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Sci. Signal., 14 May 2013
Vol. 6, Issue 275, p. pc13
[DOI: 10.1126/scisignal.2004292]


Science Signaling Podcast: 14 May 2013

Chen Dong1 and Annalisa M. VanHook2

1 Department of Immunology, Centers for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054, 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 an interview with Chen Dong, senior author of a Research Article that appears in the 14 May 2013 issue of Science Signaling. A group led by Dong found that the deubiquitinase USP25 modulates inflammatory signaling initiated by Toll-like receptor 4 (TLR4). Activation of TLR4 by the bacterial cell wall component lipopolysaccharide (LPS) activates two signaling pathways that promote the production of various cytokines that control inflammation. Zhong et al. report that USP25 affected signaling through one of these pathways to prevent excessive inflammation, which can damage tissues. Compared to wild-type controls, mice lacking USP25 exhibited an excessive inflammatory response and were more susceptible to septic shock following LPS treatment. Understanding the mechanisms that ensure balance in the inflammatory response is important for developing strategies to treat diseases that result from excessive inflammation.

Citation: C. Dong, A. M. VanHook, Science Signaling Podcast: 14 May 2013. Sci. Signal. 6, pc13 (2013).

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