Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 3 May 2011
Vol. 4, Issue 171, p. pc9
[DOI: 10.1126/scisignal.2002075]


Science Signaling Podcast: 3 May 2011

Thomas C. Mitchell1 and Annalisa M. VanHook2

1 Department of Microbiology and Immunology and the Institute for Cellular Therapeutics, University of Louisville School of Medicine, 570 South Preston Street, Louisville, KY 40202, USA.
2 Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue, N.W., Washington, DC 20005, USA.

Abstract: This Podcast features a conversation with the senior author of a Research Article published in the May 3 issue of Science Signaling. Thomas Mitchell discusses his group’s identification of the mechanism through which monophosphoryl lipid A (MLA) stimulates the immune system without triggering inflammation. Lipopolysaccharide (LPS) and MLA both bind to and activate Toll-like receptor 4 (TLR4), but only LPS stimulates a toxic inflammatory response. Embry et al. now show that whereas LPS triggers two pathways downstream of TLR4, MLA triggers only one of these and does not lead to activation of the inflammasome.

Citation: T. C. Mitchell, A. M. VanHook, Science Signaling Podcast: 3 May 2011. Sci. Signal. 4, pc9 (2011).

Read the Full Text

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882