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Sci. Signal., 17 November 2009
Vol. 2, Issue 97, p. ra74
[DOI: 10.1126/scisignal.2000374]

RESEARCH ARTICLES

Editor's Summary

Giving a Helping Hand
The obligate intracellular parasite Trypanosoma cruzi, the causative agent of Chagas’ disease, binds to cell-surface receptors before being internalized in phagolysomes. It then escapes to the cytosol of the host cell, where it differentiates and replicates before spreading to infect other cells. Strategies that keep the infected cell alive while the parasite is differentiating and replicating increase the chances of spreading the infection. Parasite-derived neurotrophic factor (PDNF), a protein at the surface of T. cruzi, binds to the receptor tyrosine kinases TrkA and TrkC, which leads to the activation of the phosphatidylinositol 3-kinase (PI3K)–Akt pathway in the host cell, which is important for cell survival. However, given that the interaction between PDNF and the Trks occurs early in infection, activation of Akt at this stage is not likely to ensure long-term survival of the host cell. Chuenkova and PereiraPerrin now show that upon escape of T. cruzi into the cytosol of the host, PDNF becomes both a substrate and an activator of Akt. Cells infected with T. cruzi were more resistant to the effects of proapoptotic cytokines than were uninfected cells. Together, these data suggest that PDNF targets Akt signaling both extracellularly and intracellularly to help the cells survive long enough for productive infection to occur.

Citation: M. V. Chuenkova, M. PereiraPerrin, Trypanosoma cruzi Targets Akt in Host Cells as an Intracellular Antiapoptotic Strategy. Sci. Signal. 2, ra74 (2009).

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Multigene Families in Trypanosoma cruzi and Their Role in Infectivity.
L. M. De Pablos and A. Osuna (2012)
Infect. Immun. 80, 2258-2264
   Abstract »    Full Text »    PDF »
Neurotrophin Receptor TrkC Is an Entry Receptor for Trypanosoma cruzi in Neural, Glial, and Epithelial Cells.
C. Weinkauf, R. Salvador, and M. PereiraPerrin (2011)
Infect. Immun. 79, 4081-4087
   Abstract »    Full Text »    PDF »

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