Scheel Olaf, Papavlassopoulos Martin, Blunck Rikard, Gebert Andreas, Hartung Thomas, Zähringer Ulrich, Seydel Ulrich, Schromm Andra B
Research Center Borstel, Department of Immunochemistry and Biochemical Microbiology, Division of Biophysics, Parkallee 10, 23845 Borstel, Germany.
Infect Immun. 2006 Jul;74(7):4354-6. doi: 10.1128/IAI.01783-05.
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.
在对人类巨噬细胞进行膜片钳实验时,我们发现大电导钙激活钾通道(MaxiK)可被脂多糖、肽聚糖和白细胞介素-1激活。由几种Toll样受体(TLR)配体和白细胞介素-1引发的细胞因子产生会被MaxiK阻断所抑制。这为MaxiK通道与TLR信号复合物之间的功能关联提供了证据。