The function of ENSG00000102452 (NALCN, sodium leak channel, non-selective) is as follows. Voltage-sensing, pore-forming subunit of the NALCN channelosome complex, which regulates the resting membrane potential by depolarizing sodium leak currents (PubMed:17448995, PubMed:32494638, PubMed:33203861, PubMed:35387979, PubMed:34929720). The NALCN channelosome complex is a voltage-gated ion channel responsible for the resting Na(+) permeability that controls neuronal excitability (PubMed:17448995, PubMed:31409833, PubMed:35387979, PubMed:34929720). The NALCN channelosome is constitutively active and conducts monovalent cations but is blocked by physiological concentrations of extracellular divalent cations (PubMed:32494638). In addition to its role in regulating neuronal excitability, is required for normal respiratory rhythm, systemic osmoregulation by controlling the serum sodium concentration and in the regulation of the intestinal pace-making activity in the interstitial cells of Cajal (By similarity). The NALCN channelosome is also activated by neuropeptides such as neurotensin and substance P (SP) through a SRC family kinases-dependent pathway (By similarity). In addition, NALCN activity is enhanced/modulated by several GPCRs, such as CHRM3 (By similarity). {ECO:0000250|UniProtKB:Q8BXR5, ECO:0000269|PubMed:17448995, ECO:0000269|PubMed:31409833, ECO:0000269|PubMed:32494638, ECO:0000269|PubMed:33203861, ECO:0000269|PubMed:34929720, ECO:0000269|PubMed:35387979}.