SLO2.1/NALCN a sodium signaling complex that regulates uterine activity.

ABSTRACT: Depolarization of the myometrial smooth muscle cell (MSMC) resting membrane potential is necessary for the uterus to transition from a quiescent state to a contractile state. The molecular mechanisms involved in this transition are not completely understood. Here, we report that a coupled system between the Na⁺-activated K⁺ channel (SLO2.1) and the non-selective Na⁺ leak channel (NALCN) determines the MSMC membrane potential. Our data indicate that Na⁺ entering through NALCN acts as an intracellular signaling molecule that activates SLO2.1. Potassium efflux through SLO2.1 hyperpolarizes the membrane. A decrease in SLO2.1/NALCN activity induces membrane depolarization, triggering Ca²⁺ entry through voltage-dependent Ca²⁺ chan

SUBMITTER: Ferreira JJ 

PROVIDER: S-EPMC8551532 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature