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Infection and Immunity, July 2006, p. 4354-4356, Vol. 74, No. 7
0019-9567/06/$08.00+0 doi:10.1128/IAI.01783-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Department of Immunochemistry and Biochemical Microbiology, Research Center Borstel-Center for Medicine and Biosciences, 23845 Borstel,1 Institute of Anatomy, University of Lübeck, 23538 Lübeck,3 Department of Biochemical Pharmacology, University of Constance, 78457 Constance, Germany,4 Department of Physiology, David Geffen School of Medicine at University of CaliforniaLos Angeles, Los Angeles, California 900952
Received 3 November 2005/ Returned for modification 22 December 2005/ Accepted 18 March 2006
Performing patch-clamp experiments on human macrophages, we show that the K+ channel MaxiK is activated by lipopolysaccharide, peptidoglycan, and interleukin-1. Cytokine production initiated by several Toll-like receptor (TLR) ligands and by interleukin-1 is inhibited by MaxiK blockade. This provides evidence for functional association of the MaxiK channel and TLR signaling complexes.
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