Cation channel with high affinity for sodium, which is gated by extracellular protons and inhibited by the diuretic amiloride. Generates a biphasic current with a fast inactivating and a slow sustained phase. In sensory neurons is proposed to mediate the pain induced by acidosis that occurs in ischemic, damaged or inflamed tissue. May be involved in hyperalgesia. May play a role in mechanoreception. Heteromeric channel assembly seems to modulate channel properties. Homotrimer or heterotrimer with other ASIC proteins (By similarity). Interacts with DLG4 and ASIC2 (By similarity). Interacts with LIN7B, MAGI1/BAIAP1 and GOPC. Interacts with STOM; this regulates channel activity. Cell surface expression may be stabilized by interaction with LIN7B and cytoplasmic retention by interaction with DLG4 (By similarity). In part cytoplasmic in cochlea cells. Expressed in liver, lung, kidney, testis, brain, eye and cochlea. Expressed in spiral ganglion and sensory hair cells of the organ of Corti in the cochlea (at protein level). Expressed in dorsal root ganglion innervating muscles and spinal chord. Expressed in peripheral sensory nerve termimals like nerves of the Meissner corpuscle, palisades of lanceolate nerve endings, site of mechanoreception in guard hair follicles, and Merkel cell-neurite complexes. Phosphorylated by PKA. Phosphorylated by PKC. In vitro, PRKCABP/PICK-1 is necessary for PKC phosphorylation and activation of a ASIC3/ACCN3-ASIC2/ASIC2b channel, but does not activate a homomeric ASIC3/ACCN3 channel (By similarity). Mice display altered responses to mechanical and acid stimuli. They do not develop chronic hyperalgesia induced by repeated acid injection. Sensitized and potentiated by NPFF and NPSF. Inhibited by anti-inflammatory drugs, like salicylic acid (By similarity). Potentiated by FMRFamide-related neuropeptides. Regulated by lactate and Ca(2+). Belongs to the amiloride-sensitive sodium channel (TC 1.A.6) family. ASIC3 subfamily.