NALCN Membrane Protein Introduction

Introduction of NALCN

The sodium leak channel non-selective protein (NALCN) in humans is encoded by the NALCN gene. It belongs to the transmembrane cation channel superfamily and is a voltage-independent cation non-selective channel that is permeable to sodium, potassium and calcium ions. The channel is described as having two transmembrane helices on the flanks of the loop that determine the ion selectivity of the channels. Many eukaryotic channels have four additional transmembrane helices associated with voltage gating.

Basic Information of NALCN
Protein Name	Sodium leak channel non-selective protein
Gene Name	NALCN
Aliases	VGCNL1
Organism	Homo sapiens (Human)
UniProt ID	Q8IZF0
Transmembrane Times	24
Length (aa)	1738
Sequence	MLKRKQSSRVEAQPVTDFGPDESLSDNADILWINKPWVHSLLRICAIISVISVCMNTPMTFEHYPPLQYVTFTLDTLLMFLYTAEMIAKMHIRGIVKGDSSYVKDRWCVFDGFMVFCLWVSLVLQVFEIADIVDQMSPWGMLRIPRPLIMIRAFRIYFRFELPRTRITNILKRSGEQIWSVSIFLLFFLLLYGILGVQMFGTFTYHCVVNDTKPGNVTWNSLAIPDTHCSPELEEGYQCPPGFKCMDLEDLGLSRQELGYSGFNEIGTSIFTVYEAASQEGWVFLMYRAIDSFPRWRSYFYFITLIFFLAWLVKNVFIAVIIETFAEIRVQFQQMWGSRSSTTSTATTQMFHEDAAGGWQLVAVDVNKPQGRAPACLQKMMRSSVFHMFILSMVTVDVIVAASNYYKGENFRRQYDEFYLAEVAFTVLFDLEALLKIWCLGFTGYISSSLHKFELLLVIGTTLHVYPDLYHSQFTYFQVLRVVRLIKISPALEDFVYKIFGPGKKLGSLVVFTASLLIVMSAISLQMFCFVEELDRFTTFPRAFMSMFQILTQEGWVDVMDQTLNAVGHMWAPVVAIYFILYHLFATLILLSLFVAVILDNLELDEDLKKLKQLKQSEANADTKEKLPLRLRIFEKFPNRPQMVKISKLPSDFTVPKIRESFMKQFIDRQQQDTCCLLRSLPTTSSSSCDHSKRSAIEDNKYIDQKLRKSVFSIRARNLLEKETAVTKILRACTRQRMLSGSFEGQPAKERSILSVQHHIRQERRSLRHGSNSQRISRGKSLETLTQDHSNTVRYRNAQREDSEIKMIQEKKEQAEMKRKVQEEELRENHPYFDKPLFIVGREHRFRNFCRVVVRARFNASKTDPVTGAVKNTKYHQLYDLLGLVTYLDWVMIIVTICSCISMMFESPFRRVMHAPTLQIAEYVFVIFMSIELNLKIMADGLFFTPTAVIRDFGGVMDIFIYLVSLIFLCWMPQNVPAESGAQLLMVLRCLRPLRIFKLVPQMRKVVRELFSGFKEIFLVSILLLTLMLVFASFGVQLFAGKLAKCNDPNIIRREDCNGIFRINVSVSKNLNLKLRPGEKKPGFWVPRVWANPRNFNFDNVGNAMLALFEVLSLKGWVEVRDVIIHRVGPIHGIYIHVFVFLGCMIGLTLFVGVVIANFNENKGTALLTVDQRRWEDLKSRLKIAQPLHLPPRPDNDGFRAKMYDITQHPFFKRTIALLVLAQSVLLSVKWDVEDPVTVPLATMSVVFTFIFVLEVTMKIIAMSPAGFWQSRRNRYDLLVTSLGVVWVVLHFALLNAYTYMMGACVIVFRFFSICGKHVTLKMLLLTVVVSMYKSFFIIVGMFLLLLCYAFAGVVLFGTVKYGENINRHANFSSAGKAITVLFRIVTGEDWNKIMHDCMVQPPFCTPDEFTYWATDCGNYAGALMYFCSFYVIIAYIMLNLLVAIIVENFSLFYSTEEDQLLSYNDLRHFQIIWNMVDDKREGVIPTFRVKFLLRLLRGRLEVDLDKDKLLFKHMCYEMERLHNGGDVTFHDVLSMLSYRSVDIRKSLQLEELLAREQLEYTIEEEVAKQTIRMWLKKCLKRIRAKQQQSCSIIHSLRESQQQELSRFLNPPSIETTQPSEDTNANSQDNSMQPETSSQQQLLSPTLSDRGGSRQDAADAGKPQRKFGQWRLPSAPKPISHSVSSVNLRFGGRTTMKSVVCKMNPMTDAASCGSEVKKWWTRQLTVESDESGDDLLDI

Function of NALCN Membrane Protein

NALCN regulates resting membrane potential and controls neuronal excitability. Neuropeptides, such as neurotensin, activates NALCN through the SRC family kinase-dependent pathway, thereby activating action potentials. In addition, NALCN activity is also associated with several GPCRs, which are involved in systemic osmoregulation by controlling serum sodium concentrations and are required for normal respiratory rhythm and neonatal survival. NALCN is part of the reason for material depolarization and regulation of intestinal pacing activity in stromal cells. Moreover, it plays a key role in maintaining the spontaneous regulation of nigral reticulocytes and the physiological regulation of neuronal excitability.

NALCN Membrane Protein Introduction Fig.1 Structure of voltage-gated sodium channels. (Yu, 2014)

Application of NALCN Membrane Protein in Literature

Cochetbissuel M., et al. The sodium leak channel, NALCN, in health and disease. Frontiers in Cellular Neuroscience. 2014, 8(4): 132. PubMed ID: 24904279

The authors focused on the sodium leak, G protein-coupled receptors (GPCRs)-activated NALCN channel and summarized the existing knowledge of NALCN pathways in physiology and disease.
Al-Sayed M., et al. Mutations in NALCN, cause an autosomal-recessive syndrome with severe hypotonia, speech impairment, and cognitive delay. American Journal of Human Genetics. 2013, 93(4):721-726. PubMed ID: 24075186

The authors used homozygous mapping of SNPs, targeted sequencing and profiling exome sequencing in two unrelated families of NALCNs, and finally identified specific mutations that led to autosomal recessive syndrome.
Köroğlu Ç., et al. Recessive truncating NALCN mutation in infantile neuroaxonal dystrophy with facial dysmorphism. Journal of Medical Genetics. 2013, 50(8):515-520. PubMed ID: 23749988

The authors tested infants with idiopathic severe growth retardation and NALCN mutations, suggesting that NALCN is responsible for INAD facial deformity and broadens the genetic profile associated with axonal dystrophy.
Lu B., et al. The neuronal channel NALCN contributes resting sodium permeability and is required for normal respiratory rhythm. Cell. 2007, 129(2):371-383. PubMed ID: 17448995

This paper showed that NALCN formed a voltage-independent non-selective cation channel that controlled neuronal excitability and affected the respiratory rhythm of mice.
Yu F.H., et al. Overview of molecular relationships in the voltage-gated ion channel superfamily. Pharmacological Reviews. 2005, 57(4):387-395. PubMed ID: 16382097

This review reviewed the molecular and evolutionary relationships in the cation channel superfamily, which are associated with a variety of physiological activities.

NALCN Preparation Options

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Reference

Yu F H, et al. (2014). Overview of molecular relationships in the voltage-gated ion channel superfamily. Pharmacological Reviews. 57(4), 387-395.

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