BK通道
化学
溶酶体
胞浆
细胞生物学
炎症体
炎症
程序性细胞死亡
生物物理学
生物化学
膜电位
细胞凋亡
生物
酶
免疫学
受体
作者
Rebekah L. Kendall,Andrij Holian
标识
DOI:10.1080/08958378.2024.2305112
摘要
Background Lysosomal ion channels are proposed therapeutic targets for a number of diseases, including those driven by NLRP3 inflammasome-mediated inflammation. Here, the specific role of the lysosomal big conductance Ca2+-activated K+ (BK) channel was evaluated in a silica model of inflammation in murine macrophages. A specific-inhibitor of BK channel function, paxilline (PAX), and activators NS11021 and NS1619 were utilized to evaluate the role of lysosomal BK channel activity in silica-induced lysosomal membrane permeabilization (LMP) and NLRP3 inflammasome activation resulting in IL-1β release.
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