Auxiliary subunit of the NALCN sodium channel complex (PubMed:32620897, PubMed:19092807, PubMed:21040849). The NALCN sodium channel complex is a voltage-gated ion channel responsible for the resting Na(+) permeability that controls neuronal excitability (PubMed:32620897). This complex is activated by neuropeptides substance P, neurotensin. In addition, the channel is inhibited by extracellular Ca(2+) through the Ca(2+)-sensing receptor. UNC80 is essential for NALCN sensitivity to extracellular calcium. NALCN complex consists of NALCN and auxiliary subunits, UNC79, UNC80 and NACL1 (PubMed:32620897, PubMed:19092807, PubMed:21040849, PubMed:26708751). These auxiliary subunits are essential for the NALCN complex function (PubMed:32620897). Interacts (via N-terminus half) with NALCN; this interaction facilitates NALCN surface localization (PubMed:19092807,PubMed:21040849,PubMed:32620897). Interacts (via C-terminus) with UNC79 (PubMed:19092807, PubMed:21040849, PubMed:32620897, PubMed:26708751). UNC80 bridges NALCN to UNC79 (PubMed:21040849, PubMed:32620897). In neurons, located in soma and dendrites. Named isoforms=2. Expressed almost exclusively in the brain (PubMed:26708753). Expressed in hippocampus and ventral tegmental area neurons (PubMed:19092807). Phosphorylated on tyrosine residues. Knockout leads to severe apnea and neonatal lethality. No mice pups survive beyond 24 hours of birth. Hippocampal neurons show decreased NALCN-dependent sodium leak current. Belongs to the unc-80 family.