SCN9A

Summary

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

Top Publications

  1. pmc Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7
    Chongyang Han
    Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China
    Mol Pain 3:3. 2007
  2. ncbi Loss-of-function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations
    Y P Goldberg
    Xenon Pharmaceuticals Inc, 3650 Gilmore Way, Burnaby, BC V5G4W8, Canada
    Clin Genet 71:311-9. 2007
  3. ncbi A stop codon mutation in SCN9A causes lack of pain sensation
    Sultan Ahmad
    Department of Molecular Sciences, AstraZeneca R and D Montreal, Ville St Laurent, Quebec, Canada
    Hum Mol Genet 16:2114-21. 2007
  4. ncbi Characterization of a new class of potent inhibitors of the voltage-gated sodium channel Nav1.7
    Brande S Williams
    Department of Ion Channels, Merck Research Laboratories, P O Box 2000, Rahway, New Jersey 07065, USA
    Biochemistry 46:14693-703. 2007
  5. doi Hepatic and branchial glutathione S-transferases of two fish species: substrate specificity and biotransformation of microcystin-LR
    I Setlíková
    Faculty of Agriculture, University of South Bohemia in Ceske Budejovice, Ceske Budejovice, Czech Republic
    Comp Biochem Physiol C Toxicol Pharmacol 149:515-23. 2009
  6. pmc Structure and functional expression of a new member of the tetrodotoxin-sensitive voltage-activated sodium channel family from human neuroendocrine cells
    N Klugbauer
    Institut für Pharmakologie und Toxikologie Technischen Universität München, Germany
    EMBO J 14:1084-90. 1995
  7. ncbi A novel tetrodotoxin-sensitive, voltage-gated sodium channel expressed in rat and human dorsal root ganglia
    L Sangameswaran
    Center for Biological Research, Neurobiology Unit, Roche Bioscience, Palo Alto, California 94304, USA
    J Biol Chem 272:14805-9. 1997
  8. pmc Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia
    Y Yang
    Department of Dermatology, Peking University First Hospital, Beijing, China
    J Med Genet 41:171-4. 2004
  9. ncbi Expression of alternatively spliced sodium channel alpha-subunit genes. Unique splicing patterns are observed in dorsal root ganglia
    Christopher K Raymond
    Rosetta Inpharmatics LLC, Seattle, Washington 98109, USA
    J Biol Chem 279:46234-41. 2004
  10. ncbi Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons
    S D Dib-Hajj
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain 128:1847-54. 2005

Research Grants

  1. Harnessing gating-pore currents to identify novel Nav1.7 modulators
    Theodore R Cummins; Fiscal Year: 2012
  2. GING K WANG; Fiscal Year: 2014
  3. Design, Synthesis and Evaluation of Novel Isoform-Selective Sodium Channel Inhibi
    JOHN VINCENT MULCAHY; Fiscal Year: 2013
  4. Evolving membrane proteins for high-level expression in modified mammalian cells
    Michael J Betenbaugh; Fiscal Year: 2013
  5. Stephen Waxman; Fiscal Year: 2016
  6. Theodore J Price; Fiscal Year: 2016
  7. Theodore R Cummins; Fiscal Year: 2016
  8. Pharmacology and biophysics of the voltage-gated sodium channel Nav1.7: a therape
    Seok Yong Lee; Fiscal Year: 2011
  9. Trigeminal Neuropathic Pain Mechanisms
    Michael Henry; Fiscal Year: 2006
  10. Samuel M Wu; Fiscal Year: 2016

Detail Information

Publications180 found, 100 shown here

  1. pmc Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7
    Chongyang Han
    Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100050, China
    Mol Pain 3:3. 2007
    ..Inherited erythromelalgia has recently been linked to mutations in the gene SCN9A, which encodes the voltage-gated sodium channel Nav1.7. Nav1...
  2. ncbi Loss-of-function mutations in the Nav1.7 gene underlie congenital indifference to pain in multiple human populations
    Y P Goldberg
    Xenon Pharmaceuticals Inc, 3650 Gilmore Way, Burnaby, BC V5G4W8, Canada
    Clin Genet 71:311-9. 2007
    ..From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Nav1.7...
  3. ncbi A stop codon mutation in SCN9A causes lack of pain sensation
    Sultan Ahmad
    Department of Molecular Sciences, AstraZeneca R and D Montreal, Ville St Laurent, Quebec, Canada
    Hum Mol Genet 16:2114-21. 2007
    ..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...
  4. ncbi Characterization of a new class of potent inhibitors of the voltage-gated sodium channel Nav1.7
    Brande S Williams
    Department of Ion Channels, Merck Research Laboratories, P O Box 2000, Rahway, New Jersey 07065, USA
    Biochemistry 46:14693-703. 2007
    ..7 channel subtype, and with appropriate pharmacokinetic and drug metabolism properties, these compounds could be developed as analgesic agents...
  5. doi Hepatic and branchial glutathione S-transferases of two fish species: substrate specificity and biotransformation of microcystin-LR
    I Setlíková
    Faculty of Agriculture, University of South Bohemia in Ceske Budejovice, Ceske Budejovice, Czech Republic
    Comp Biochem Physiol C Toxicol Pharmacol 149:515-23. 2009
    ..CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), 4-nitrobenzyl chloride (pNBC) and ethacrynic acid (ETHA). Biotransformation rate of MC-LR was determined by high performance liquid chromatography (HPLC)...
  6. pmc Structure and functional expression of a new member of the tetrodotoxin-sensitive voltage-activated sodium channel family from human neuroendocrine cells
    N Klugbauer
    Institut für Pharmakologie und Toxikologie Technischen Universität München, Germany
    EMBO J 14:1084-90. 1995
    ..The cDNA of hNE-Na (human neuroendocrine sodium channel) encodes a 1977 amino acid protein which phylogenetically represents a link between sodium channels ..
  7. ncbi A novel tetrodotoxin-sensitive, voltage-gated sodium channel expressed in rat and human dorsal root ganglia
    L Sangameswaran
    Center for Biological Research, Neurobiology Unit, Roche Bioscience, Palo Alto, California 94304, USA
    J Biol Chem 272:14805-9. 1997
    ..cellular expression, and functional analysis of a novel tetrodotoxin-sensitive peripheral sodium channel (PN), PN1. PN1 mRNA is expressed in many different tissues...
  8. pmc Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia
    Y Yang
    Department of Dermatology, Peking University First Hospital, Beijing, China
    J Med Genet 41:171-4. 2004
    ..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...
  9. ncbi Expression of alternatively spliced sodium channel alpha-subunit genes. Unique splicing patterns are observed in dorsal root ganglia
    Christopher K Raymond
    Rosetta Inpharmatics LLC, Seattle, Washington 98109, USA
    J Biol Chem 279:46234-41. 2004
    ..6), SCN9A (Na(v)1.7), and SCN11A (Na(v)1.9) was characterized in detail...
  10. ncbi Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons
    S D Dib-Hajj
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain 128:1847-54. 2005
    ..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...
  11. ncbi A potential novel marker for human prostate cancer: voltage-gated sodium channel expression in vivo
    J K J Diss
    Department of Biological Sciences, Neuroscience Solutions to Cancer Research Group, Imperial College London, South Kensington Campus, London, UK
    Prostate Cancer Prostatic Dis 8:266-73. 2005
    ..It is concluded that VGSCalpha expression increases significantly in CaP in vivo and that Nav1.7 is a potential functional diagnostic marker...
  12. ncbi Autosomal dominant erythermalgia associated with a novel mutation in the voltage-gated sodium channel alpha subunit Nav1.7
    Jan J Michiels
    Haemostasis and Thrombosis Research, Department of Haematology, Antwerp University Hospital, University of Antwerp, Antwerp, Belgium
    Arch Neurol 62:1587-90. 2005
    ..Autosomal dominant primary erythermalgia is a rare disorder characterized by recurrent attacks of red, warm, and painful hands and/or feet...
  13. ncbi Sporadic onset of erythermalgia: a gain-of-function mutation in Nav1.7
    Chongyang Han
    Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
    Ann Neurol 59:553-8. 2006
    ..We investigated the role of Na(v)1.7 in a sporadic case of erythermalgia in a Chinese family...
  14. ncbi Inherited erythermalgia: limb pain from an S4 charge-neutral Na channelopathy
    Jin Sung Choi
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    Neurology 67:1563-7. 2006
    ..7 sodium channel, which is preferentially expressed in nociceptors. Thus far, Na(v)1.7 mutations within intracellular linker parts of the channel have been physiologically characterized...
  15. ncbi Size matters: Erythromelalgia mutation S241T in Nav1.7 alters channel gating
    Angelika Lampert
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Biol Chem 281:36029-35. 2006
    ..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...
  16. ncbi Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons
    T Patrick Harty
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 26:12566-75. 2006
    ..Thus, A863P mutant channels produce hyperexcitability in DRG neurons, which contributes to the pathophysiology of IEM...
  17. ncbi SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes
    Caroline R Fertleman
    Department of Paediatrics and Child Health, Royal Free and University College Medical School, University College London, 5 University Street, London WC1E 6JJ, United Kingdom
    Neuron 52:767-74. 2006
    ..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...
  18. ncbi An SCN9A channelopathy causes congenital inability to experience pain
    James J Cox
    Department of Medical Genetics, Cambridge Institute for Medical Research, Wellcome MRC Building, Addenbrooke s Hospital, Cambridge CB2 0XY, UK
    Nature 444:894-8. 2006
    ..3. This region contains the gene SCN9A, encoding the alpha-subunit of the voltage-gated sodium channel, Na(v)1...
  19. ncbi Characterization of a familial case with primary erythromelalgia from Taiwan
    Ming Jen Lee
    Department of Neurology, National Taiwan University Hospital, 7 Chung Shan South Road, Taipei 100, Taiwan
    J Neurol 254:210-4. 2007
    ..that the disease segregates with a novel mutation in the alpha subunit of the voltage-gated sodium channel (SCN9A or Na(v)1.7)...
  20. ncbi A case of inherited erythromelalgia
    Steven P Novella
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06520 8018, USA
    Nat Clin Pract Neurol 3:229-34. 2007
    ..The episodes were triggered by heat or exertion. His medical history revealed an extensive six-generation family history of similar symptoms...
  21. ncbi From genes to pain: Na v 1.7 and human pain disorders
    Sulayman D Dib-Hajj
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Trends Neurosci 30:555-63. 2007
    ..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...
  22. pmc Epidermal growth factor potentiates in vitro metastatic behaviour of human prostate cancer PC-3M cells: involvement of voltage-gated sodium channel
    Pinar Uysal-Onganer
    Neuroscience Solutions to Cancer Research Group, Division of Cell and Molecular Biology, Sir Alexander Fleming Building, Imperial College London, South Kensington Campus, London SW7 2AZ, UK
    Mol Cancer 6:76. 2007
    ..Protein expression was studied by Western blots and immunocytochemistry and digital image analysis. Functional assays involved measurements of transverse migration, endocytic membrane activity and Matrigel invasion...
  23. pmc Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders
    Joost P H Drenth
    Department of Medicine, Division of Gastroenterology and Hepatology, University Medical Center St Radboud, Nijmegen, The Netherlands
    J Clin Invest 117:3603-9. 2007
    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...
  24. ncbi When adaptive processes go awry: gain-of-function in SCN9A
    F B J Young
    Centre for Molecular Medicine and Therapeutics, 950 West 28th Avenue, Vancouver, BC V5Z 4H4, Canada
    Clin Genet 73:34-6. 2008
  25. doi Primary erythermalgia as a sodium channelopathy: screening for SCN9A mutations: exclusion of a causal role of SCN10A and SCN11A
    Joost P H Drenth
    Division of Gastroenterology and Hepatology, Department of Medicine, University Medical Center St Radboud, PO Box 9101, 6500 HB Nijmegen, The Netherlands
    Arch Dermatol 144:320-4. 2008
    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.
  26. pmc Compound heterozygosity in sodium channel Nav1.7 in a family with hereditary erythermalgia
    Mark E Samuels
    Département de Médicine, Centre de Recherche du CHUM, Local M 5226, Hopital Notre Dame, 1560 rue Sherbrooke Est, Montreal QC H2L 4M1, Canada
    Mol Pain 4:21. 2008
    ..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...
  27. pmc Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable
    Sulayman D Dib-Hajj
    Deptartment of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 4:37. 2008
    ..is 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...
  28. doi 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
    M Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 28:11079-88. 2008
    ..These observations indicate that IEM and PEPD mutants are part of a physiological continuum that can produce a continuum of clinical phenotypes...
  29. doi Function and role of voltage-gated sodium channel NaV1.7 expressed in aortic smooth muscle cells
    Kentaro Meguro
    Dept of Cardiovascular Medicine, Univ of Tokyo Graduate School of Medicine, Hongo 7 3 1, Bunkyo ku, Tokyo 113 8655, Japan
    Am J Physiol Heart Circ Physiol 296:H211-9. 2009
    ..In contrast to native aorta, cultured hASMCs strongly expressed SCN9A encoding Na(V)1.7, as determined by quantitative RT-PCR...
  30. doi Two novel SCN9A mutations causing insensitivity to pain
    K B Nilsen
    Department of Neuroscience, Norwegian University of Science and Technology, Edvard Griegs gate 8, 7489 Trondheim, Norway
    Pain 143:155-8. 2009
    ..Different mutations in the SCN9A gene causing loss of function of the voltage-gated sodium channel Nav1...
  31. pmc A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia
    Tanya Z Fischer
    Department of Neurology, Yale University School of Medicine, New Haven, CT 16510, USA
    Ann Neurol 65:733-41. 2009
    ..Inherited erythromelalgia (IEM) has been linked to gain-of-function mutations of Na(v)1.7. We now report a novel mutation (V400M) in a three-generation Canadian family in which pain is relieved by carbamazepine (CBZ)...
  32. pmc Alternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T
    Brian W Jarecki
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA
    Channels (Austin) 3:259-67. 2009
    ....
  33. doi Abnormal expression of voltage-gated sodium channels Nav1.7, Nav1.3 and Nav1.8 in trigeminal neuralgia
    S R D T Siqueira
    School of Arts, Science and Humanities, University of Sao Paulo, Brazil
    Neuroscience 164:573-7. 2009
    ..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...
  34. pmc A role of SCN9A in human epilepsies, as a cause of febrile seizures and as a potential modifier of Dravet syndrome
    Nanda A Singh
    Department of Human Genetics, University of Utah, Salt Lake City, Utah, United States of America
    PLoS Genet 5:e1000649. 2009
    ..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...
  35. doi Erythromelalgia mutation L823R shifts activation and inactivation of threshold sodium channel Nav1.7 to hyperpolarized potentials
    Angelika Lampert
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Biochem Biophys Res Commun 390:319-24. 2009
    ..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...
  36. doi A sodium channel gene SCN9A polymorphism that increases nociceptor excitability
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven CT
    Ann Neurol 66:862-6. 2009
    Sodium channel Na(V)1.7, encoded by the SCN9A gene, is preferentially expressed in nociceptive primary sensory neurons, where it amplifies small depolarizations...
  37. doi Familial pain syndromes from mutations of the NaV1.7 sodium channel
    Tanya Z Fischer
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA
    Ann N Y Acad Sci 1184:196-207. 2010
    ..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...
  38. pmc Pain perception is altered by a nucleotide polymorphism in SCN9A
    Frank Reimann
    Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke s Hospital, Cambridge CB2 0XY, United Kingdom
    Proc Natl Acad Sci U S A 107:5148-53. 2010
    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...
  39. pmc Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders
    Xiaoyang Cheng
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT, USA
    Mol Pain 6:24. 2010
    ....
  40. doi Alternative splicing may contribute to time-dependent manifestation of inherited erythromelalgia
    Jin Sung Choi
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Brain 133:1823-35. 2010
    ..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...
  41. pmc A nonsense mutation in the SCN9A gene in congenital insensitivity to pain
    Mazen Kurban
    Department of Dermatology, Columbia University, New York, NY, USA
    Dermatology 221:179-83. 2010
    ..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.
  42. pmc Congenital insensitivity to pain: novel SCN9A missense and in-frame deletion mutations
    James J Cox
    Department of Medical Genetics, University of Cambridge, UK
    Hum Mutat 31:E1670-86. 2010
    ..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 ..
  43. pmc Two novel mutations of SCN9A (Nav1.7) are associated with partial congenital insensitivity to pain
    Roland Staud
    Department of Medicine, University of Florida, Gainesville, FL 32610, United States
    Eur J Pain 15:223-30. 2011
    ..Sequence analysis of genomic DNA revealed two novel SCN9A mutations in this index case (IC)...
  44. doi Chronic non-paroxysmal neuropathic pain - Novel phenotype of mutation in the sodium channel SCN9A gene
    Ron Dabby
    Department of Neurology, Wolfson Medical Center, Holon, Israel Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
    J Neurol Sci 301:90-2. 2011
    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)...
  45. pmc Loss-of-function mutations in sodium channel Nav1.7 cause anosmia
    Jan Weiss
    Department of Physiology, University of Saarland School of Medicine, 66421 Homburg, Germany
    Nature 472:186-90. 2011
    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...
  46. doi Gain of function Naν1.7 mutations in idiopathic small fiber neuropathy
    Catharina G Faber
    Department of Neurology, University Medical Center Maastricht, Maastricht, The Netherlands
    Ann Neurol 71:26-39. 2012
    ..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...
  47. doi Deletion mutation of sodium channel Na(V)1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability
    Xiaoyang Cheng
    Department of Neurology and Centre for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT, USA
    Brain 134:1972-86. 2011
    ..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...
  48. pmc A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia
    Gilberto Vargas-Alarcon
    Department of Molecular Biology, National Institute of Cardiology Ignacio Chavez, Mexico City, Mexico
    BMC Musculoskelet Disord 13:23. 2012
    ..7) act as molecular gatekeepers for pain detection. Nav1.7 is encoded in gene SCN9A of chromosome 2q24...
  49. doi Nav1.7-related small fiber neuropathy: impaired slow-inactivation and DRG neuron hyperexcitability
    C Han
    Department of Neurology, Yale University School of Medicine, New Haven, CT, USA
    Neurology 78:1635-43. 2012
    ..Here we show that the I739V Na(v)1.7 variant in a patient with biopsy-confirmed I-SFN impairs slow-inactivation within DRG neurons and increases their excitability...
  50. pmc Infrequent SCN9A mutations in congenital insensitivity to pain and erythromelalgia
    Christopher J Klein
    Department of Neurology, Division of Peripheral Nerve Diseases, Mayo Clinic, Rochester, MN 55905, USA
    J Neurol Neurosurg Psychiatry 84:386-91. 2013
    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...
  51. doi The Na(V)1.7 sodium channel: from molecule to man
    Sulayman D Dib-Hajj
    Department of Neurology, and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Nat Rev Neurosci 14:49-62. 2013
    ..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...
  52. pmc A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockers
    Min Tzu Wu
    Graduate Institute of Zoology, College of Life Sciences, National Taiwan University, Taipei, Taiwan
    PLoS ONE 8:e55212. 2013
    ..Mutations in human SCN9A gene, encoding the α-subunit of the voltage-gated sodium channel, Na(v)1.7, were found to be responsible for PE...
  53. ncbi International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels
    William A Catterall
    Department of Pharmacology, University of Washington, Mailstop 357280, Seattle, WA 98195 7280
    Pharmacol Rev 57:397-409. 2005
    ..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...
  54. doi Two novel SCN9A gene heterozygous mutations may cause partial deletion of pain perception
    Ruimei Yuan
    Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
    Pain Med 12:1510-4. 2011
    ..Our purpose was to investigate why this protection disappears or almost disappears for patients with congenital indifference to pain (CIP)...
  55. pmc Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 7:92. 2011
    ..In this paper we describe three patients who house the NaV1.7/I228M variant...
  56. ncbi SCN9A mutations define primary erythermalgia as a neuropathic disorder of voltage gated sodium channels
    Joost P H Drenth
    Department of Medicine, Division of Gastroenterology and Hepatology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands
    J Invest Dermatol 124:1333-8. 2005
    ..Recently, Yang et al identified two missense mutations of the sodium channel alpha subunit SCN9A in patients with erythermalgia...
  57. pmc A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity
    Patrick L Sheets
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, 950 West Walnut St, R2 468, Indianapolis, IN 46202, USA
    J Physiol 581:1019-31. 2007
    ..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...
  58. ncbi Voltage-gated ion channel Nav1.7 innervation in patients with idiopathic rectal hypersensitivity and paroxysmal extreme pain disorder (familial rectal pain)
    Yiangos Yiangou
    Peripheral Neuropathy Unit, Imperial College London, Hammersmith Hospital, London, UK
    Neurosci Lett 427:77-82. 2007
    ..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...
  59. pmc Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade
    Xiaoyang Cheng
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Mol Pain 4:1. 2008
    ..7 mutations reported to date, which have been localized in the voltage sensor S4, the linker joining segments S4 and S5 or pore-lining segments S5 and S6 in DI, II and III...
  60. pmc Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation
    Brian W Jarecki
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    J Physiol 586:4137-53. 2008
    ..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...
  61. ncbi Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy
    Theodore R Cummins
    Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
    J Neurosci 24:8232-6. 2004
    ....
  62. pmc The primary erythermalgia-susceptibility gene is located on chromosome 2q31-32
    J P Drenth
    Department of Medicine, Division of Gastroenterology, University Medical Center St Radboud, 6500 HB Nijmegen, The Netherlands
    Am J Hum Genet 68:1277-82. 2001
    ..Identification of the primary erythermalgia gene will allow a better clinical classification of this pleomorphic group of disorders...
  63. doi Dorsal root ganglia, sodium channels, and fibromyalgia sympathetic pain
    Manuel Martinez-Lavin
    National Institute of Cardiology, Rheumatology Department, Juan Badiano 1, 14080 Mexico City, Mexico
    Med Hypotheses 72:64-6. 2009
    ..If this hypothesis proves to be true, then sodium channel blockers could become therapeutic options for FM pain...
  64. doi Involvement of voltage-gated sodium channels blockade in the analgesic effects of orphenadrine
    Jean Francois Desaphy
    Sezione di Farmacologia, Dipartimento Farmacobiologico, Facolta di Farmacia, Universita di Bari, Bari, Italy
    Pain 142:225-35. 2009
    ..On the other hand, block of Nav1.1 and Nav1.5 may contribute to the proconvulsive and proarrhythmic adverse reactions, especially observed during overdose...
  65. pmc Voltage-gated sodium channels in taste bud cells
    Na Gao
    Senomyx, Inc, 4767 Nexus Centre Drive, San Diego, CA 92121, USA
    BMC Neurosci 10:20. 2009
    ..The molecular identity of the voltage-gated sodium channels that sense depolarizing signals and subsequently initiate action potentials coding taste information to gustatory nerve fibers is unknown...
  66. doi Sodium channel activity modulates multiple functions in microglia
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, Connecticut 06518, USA
    Glia 57:1072-81. 2009
    ..6) indicate that Nav1.6 plays a role in microglial migration. The results demonstrate that the activity of sodium channels contributes to effector roles of activated microglia...
  67. ncbi Downregulation of neuronal sodium channel subunits Nav1.1 and Nav1.6 in the sinoatrial node from volume-overloaded heart failure rat
    Yuan Du
    Department of Cardiovascular Medicine, First Hospital of Xi an Jiaotong University, No 277 West Yanta Road, Xi an, Shaanxi, 710061, China
    Pflugers Arch 454:451-9. 2007
    ..1 and Nav1.6 expression contributes to HF-induced SAN dysfunction. These findings provide additional information about molecular basis of disease-related impairment of SAN function...
  68. doi Increased nerve fiber expression of sensory sodium channels Nav1.7, Nav1.8, And Nav1.9 in rhinitis
    Siew M Keh
    Peripheral Neuropathy Unit, Hammersmith Hospital, Faculty of Medicine, Imperial College London, London, UK
    Laryngoscope 118:573-9. 2008
    ..Voltage-gated sodium channels Nav1.7, Nav1.8, and Nav1.9 are involved in nerve action potentials and have been proposed to underlie neuronal hypersensitivity. We have therefore studied their levels in allergic and nonallergic rhinitis...
  69. doi Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas
    Joel A Black
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, USA
    Ann Neurol 64:644-53. 2008
    ..We also examined the expression of two mitogen-activated protein (MAP) kinases, activated p38 and extracellular signal-regulated kinases 1 and 2 (ERK1/2), which are known to contribute to chronic pain, within these human neuromas...
  70. doi ERK1/2 mitogen-activated protein kinase phosphorylates sodium channel Na(v)1.7 and alters its gating properties
    Severine Stamboulian
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 30:1637-47. 2010
    ..7 by pERK1/2, which unlike the modulation of Na(v)1.6 and Na(v)1.8 by pp38, regulates gating properties of this channel but not its current density and contributes to the effects of MAPKs on DRG neuron excitability...
  71. doi Mexiletine-responsive erythromelalgia due to a new Na(v)1.7 mutation showing use-dependent current fall-off
    Jin Sung Choi
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Exp Neurol 216:383-9. 2009
    ..We report here a new IEM Na(v)1.7 mutation in this patient, and its response to mexiletine. SCN9A exons from the proband were amplified and sequenced...
  72. doi A new Nav1.7 sodium channel mutation I234T in a child with severe pain
    Hye Sook Ahn
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Eur J Pain 14:944-50. 2010
    ..Although enhanced slow-inactivation may attenuate the gain-of-function of the I234T mutation, the shift in activation appears to be dominant, and is consistent with the severe pain symptoms reported in this patient...
  73. ncbi Prognostic factors of rectum carcinoma--experience of the German Multicentre Study SGCRC. German Study Group Colo-Rectal Carcinoma
    P Hermanek
    University of Erlangren, Germany
    Tumori 81:60-4. 1995
    ..Stage III is prognostically inhomogeneous: pN1: 5-year survival 47% (39-55%), pN2, 3: 34% (27-41%) (p < 0.01)...
  74. pmc A pore-blocking hydrophobic motif at the cytoplasmic aperture of the closed-state Nav1.7 channel is disrupted by the erythromelalgia-associated F1449V mutation
    Angelika Lampert
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    J Biol Chem 283:24118-27. 2008
    ..We propose that the four aromatic residues contribute to the gate at the cytoplasmic pore aperture, and that their ring side chains form a hydrophobic plug which stabilizes the closed state of Na(v)1.7...
  75. doi Genetics and molecular pathophysiology of Na(v)1.7-related pain syndromes
    Sulayman D Dib-Hajj
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Adv Genet 63:85-110. 2008
    b>SCN9A, the gene which encodes voltage-gated sodium channel Na(v)1.7, is located on human chromosome 2 within a cluster of other members of this gene family. Na(v)1...
  76. pmc Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents
    Jonathan W Theile
    Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    J Physiol 589:597-608. 2011
    ..This knowledge provides us with a better understanding of the mechanism of I(NaR) generation and may lead to the development of specialized treatment for pain disorders associated with I(NaR)...
  77. doi Kinetic modeling of Nav1.7 provides insight into erythromelalgia-associated F1449V mutation
    Meron Gurkiewicz
    The Leslie and Susan Gonda Multidisciplinary Brain Research Center, Bar Ilan University, Ramat Gan 52900, Israel
    J Neurophysiol 105:1546-57. 2011
    ..Thus a point mutation in position F1449, while phenotypically most probably affecting the activation gate, may also modify channel functions mediated by structures in more distant areas of the channel protein...
  78. ncbi Male breast cancer--a reappraisal of clinical and biologic indicators of prognosis
    S Andre
    Departamento de Patologia Morfologica, Instituto Portugues de Oncologia de Francisco Gentil, Centro de Lisboa, Portugal
    Acta Oncol 40:472-8. 2001
    ..Clinically useful information on the probability of relapse can be added by determining c-erbB-2 (p = 0.02) and progesterone receptors (p = 0.04) in stage III and tumor ploidy (p = 0.04) in pN1 subgroups of patients.
  79. pmc Can robots patch-clamp as well as humans? Characterization of a novel sodium channel mutation
    M Estacion
    Department of Neurology, Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    J Physiol 588:1915-27. 2010
    ....
  80. pmc Pattern of regional metastases and prognostic factors in differentiated thyroid carcinoma
    G Spriano
    Department of Otolaryngology, Head and Neck Surgery, Regina Elena National Cancer Institute, Rome, Italy
    Acta Otorhinolaryngol Ital 29:312-6. 2009
    ..After surgery, 12 patients were lost to follow-up, 8 resulted pathologically negative, therefore only 77 cases of pN1 well-differentiated thyroid carcinoma were studied...
  81. doi No mutations in the voltage-gated NaV1.7 sodium channel alpha1 subunit gene SCN9A in familial complex regional pain syndrome
    A M de Rooij
    Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands
    Eur J Neurol 17:808-14. 2010
    Mutations in the voltage-gated Na(V)1.7 Na(+) channel alpha1 gene SCN9A have been linked to pain disorders, such as inherited primary erythromelalgia and paroxysmal extreme pain disorder...
  82. doi Nav1.7 sodium channel-induced Ca2+ influx decreases tau phosphorylation via glycogen synthase kinase-3beta in adrenal chromaffin cells
    Tasuku Kanai
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889 1692, Japan
    Neurochem Int 54:497-505. 2009
    ....
  83. doi Results of selective neck dissection in the primary management of head and neck squamous cell carcinoma
    Sandra Schmitz
    Department of Head and Neck Surgery, St Luc University Hospital and Cancer Center, Universite Catholique de Louvain, Brussels, Belgium
    Eur Arch Otorhinolaryngol 266:437-43. 2009
    ..5% (3/194); 16% (39/249) were staged pN1 and postoperative radiotherapy (PORT) was proposed in 21 of these patients. The failure rate with PORT was 9...
  84. doi Genetic categorization of Echinococcus granulosus from humans and herbivorous hosts in Iran using an integrated mutation scanning-phylogenetic approach
    Mitra Sharbatkhori
    Department of Veterinary Science, The University of Melbourne, Werribee, Victoria, Australia
    Electrophoresis 30:2648-55. 2009
    ..granulosus revealed five (pc1-pc5) and nine (pn1-pn9) electrophoretic profiles, respectively...
  85. ncbi Male breast carcinoma. I. A study of the total material reported to the Swedish Cancer Registry 1958-1967 with respect to clinical and histopathologic parameters
    R Hultborn
    Department of Oncology, University of Gothenburg, Sweden
    Acta Oncol 26:241-56. 1987
    ..A similar difference was found between pN0 and pN1 tumours. This difference might reflect the progression rate of male breast cancer...
  86. doi Nav1.7-Ca2+ influx-induced increased phosphorylations of extracellular signal-regulated kinase (ERK) and p38 attenuate tau phosphorylation via glycogen synthase kinase-3beta: priming of Nav1.7 gating by ERK and p38
    Takayuki Nemoto
    Department of Pharmacology, Miyazaki Medical College, University of Miyazaki, Miyazaki 889 1692, Japan
    Eur J Pharmacol 640:20-8. 2010
    ..In veratridine-nontreated cells, basal constitutive activities of ERK1/ERK2 and p38 primed Nav1.7 to increase 22Na+ influx...
  87. ncbi Moracizine and ethacizine effects on membrane receptors
    E I Ratner
    Cardiology Research Center of the USSR, Moscow
    Arzneimittelforschung 39:766-9. 1989
    Interaction of the antiarrhythmics moracizine (moricizine, ethmozine, ETHM) and ethacizine (ETHA), the ethyl ester hydrochlorides of 10-(3-R-propionyl)-phenothiazine-2-carbamic acid (where R is morpholine or diethylamine, respectively), ..
  88. doi Nodal staging in colorectal cancer: should distant lymph nodes be recovered in surgical specimens?
    Marc Pusztaszeri
    Department of Pathology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
    Hum Pathol 40:552-7. 2009
    ..There were 169 pN0, 104 pN1, and 72 pN2 cases...
  89. ncbi Leukotriene receptor antagonism and augmentation of beta-receptor-mediated events by LY171883
    L E Rinkema
    Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana 46285
    J Pharm Pharmacol 42:620-5. 1990
    LY171883, (1-[2-hydroxy-3-propyl-4-[4(1H-tetrazol-5-yl)butoxy)phenyl]etha none), a leukotriene (LT) D4/E4 receptor antagonist, was assessed in comparison with two well known phosphodiesterase inhibitors, isobutylmethyl-xanthine (IBMX) and ..
  90. ncbi [Expression and function of voltage-gated Na+ channel isoforms in rat sinoatrial node]
    Xin Huang
    Department of Cardiology, First Affiliated Hospital, Ion Channel Disease Laboratory, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry, Medical School of Xi an Jiaotong University, Xi an 710061, China
    Nan Fang Yi Ke Da Xue Xue Bao 27:52-5. 2007
    ..To detect the expression of voltage-gated Na(+) channel (NaCh) isoforms in rat sinoatrial node and explore their functions...
  91. pmc Effects of ranolazine on wild-type and mutant hNav1.7 channels and on DRG neuron excitability
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 6:35. 2010
    A direct role of sodium channels in pain has recently been confirmed by establishing a monogenic link between SCN9A, the gene which encodes sodium channel Nav1...
  92. ncbi Lymphadenectomy in gastric cancer: influence on prognosis of lymph node count
    A Giuliani
    Dept of Surgery Pietro Valdoni, University La Sapienza, Rome, Italy
    J Exp Clin Cancer Res 23:215-24. 2004
    ..044) were independently associated with the number of lymph nodes involved (pN0, pN1 1-7, pN2 >7)...
  93. ncbi Acute toxicity of adjuvant radiotherapy in locally advanced differentiated thyroid carcinoma. First results of the multicenter study differentiated thyroid carcinoma (MSDS)
    Andreas Schuck
    Department of Radiotherapy, University Hospital Munster, Germany
    Strahlenther Onkol 179:832-9. 2003
    ..Radiation-associated toxicity has been prospectively evaluated...
  94. ncbi [Ductal carcinoma in situ of the breast with microinvasion. Role of sentinel lymph node biopsy]
    G Le Bouedec
    Service de Chirurgie, centre Jean Perrin centre de lutte contre le cancer d Auvergne, 58, rue Montalembert, BP 392, 63011 Clermont Ferrand Cedex 01, France
    Gynecol Obstet Fertil 35:317-22. 2007
    ..To investigate the role of sentinel lymph node biopsy for microinvasive ductal carcinoma in situ of the breast...
  95. ncbi Squamous cell carcinoma from an unknown head and neck primary site: a "selective treatment" approach
    Rajan S Patel
    Sydney Head and Neck Cancer Institute, Level 6, Gloucester House, Royal Prince Alfred Hospital, Camperdown, NSW, Australia
    Arch Otolaryngol Head Neck Surg 133:1282-7. 2007
    ....
  96. doi Hemolysin EthA in Edwardsiella tarda is essential for fish invasion in vivo and in vitro and regulated by two-component system EsrA-EsrB and nucleoid protein HhaEt
    Xin Wang
    State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, PR China
    Fish Shellfish Immunol 29:1082-91. 2010
    ..A hemolysis-associated 147 kDa protein, EthA, was found to be up-regulated in the ECPs of ΔesrB. The deletion of ethA gene in E...
  97. pmc EthA, a common activator of thiocarbamide-containing drugs acting on different mycobacterial targets
    Lynn G Dover
    School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom
    Antimicrob Agents Chemother 51:1055-63. 2007
    ..Herein, through the use of genetically defined strains of Mycobacterium bovis BCG we provide evidence that EthA, previously shown to activate ethionamide, also converts isoxyl (ISO) and thiacetazone (TAC) into reactive species...
  98. ncbi Changes in the expression of NaV1.7, NaV1.8 and NaV1.9 in a distinct population of dorsal root ganglia innervating the rat knee joint in a model of chronic inflammatory joint pain
    Iain T Strickland
    Division of Neuroscience, University of Edinburgh, Medical College, 1 George Sq, Edinburgh EH8 9JZ, UK
    Eur J Pain 12:564-72. 2008
    ..The increased presence of these channels suggests that Na(V)1.7, Na(V)1.8 and Na(V)1.9 play a role, at least in part, in the maintenance of chronic inflammatory pain several weeks after the initial insult...
  99. ncbi Gastric cancer: correlation between clinicopathological factors and survival of patients (III)
    Daniela Lazar
    Department of Gastroenterology and Hepatology, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania
    Rom J Morphol Embryol 50:369-79. 2009
    ....
  100. ncbi [Selective neck dissection in the treatment of pN1/2 lymph node metastases in the neck]
    Rajko Jovic
    Klinika za bolesti uva, grla i nosa, Klinicki centar Novi Sad
    Med Pregl 56:221-6. 2003
    ..The aim of this paper was to establish the extent to which, with good control of primary process, we can control spreading of malignant disease by means of selective neck dissection...
  101. ncbi Skip metastasis in nonsmall cell lung carcinoma: predictive markers and isolated tumor cells in N1 lymph nodes
    Klaus L Prenzel
    Department of Visceral and Vascular Surgery, University of Cologne, Cologne, Germany
    Cancer 100:1909-17. 2004
    ..In patients with pN2 skip metastases, micrometastases to N1 lymph nodes, which only mimic skip metastases, have not been investigated...

Research Grants32

  1. Harnessing gating-pore currents to identify novel Nav1.7 modulators
    Theodore R Cummins; Fiscal Year: 2012
    ....
  2. GING K WANG; Fiscal Year: 2014
    ..Our goals are to delimit such a receptor in peripheral Nav1.7 and Nav1.8 channels, to resolve the drug/receptor interactions during state transitions, and to explore this receptor site for novel pain therapeutics. ..
  3. Design, Synthesis and Evaluation of Novel Isoform-Selective Sodium Channel Inhibi
    JOHN VINCENT MULCAHY; Fiscal Year: 2013
    ..7 as a target for pain treatment, and 3) a high-affinity, isoform-selective sodium channel antagonist as a lead compound for optimization toward a next-generation pain therapeutic. ..
  4. Evolving membrane proteins for high-level expression in modified mammalian cells
    Michael J Betenbaugh; Fiscal Year: 2013
    ..This project will provide a new paradigm for expressing high yields of complex MMPs based on protein and cellular evolution strategies. ..
  5. Stephen Waxman; Fiscal Year: 2016
    ..Our aim is to discover molecules that affect DRG neuron behavior, so that we can identify more effective treatments for neuropathic and inflammatory pain. ..
  6. Theodore J Price; Fiscal Year: 2016
    ..7 interactions. Hence, the present application will utilize a multidisciplinary approach to tackle the problem of post-surgical pain with the goal of advancing novel therapies toward the clinic. ..
  7. Theodore R Cummins; Fiscal Year: 2016
    ....
  8. Pharmacology and biophysics of the voltage-gated sodium channel Nav1.7: a therape
    Seok Yong Lee; Fiscal Year: 2011
    ..My proposed research, if successful, will pave the way for the development of new analgesics and further our understanding of the mechanisms of voltage sensing in voltage-gated sodium channels in health and in disease. ..
  9. Trigeminal Neuropathic Pain Mechanisms
    Michael Henry; Fiscal Year: 2006
    ..Identification of specific sodium channel alterations after injury may help develop more selective treatments for neuropathic pain. ..
  10. Samuel M Wu; Fiscal Year: 2016
    ..with 15 qualifying NEI R01 grants, 2 NEI R21 grants, 1 U10 grant, 1 NEI-funded Research Development Center grant (PN1) and 2 NEI-funded training (T32) grants at Baylor College of Medicine...
  11. Computational investigation of neuropathic changes in primary afferent excitabili
    Steven A Prescott; Fiscal Year: 2012
    ....
  12. REGULATION OF EXTRACELLULAR PROTEOLYSIS BY SERPINS
    DANIEL KNAUER; Fiscal Year: 2004
    ..We will also investigate the role of HSPG's in the post-endocytic retention/trafficking of PN1 :Protease complexes, a phenomenon that was recently described in our laboratory...
  13. NOVEL PROTEIN ASSOCIATED WITH HEART DEVELOPMENT
    LARRY LEMANSKI; Fiscal Year: 2001
    ..A cDNA library constructed from this RNA and a clone (pN1) with a unique partial nucleotide sequence was identified and its deduced 88 amino acid sequence was given the name,..
  14. POSTNATAL ETHANOL EXPOSURE AND NEUROCHEMICAL DEVELOPMENT
    Kim Light; Fiscal Year: 1993
    ..Exposure periods will include postnatal day one (PN1) to PN10, PN1-PN5, and PN5-PN10...
  15. NEUROTOXICITY OF METHYLMERCURY ACROSS THE LIFESPAN
    M Newland; Fiscal Year: 2005
    ..Offspring will be maintained on the different diets and used as follows: 1) Hg and Se or FA profile determination PN1; 2) FI schedule performance in transition with drug challenges: 3) Targeted percentile schdule performance, and 4) ..
  16. BIOPHYSICAL STUDIES OF LRP LIGANDS INTERACTIONS
    ELIZABETH KOMIVES; Fiscal Year: 2003
    ..is interested in the LRP-mediated clearance of thrombin-PNI complexes, because the balance between thrombin and PN1 is upset in AD, and experiments have show l that thrombin acts to inhibit neurite outgrowth and promote synapse ..
  17. Recombinant Herpes Injection into Trigeminal Ganglia
    David Yeomans; Fiscal Year: 2004
    ..In so doing, we hope to provide initial support for what may be a new long-lasting treatment for trigeminal nerve-related pain. ..
  18. NOCICEPTOR SELECTIVE ANALGESIA
    David Yeomans; Fiscal Year: 2001
    ....
  19. In Vivo Genetic Manipulation of Neuronal Excitability
    David Yeomans; Fiscal Year: 2004
    ..7 channels in chronic pain patients, providing a long-term genetic therapy for their pain. ..
  20. Chronic Compression of the Trigeminal Ganglia
    David Yeomans; Fiscal Year: 2009
    ..These mechanistic studies, in turn, can lead to the determination of new targets for pharmacdceutical development, as well as for gene therapy approaches. ..
  21. Structural Mechanisms for the Inhibition of Thrombosis
    JAMES HUNTINGTON; Fiscal Year: 2009
    ....
  22. Peripheral and Central Mechanism of Pain in Patients with Fibromyalgia
    ROLAND M STAUD; Fiscal Year: 2010
    ..Either way, we will provide evidence that will characterize the role of local anesthesia, placebo analgesia, or both. Thus patients with FM and other similar pain syndromes may strongly benefit from the results of our study. ..
  23. TRAINING IN MOLECULAR NEUROBIOLOGY
    William Catterall; Fiscal Year: 2008
    ..The training program will integrate the substantial expertise of this group of faculty in a coordinated pre-doctoral and post-doctoral training effort. ..
  24. MECHANISMS OF CHLORPYRIFOS DEVELOPMENTAL NEUROTOXICITY
    Theodore Slotkin; Fiscal Year: 2004
    ..Molecular mechanisms of developmental neurotoxicity can be determined and linked to eventual alterations in behavioral performance. ..
  25. MECHANISM OF PAIN IN PATIENTS WITH FIBROMYALGIA SYNDROME
    Roland Staud; Fiscal Year: 2008
    ..In addition, our findings may contribute to the understanding of pain mechanisms related to other chronic pain disorders. ..
  26. Ionic Basis of the Brugada Syndrome
    Hong Sheng Wang; Fiscal Year: 2008
    ..Our proposed study closely fits the stated purpose of the R21 Program Announcement because it is innovative and exploratory, and it is consistent with the goal of the funding program. [unreadable] [unreadable] [unreadable]..
  27. DRUGS AND DEVELOPMENT OF THE ADRENERGIC NERVOUS SYSTEM
    Theodore Slotkin; Fiscal Year: 2003
    ....
  28. NEUROTROPHIN 3 IN NEURONAL INJURY AND DISEASE
    Douglas Wright; Fiscal Year: 2002
    ..Results from these studies will define new biological actions of NT-3 and reveal how manipulation of the trophic support of neurons may be useful to treat pathologic neural conditions. ..
  29. THERAPEUTIC NA+ CHANNEL BLOCKERS: RECEPTOR & DRUG DESIGN
    GING WANG; Fiscal Year: 2007
    ..Such drugs, either taken orally or injected locally, may be beneficial for patients with chronic and intractable cancer pain. ..
  30. MOLECULAR BASIS OF LIGAND/SODIUM CHANNEL INTERACTIONS
    GING WANG; Fiscal Year: 2002
    ....
  31. Ensemble coding in olfactory cortex
    Donald Wilson; Fiscal Year: 2006
    ..This combination is ideally suited for the R21 mechanism. ..
  32. Fetal & Adolescent Nicotine Effects on CNS 5HT Systems
    Theodore Slotkin; Fiscal Year: 2003
    ..abstract_text> ..