Gene Symbol: SCN9A
Description: sodium voltage-gated channel alpha subunit 9
Alias: ETHA, FEB3B, GEFSP7, HSAN2D, NE-NA, NENA, Nav1.7, PN1, SFNP, sodium channel protein type 9 subunit alpha, hNE-Na, neuroendocrine sodium channel, peripheral sodium channel 1, sodium channel protein type IX subunit alpha, sodium channel, voltage-gated, type IX, alpha polypeptide, sodium channel, voltage-gated, type IX, alpha subunit, voltage-gated sodium channel alpha subunit Nav1.7, voltage-gated sodium channel subunit alpha Nav1.7
Species: human
Products:     SCN9A

Top Publications

  1. Goldberg Y, Macfarlane J, MacDonald M, Thompson J, Dube M, Mattice M, et al. Loss-of-function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations. Clin Genet. 2007;71:311-9 pubmed
    ..From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Nav1.7...
  2. Ahmad S, Dahllund L, Eriksson A, Hellgren D, Karlsson U, Lund P, et al. A stop codon mutation in SCN9A causes lack of pain sensation. Hum Mol Genet. 2007;16:2114-21 pubmed
    ..3-2q31.1). Screening of candidate genes in this region identified a protein-truncating mutation in SCN9A, which encodes for the voltage-gated sodium channel Na(v)1.7...
  3. Nilsen K, Nicholas A, Woods C, Mellgren S, Nebuchennykh M, Aasly J. Two novel SCN9A mutations causing insensitivity to pain. Pain. 2009;143:155-8 pubmed publisher
    ..Different mutations in the SCN9A gene causing loss of function of the voltage-gated sodium channel Nav1...
  4. Singh N, Pappas C, Dahle E, Claes L, Pruess T, De Jonghe P, et al. A role of SCN9A in human epilepsies, as a cause of febrile seizures and as a potential modifier of Dravet syndrome. PLoS Genet. 2009;5:e1000649 pubmed publisher
    ..large Utah family with significant linkage to chromosome 2q24 led us to identify a new febrile seizure (FS) gene, SCN9A encoding Na(v)1.7. In 21 affected members, we uncovered a potential mutation in a highly conserved amino acid, p...
  5. Choi J, Cheng X, Foster E, Leffler A, Tyrrell L, Te Morsche R, et al. Alternative splicing may contribute to time-dependent manifestation of inherited erythromelalgia. Brain. 2010;133:1823-35 pubmed publisher
    ..This study shows that a change in relative expression of splice isoforms can contribute to time-dependent manifestation of the functional phenotype of a sodium channelopathy. ..
  6. Wu M, Huang P, Yen C, Chen C, Lee M. A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockers. PLoS ONE. 2013;8:e55212 pubmed publisher
    ..Mutations in human SCN9A gene, encoding the ?-subunit of the voltage-gated sodium channel, Na(v)1.7, were found to be responsible for PE...
  7. Jarecki B, Sheets P, Jackson J, Cummins T. Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation. J Physiol. 2008;586:4137-53 pubmed publisher
    ..7 in a residue-specific manner and (2) disruption of the fast-inactivated state by PEPD mutations can be more moderate than previously indicated, which has important implications for the pathophysiology of PEPD. ..
  8. Raymond C, Castle J, Garrett Engele P, Armour C, Kan Z, Tsinoremas N, et al. Expression of alternatively spliced sodium channel alpha-subunit genes. Unique splicing patterns are observed in dorsal root ganglia. J Biol Chem. 2004;279:46234-41 pubmed
    ..6), SCN9A (Na(v)1.7), and SCN11A (Na(v)1.9) was characterized in detail...
  9. Novella S, Hisama F, Dib Hajj S, Waxman S. A case of inherited erythromelalgia. Nat Clin Pract Neurol. 2007;3:229-34 pubmed
    ..Neurological examination, MRI brain scan, electromyography, skin biopsy, laboratory blood testing, and DNA analysis. Juvenile onset primary erythromelalgia. Genetic counseling, and symptomatic management of neuropathic pain. ..

More Information


  1. Fischer T, Gilmore E, Estacion M, Eastman E, Taylor S, Melanson M, et al. A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia. Ann Neurol. 2009;65:733-41 pubmed publisher
    ..We extracted genomic DNA from blood samples of eight members of the family, and the sequence of SCN9A coding exons was compared with the reference Na(v)1.7 complementary DNA. Wild-type Na(v)1...
  2. Cheng X, Dib Hajj S, Tyrrell L, Wright D, Fischer T, Waxman S. Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders. Mol Pain. 2010;6:24 pubmed publisher
    ..Our results provide evidence for differential roles of the DIII/S4-S5 linker N- and C-termini in channel inactivation and activation, and demonstrate the cellular basis for pain in patients carrying these mutations. ..
  3. Dib Hajj S, Cummins T, Black J, Waxman S. From genes to pain: Na v 1.7 and human pain disorders. Trends Neurosci. 2007;30:555-63 pubmed
    ..The contribution of Na(v)1.7 to acquired and inherited pain states and the absence of motor, cognitive and cardiac deficits in patients lacking this channel make it an attractive target for the treatment of neuropathic pain. ..
  4. Dabby R, Sadeh M, Gilad R, Lampl Y, Cohen S, Inbar S, et al. Chronic non-paroxysmal neuropathic pain - Novel phenotype of mutation in the sodium channel SCN9A gene. J Neurol Sci. 2011;301:90-2 pubmed publisher
    Gain-of-function mutations in the SCN9A gene (encoding to NaV1.7 voltage-gated sodium channel) cause two rare paroxysmal pain disorders: inherited erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEDP)...
  5. Michiels J, Te Morsche R, Jansen J, Drenth J. Autosomal dominant erythermalgia associated with a novel mutation in the voltage-gated sodium channel alpha subunit Nav1.7. Arch Neurol. 2005;62:1587-90 pubmed
    ..7. Primary erythermalgia may be a neuropathic disorder of the small peripheral sensory and sympathetic neurons, and may be caused by hyperexcitability of Nav1.7. ..
  6. Dib Hajj S, Yang Y, Black J, Waxman S. The Na(V)1.7 sodium channel: from molecule to man. Nat Rev Neurosci. 2013;14:49-62 pubmed publisher
    ..7 is a major contributor to pain signalling in humans, and homology modelling based on crystal structures of ion channels suggests an atomic-level structural basis for the altered gating of mutant Na(V)1.7 that causes pain. ..
  7. Duan G, Xiang G, Zhang X, Yuan R, Zhan H, Qi D. A single-nucleotide polymorphism in SCN9A may decrease postoperative pain sensitivity in the general population. Anesthesiology. 2013;118:436-42 pubmed publisher
    This study aimed to explore the role of a nonsynonymous single-nucleotide polymorphism, 3312G>T, in SCN9A, which was identified in probands with congenital indifference to pain, but which is also present in normal controls, in the ..
  8. Drenth J, Finley W, Breedveld G, Testers L, Michiels J, Guillet G, et al. The primary erythermalgia-susceptibility gene is located on chromosome 2q31-32. Am J Hum Genet. 2001;68:1277-82 pubmed
    ..Identification of the primary erythermalgia gene will allow a better clinical classification of this pleomorphic group of disorders. ..
  9. Yiangou Y, Facer P, Chessell I, Bountra C, Chan C, Fertleman C, et al. Voltage-gated ion channel Nav1.7 innervation in patients with idiopathic rectal hypersensitivity and paroxysmal extreme pain disorder (familial rectal pain). Neurosci Lett. 2007;427:77-82 pubmed
    ..7 immunoreactivity or expression. Drugs that target Na(v)1.7-expressing nerve terminals may be useful for treating rectal hypersensitivity, and combining these with TRPV1 antagonists may enhance efficacy. ..
  10. Estacion M, Dib Hajj S, Benke P, Te Morsche R, Eastman E, MacAla L, et al. NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders. J Neurosci. 2008;28:11079-88 pubmed publisher
    ..These observations indicate that IEM and PEPD mutants are part of a physiological continuum that can produce a continuum of clinical phenotypes. ..
  11. Siqueira S, Alves B, Malpartida H, Teixeira M, Siqueira J. Abnormal expression of voltage-gated sodium channels Nav1.7, Nav1.3 and Nav1.8 in trigeminal neuralgia. Neuroscience. 2009;164:573-7 pubmed publisher
    ..7 was downregulated in TN (P=0.017) and Nav1.3 was upregulated in these patients (P=0.043). We propose a physiopathological mechanism for these findings. Besides vascular compression of TN, this disease might be also a channelopathy. ..
  12. Samuels M, Te Morsche R, Lynch M, Drenth J. Compound heterozygosity in sodium channel Nav1.7 in a family with hereditary erythermalgia. Mol Pain. 2008;4:21 pubmed publisher
    ..This is the second reported study of potential compound heterozygosity for coding polymorphisms in Nav1.7, the first being in a patient with paroxysmal extreme pain disorder. ..
  13. Harty T, Dib Hajj S, Tyrrell L, Blackman R, Hisama F, Rose J, et al. Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons. J Neurosci. 2006;26:12566-75 pubmed
    ..Thus, A863P mutant channels produce hyperexcitability in DRG neurons, which contributes to the pathophysiology of IEM. ..
  14. Han C, Hoeijmakers J, Ahn H, Zhao P, Shah P, Lauria G, et al. Nav1.7-related small fiber neuropathy: impaired slow-inactivation and DRG neuron hyperexcitability. Neurology. 2012;78:1635-43 pubmed publisher skin biopsy, quantitative sensory testing, nerve conduction studies, screening of genomic DNA for variants in SCN9A, and functional analysis. Voltage-clamp analysis following expression within DRG neurons revealed that the Na(v)1...
  15. Cummins T, Dib Hajj S, Waxman S. Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. J Neurosci. 2004;24:8232-6 pubmed
  16. Yang Y, Wang Y, Li S, Xu Z, Li H, Ma L, et al. Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia. J Med Genet. 2004;41:171-4 pubmed
    ..analysis in a Chinese family with primary erythermalgia, and screened the mutations in the two candidate genes, SCN9A and GCA, in the family and a sporadic patient. Linkage analysis yielded a maximum lod score of 2...
  17. Fischer T, Waxman S. Familial pain syndromes from mutations of the NaV1.7 sodium channel. Ann N Y Acad Sci. 2010;1184:196-207 pubmed publisher
    ..7 channel may provide a unique target for the pharmacotherapy of pain in humans. In this review article we summarize current knowledge regarding several different disease manifestations arising from changes within the Na(v)1.7 channel. ..
  18. Reimann F, Cox J, Belfer I, Diatchenko L, Zaykin D, McHale D, et al. Pain perception is altered by a nucleotide polymorphism in SCN9A. Proc Natl Acad Sci U S A. 2010;107:5148-53 pubmed publisher
    The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe episodic pain in paroxysmal extreme pain disorder and primary erythermalgia...
  19. Staud R, Price D, Janicke D, Andrade E, Hadjipanayis A, Eaton W, et al. Two novel mutations of SCN9A (Nav1.7) are associated with partial congenital insensitivity to pain. Eur J Pain. 2011;15:223-30 pubmed publisher
    ..Sequence analysis of genomic DNA revealed two novel SCN9A mutations in this index case (IC)...
  20. Sangameswaran L, Fish L, Koch B, Rabert D, Delgado S, Ilnicka M, et al. A novel tetrodotoxin-sensitive, voltage-gated sodium channel expressed in rat and human dorsal root ganglia. J Biol Chem. 1997;272:14805-9 pubmed
    ..cellular expression, and functional analysis of a novel tetrodotoxin-sensitive peripheral sodium channel (PN), PN1. PN1 mRNA is expressed in many different tissues...
  21. Young F. When adaptive processes go awry: gain-of-function in SCN9A. Clin Genet. 2008;73:34-6 pubmed
  22. Diss J, Stewart D, Pani F, Foster C, Walker M, Patel A, et al. A potential novel marker for human prostate cancer: voltage-gated sodium channel expression in vivo. Prostate Cancer Prostatic Dis. 2005;8:266-73 pubmed
    ..It is concluded that VGSCalpha expression increases significantly in CaP in vivo and that Nav1.7 is a potential functional diagnostic marker. ..
  23. Fertleman C, Baker M, Parker K, Moffatt S, Elmslie F, Abrahamsen B, et al. SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. Neuron. 2006;52:767-74 pubmed
    ..A genome-wide linkage search followed by mutational analysis of the candidate gene SCN9A, which encodes hNa(v)1.7, identified eight missense mutations in 11 families and 2 sporadic cases...
  24. Sheets P, Jackson J, Waxman S, Dib Hajj S, Cummins T. A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity. J Physiol. 2007;581:1019-31 pubmed
    ..7 and suggests that the response of individuals with hereditary erythromelalgia to lidocaine treatment may be determined, at least in part, by their specific genotype. ..
  25. Lee M, Yu H, Hsieh S, Stephenson D, Lu C, Yang C. Characterization of a familial case with primary erythromelalgia from Taiwan. J Neurol. 2007;254:210-4 pubmed
    ..that the disease segregates with a novel mutation in the alpha subunit of the voltage-gated sodium channel (SCN9A or Na(v)1.7)...
  26. Weiss J, Pyrski M, Jacobi E, Bufe B, Willnecker V, Schick B, et al. Loss-of-function mutations in sodium channel Nav1.7 cause anosmia. Nature. 2011;472:186-90 pubmed publisher
    Loss of function of the gene SCN9A, encoding the voltage-gated sodium channel Na(v)1.7, causes a congenital inability to experience pain in humans. Here we show that Na(v)1...
  27. Cox J, Sheynin J, Shorer Z, Reimann F, Nicholas A, Zubovic L, et al. Congenital insensitivity to pain: novel SCN9A missense and in-frame deletion mutations. Hum Mutat. 2010;31:E1670-86 pubmed publisher
    ..7, a protein highly expressed in pain-sensing neurons. Mutations in SCN9A cause three human pain disorders: bi-allelic loss of function mutations result in Channelopathy-associated ..
  28. Choi J, Dib Hajj S, Waxman S. Inherited erythermalgia: limb pain from an S4 charge-neutral Na channelopathy. Neurology. 2006;67:1563-7 pubmed
    ..These changes should increase excitability of nociceptive dorsal root ganglion neurons in which the mutant channel is present, thus contributing to pain. ..
  29. Lampert A, Dib Hajj S, Tyrrell L, Waxman S. Size matters: Erythromelalgia mutation S241T in Nav1.7 alters channel gating. J Biol Chem. 2006;281:36029-35 pubmed
    ..We conclude that the linker between S4 and S5 in domain I of Nav1.7 modulates gating of this channel, and that a larger side chain at position 241 interferes with its gating mechanisms. ..
  30. Yuan R, Zhang X, Deng Q, Si D, Wu Y, Gao F, et al. Two novel SCN9A gene heterozygous mutations may cause partial deletion of pain perception. Pain Med. 2011;12:1510-4 pubmed publisher
    ..The measures made were novel mutations within SCN9A. Sequence analysis of candidate genes of two affected individuals identified two novel heterozygous mutations (..
  31. Estacion M, Harty T, Choi J, Tyrrell L, Dib Hajj S, Waxman S. A sodium channel gene SCN9A polymorphism that increases nociceptor excitability. Ann Neurol. 2009;66:862-6 pubmed publisher
    Sodium channel Na(V)1.7, encoded by the SCN9A gene, is preferentially expressed in nociceptive primary sensory neurons, where it amplifies small depolarizations...
  32. Jarecki B, Sheets P, Xiao Y, Jackson J, Cummins T. Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T. Channels (Austin). 2009;3:259-67 pubmed
  33. Uysal Onganer P, Djamgoz M. Epidermal growth factor potentiates in vitro metastatic behaviour of human prostate cancer PC-3M cells: involvement of voltage-gated sodium channel. Mol Cancer. 2007;6:76 pubmed
    ..1) EGF has a major involvement in the upregulation of functional VGSC expression in human PCa PC-3M cells. (2) VGSC activity has a significant intermediary role in potentiating effect of EGF in human PCa. ..
  34. Dib Hajj S, Rush A, Cummins T, Hisama F, Novella S, Tyrrell L, et al. Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons. Brain. 2005;128:1847-54 pubmed
    ..We describe a novel mutation in a family with erythromelalgia in SCN9A, the gene that encodes the Na(v)1.7 sodium channel. Na(v)1...
  35. Drenth J, Te Morsche R, Mansour S, Mortimer P. Primary erythermalgia as a sodium channelopathy: screening for SCN9A mutations: exclusion of a causal role of SCN10A and SCN11A. Arch Dermatol. 2008;144:320-4 pubmed publisher
    To elucidate the rate of missense mutations in the SCN9A gene (which encodes sodium channel Na(v)1.7) (OMIM 603415) among patients with primary erythermalgia and to examine the possibility that other sodium channels can cause the disease...
  36. Estacion M, Han C, Choi J, Hoeijmakers J, Lauria G, Drenth J, et al. Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7. Mol Pain. 2011;7:92 pubmed publisher
    ..Our results demonstrate intra- and interfamily phenotypic diversity in pain syndromes produced by a gain-of-function variant of NaV1.7. ..
  37. Drenth J, Te Morsche R, Guillet G, Taieb A, Kirby R, Jansen J. SCN9A mutations define primary erythermalgia as a neuropathic disorder of voltage gated sodium channels. J Invest Dermatol. 2005;124:1333-8 pubmed
    ..Recently, Yang et al identified two missense mutations of the sodium channel alpha subunit SCN9A in patients with erythermalgia...
  38. Cheng X, Dib Hajj S, Tyrrell L, te Morsche R, Drenth J, Waxman S. Deletion mutation of sodium channel Na(V)1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability. Brain. 2011;134:1972-86 pubmed publisher
    ..7 channels. Our results suggest that despite the pivotal role of activation shift in inherited erythromelalgia development, slow inactivation may regulate clinical phenotype by altering channel availability. ..
  39. Faber C, Hoeijmakers J, Ahn H, Cheng X, Han C, Choi J, et al. Gain of function Na?1.7 mutations in idiopathic small fiber neuropathy. Ann Neurol. 2012;71:26-39 pubmed publisher
    ..identify a genetic basis for I-SFN by screening patients with biopsy-confirmed idiopathic SFN for mutations in the SCN9A gene, encoding voltage-gated sodium channel Na(V)1...
  40. Cheng X, Dib Hajj S, Tyrrell L, Waxman S. Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade. Mol Pain. 2008;4:1 pubmed publisher
    ..7, compared to the other reported cases of inherited erythromelalgia, may contribute to the later age of onset and slower progression of the symptoms reported in association with this mutation. ..
  41. Lampert A, Dib Hajj S, Eastman E, Tyrrell L, Lin Z, Yang Y, et al. Erythromelalgia mutation L823R shifts activation and inactivation of threshold sodium channel Nav1.7 to hyperpolarized potentials. Biochem Biophys Res Commun. 2009;390:319-24 pubmed publisher
    ..7 leads to a pronounced hyperpolarizing shift of activation, a change that is expected to increase nociceptor excitability despite the hyperpolarizing shift in fast-inactivation, which is unique among the IEM mutations. ..
  42. Dib Hajj S, Estacion M, Jarecki B, Tyrrell L, Fischer T, Lawden M, et al. Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable. Mol Pain. 2008;4:37 pubmed publisher an autosomal dominant painful neuropathy with many, but not all, cases linked to gain-of-function mutations in SCN9A which encodes voltage-gated sodium channel Nav1.7...
  43. Han C, Rush A, Dib Hajj S, Li S, Xu Z, Wang Y, et al. Sporadic onset of erythermalgia: a gain-of-function mutation in Nav1.7. Ann Neurol. 2006;59:553-8 pubmed
    ..Founder mutations in Na(v)1.7, which can confer hyperexcitability on peripheral sensory neurons, can underlie sporadic erythermalgia. ..
  44. Cox J, Reimann F, Nicholas A, Thornton G, Roberts E, Springell K, et al. An SCN9A channelopathy causes congenital inability to experience pain. Nature. 2006;444:894-8 pubmed
    ..3. This region contains the gene SCN9A, encoding the alpha-subunit of the voltage-gated sodium channel, Na(v)1...
  45. Vargas Alarcon G, Alvarez Leon E, Fragoso J, Vargas A, Martinez A, Vallejo M, et al. A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia. BMC Musculoskelet Disord. 2012;13:23 pubmed publisher
    ..7) act as molecular gatekeepers for pain detection. Nav1.7 is encoded in gene SCN9A of chromosome 2q24...
  46. Meguro K, Iida H, Takano H, Morita T, Sata M, Nagai R, et al. Function and role of voltage-gated sodium channel NaV1.7 expressed in aortic smooth muscle cells. Am J Physiol Heart Circ Physiol. 2009;296:H211-9 pubmed publisher
    ..In contrast to native aorta, cultured hASMCs strongly expressed SCN9A encoding Na(V)1.7, as determined by quantitative RT-PCR...
  47. Klein C, Wu Y, Kilfoyle D, Sandroni P, Davis M, Gavrilova R, et al. Infrequent SCN9A mutations in congenital insensitivity to pain and erythromelalgia. J Neurol Neurosurg Psychiatry. 2013;84:386-91 pubmed publisher
    Mutations in SCN9A have been reported in (1) congenital insensitivity to pain (CIP); (2) primary erythromelalgia; (3) paroxysmal extreme pain disorder; (4) febrile seizures and recently (5) small fibre sensory neuropathy...
  48. Klugbauer N, Lacinova L, Flockerzi V, Hofmann F. Structure and functional expression of a new member of the tetrodotoxin-sensitive voltage-activated sodium channel family from human neuroendocrine cells. EMBO J. 1995;14:1084-90 pubmed
    ..The cDNA of hNE-Na (human neuroendocrine sodium channel) encodes a 1977 amino acid protein which phylogenetically represents a link between sodium channels ..
  49. Catterall W, Goldin A, Waxman S. International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels. Pharmacol Rev. 2005;57:397-409 pubmed
    ..This article presents the molecular relationships and physiological roles of these sodium channel proteins and provides comprehensive information on their molecular, genetic, physiological, and pharmacological properties. ..
  50. Kurban M, Wajid M, Shimomura Y, Christiano A. A nonsense mutation in the SCN9A gene in congenital insensitivity to pain. Dermatology. 2010;221:179-83 pubmed publisher
    ..Clinically, CIP is characterized by insensitivity to all modalities of pain except neuropathic pain, and recurrent injuries frequently go unnoticed. CIP is caused by mutations in the SCN9A gene encoding for the Na1.7 channel.
  51. Drenth J, Waxman S. Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders. J Clin Invest. 2007;117:3603-9 pubmed
    The voltage-gated sodium-channel type IX alpha subunit, known as Na(v)1.7 and encoded by the gene SCN9A, is located in peripheral neurons and plays an important role in action potential production in these cells...
  52. Cao L, McDonnell A, Nitzsche A, Alexandrou A, Saintot P, Loucif A, et al. Pharmacological reversal of a pain phenotype in iPSC-derived sensory neurons and patients with inherited erythromelalgia. Sci Transl Med. 2016;8:335ra56 pubmed publisher
    ..7 blockers, including the clinical test agent. Given the importance of peripherally expressed sodium channels in many pain conditions, our approach may have broader utility for a wide range of pain and sensory conditions. ..
  53. Ke B, Liu N, Zhang R, Guo X, Li B, Wang X, et al. [Analysis of lymph node metastasis pattern in gastric cancer patients at stage pN1]. Zhonghua Wei Chang Wai Ke Za Zhi. 2017;20:782-786 pubmed
    To investigate the lymph node metastasis pattern in pN1 stage gastric cancer patients and to analyze its risk factors...
  54. La D, Peterson E, Bode C, Boezio A, Bregman H, Chu Moyer M, et al. The discovery of benzoxazine sulfonamide inhibitors of NaV1.7: Tools that bridge efficacy and target engagement. Bioorg Med Chem Lett. 2017;27:3477-3485 pubmed publisher
    ..The latter represents a simple and efficient means of measuring target engagement. ..
  55. García Novoa A, Acea Nebril B. Treatment of the axila in breast cancer surgery: Systematic review of its impact on survival. Cir Esp. 2017;95:503-512 pubmed publisher
    ..In patients pN1 it is proposed not to treat the axilla or replace ALND for axillary radiotherapy...