Title: Kir3.1 channel is functionally involved in TLR4-mediated signaling.

Authors: Hee-Yeon Jo, So Yong Kim, Sooyoung Lee, Sookyoung Jeong, Sung Joon Kim, Tong Mook Kang, Ki-Young Lee

Journal, date & volume: Biochem. Biophys. Res. Commun., 2011 Apr 22 , 407, 687-91

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21420934

Abstract
We aimed to study the involvement of Kir3.1 channel in TLR4-mediated signaling. LPS stimulation induced the recruitment of TLR4 and Kir3.1 into the lipid raft in THP-1 cells. Treatment with Tertiapin-Q, an inhibitor of Kir3.1, markedly abolished the recruitment of TLR4 into the lipid raft and inhibited the LPS-induced NF-κB activation, resulting in decreased production of TNF-α, IL-1β, and IL-6. To verify the specific role of the Kir3.1 channel, we generated Kir3.1-knockdown THP-1 cells. The Kir3.1(KD) THP-1 cells exhibited inhibition of NF-κB activation and production of these pro-inflammatory cytokines in response to TLR4 stimulation. Taken together, our results demonstrate that the Kir3.1 channel is involved in the TLR4-mediated signal at an early event by facilitating the recruitment of TLR4 into lipid raft.