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Sci. Signal., 14 February 2012
Vol. 5, Issue 211, p. pc4
[DOI: 10.1126/scisignal.2002905]


Science Signaling Podcast: 14 February 2012

Marc Peters-Golden1 and Annalisa M. VanHook2

1 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, MI 48109 USA.
2 Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue NW, Washington, DC 20005, USA.

Abstract: This Podcast features a conversation with authors of a Research Article published in the 7 February 2012 issue of Science Signaling. Marc Peters-Golden discusses his group’s finding that infection of alveolar macrophages with the fungus Candida albicans triggered the production of the lipid mediator prostaglandin E2 (PGE2), prevented polymerization of the actin cytoskeleton, and inhibited phagocytosis of the pathogen by the macrophages. Dephosphorylation and activation of the actin depolymerizing factor cofilin-1 was necessary for these inhibitory effects of PGE2 and was mediated by the protein phosphatase activity of PTEN (phosphatase and tensin homolog deleted on chromosome 10). Immunosuppression is associated with increased production of PGE2, which may help to explain how antifungal responses are attenuated in immunocompromised individuals.

Citation: M. Peters-Golden, A. M. VanHook, Science Signaling Podcast: 14 February 2012. Sci. Signal. 5, pc4 (2012).

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