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Nalcn is a voltage-independent, cation-nonselective channel which is permeable to sodium, potassium and calcium ions. Nalcn regulates the resting membrane potential and controls neuronal excitability (PubMed:17448995). Neuropeptides such as neurotensin and substance P (SP) stimulate the firing of action potentials by activating NALCN through a SRC family kinases-dependent pathway. In addition to its baseline activity, Nalcn activity is enhanced/modulated by several GPCRs, is required for normal respiratory rhythm and neonatal survival, is involved in systemic osmoregulation by controlling the serum sodium concentration. Nalcn is partly responsible for the substance P-induced depolarization and regulation of the intestinal pace-making activity in the interstitial cells of Cajal. Further, Nalcn plays a critical role in both maintenance of spontaneous firing of substantia nigra pars reticulata (SNr) neurons and physiological modulation of SNr neuron excitability. Diseases associated with NALCN include Congenital contractures of the limbs and face, Hypotonia, Developmental Delay and Hypotonia, Infantile Psychomotor Retardation And Characteristic Facies 1.
A530023G15Rik; AI849508; bA430M15.1; brain voltage-gated cation channel; CanIon; CLIFAHDD; FLJ23913; FLJ44659; FLJ44764; Four domain-type voltage-gated ion channel alpha-1 subunit; four repeat voltage-gated ion channel; IHPRF; IHPRF1; INNFD; MGC74524; Nalcn; Nca; Rb21; Rb21-channel; Sodium leak channel non-selective protein; sodium leak channel, non selective; sodium leak channel, non-selective; Vgcnl1; voltage gated channel like 1; voltage gated channel-like protein 1
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