Cholesterol and PIP₂ Modulation of BK_Ca Channels.

ABSTRACT: Ca²⁺/voltage-gated, large conductance K⁺ channels (BK_Ca) are formed by homotetrameric association of α (slo1) subunits. Their activity, however, is suited to tissue-specific physiology largely due to their association with regulatory subunits (β and γ types), chaperone proteins, localized signaling, and the channel's lipid microenvironment. PIP₂ and cholesterol can modulate BK_Ca activity independently of downstream signaling, yet activating Ca²⁺_i levels and regulatory subunits control ligand action. At physiological Ca²⁺_i and voltages, cholesterol and PIP₂ reduce and increase slo1 channel activity, respectively. Moreover, slo1 proteins provide sites that seem to recognize cholester

SUBMITTER: Vaithianathan T 

PROVIDER: S-EPMC10683925 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature