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• W3204335719 endingPage "103210" @default.
• W3204335719 startingPage "103210" @default.
• W3204335719 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+ channels and promoting contraction. Consistent with functional coupling, our data show that NALCN and SLO2.1 are in close proximity in human MSMCs. We propose that these arrangements of SLO2.1 and NALCN permit these channels to functionally regulate MSMC membrane potential and cell excitability and modulate uterine contractility." @default.
• W3204335719 created "2021-10-11" @default.
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• W3204335719 date "2021-11-01" @default.
• W3204335719 modified "2023-09-27" @default.
• W3204335719 title "SLO2.1/NALCN a sodium signaling complex that regulates uterine activity." @default.
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• W3204335719 doi "https://doi.org/10.1016/j.isci.2021.103210" @default.
• W3204335719 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8551532" @default.
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