediated signaling. Inhibition by YpkA could contribute to one of the most documented symptoms of Yersinia pestis infection, extensive bleeding.