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Genomes and Genes
| SCN3ASummaryGene Symbol: SCN3A Description: sodium channel, voltage-gated, type III, alpha subunit Alias: NAC3, Nav1.3, brain III voltage-gated sodium channel, sodium channel protein brain III subunit alpha, sodium channel protein type 3 subunit alpha, sodium channel protein type III subunit alpha, sodium channel, voltage-gated, type III, alpha polypeptide, voltage-gated sodium channel subtype III, voltage-gated sodium channel subunit alpha Nav1.3 Species: human Top Publications
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Publications
Voltage-gated sodium channels in taste bud cellsNa 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...
Differential evolution of voltage-gated sodium channels in tetrapods and teleost fishesJenny Widmark
Department of Neuroscience, Uppsala University, Uppsala, Sweden
Mol Biol Evol 28:859-71. 2011..of amniotes, generating the cluster SCN5A, SCN10A, and SCN11A on one chromosome and the cluster SCN1A, SCN2A, SCN3A, and SCN9A on a different chromosome...
Human and rat Nav1.3 voltage-gated sodium channels differ in inactivation properties and sensitivity to the pyrethroid insecticide tefluthrinJianguo Tan
Insecticide Toxicology Laboratory, Department of Entomology, New York State Agricultural Experiment Station, 630 W North St, Cornell University, Geneva, NY 14456, USA
Neurotoxicology 30:81-9. 2009....
[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...
Transport characteristics of N-acetyl-L-aspartate in rat astrocytes: involvement of sodium-coupled high-affinity carboxylate transporter NaC3/NaDC3-mediated transport systemTakuya Fujita
Department of Biochemical Pharmacology, Kyoto Pharmaceutical University, Jamashina ku, Kyoto, Japan
J Neurochem 93:706-14. 2005..of astrocytes from rat cerebral cortex and the involvement of NA+-coupled high-affinity carboxylate transporter NaC3 (formerly known as NaDC3) responsible for N-acetyl-L-aspartate transport...
Vasa recta voltage-gated Na+ channel Nav1.3 is regulated by calmodulinWhaseon Lee-Kwon
Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Baltimore 21201, USA
Am J Physiol Renal Physiol 292:F404-14. 2007..3C was not affected by Ca(2+) concentration. We conclude that Na(V)1.3 is expressed by DVR, binds to CaM, and is regulated by CaM and Ca(2+). Inhibition of CaM binding suppresses pericyte Na(V) currents...
Differential expression of exon 5 splice variants of sodium channel alpha subunit mRNAs in the developing mouse brainE V Gazina
Howard Florey Institute, The University of Melbourne, 3010, Victoria, Australia
Neuroscience 166:195-200. 2010Sodium channel alpha subunit genes expressed in the human brain, SCN1A, SCN2A, SCN3A and SCN8A, are subject to alternative splicing of coding exons 5N and 5A...
TNF-? contributes to up-regulation of Nav1.3 and Nav1.8 in DRG neurons following motor fiber injuryXin Hua He
Pain Research Center and Department of Physiology, Zhongshan School of Medicine of Sun Yat Sen University, Guangzhou, PR China
Pain 151:266-79. 2010..These data suggest that increased TNF-? may be responsible for up-regulation of Nav1.3 and Nav1.8 in uninjured DRG neurons following nerve injury...
Inhibition of NF-kappaB prevents mechanical allodynia induced by spinal ventral root transection and suppresses the re-expression of Nav1.3 in DRG neurons in vivo and in vitroYing Zang
Pain Research Center and Department of Physiology, Zhongshan Medical School of Sun Yat Sen University, 74 Zhongshan Rd 2, Guangzhou 510080, PR China
Brain Res 1363:151-8. 2010..The data suggested that injury to ventral root might lead to neuropathic pain and the re-expression of Nav1.3 in primary sensory neurons by activation of NF-?B...
The sodium channel {beta}3-subunit induces multiphasic gating in NaV1.3 and affects fast inactivation via distinct intracellular regionsFiona S Cusdin
Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom
J Biol Chem 285:33404-12. 2010..The complex gating behavior induced by ?3 may contribute to the known hyperexcitability of peripheral neurons under those physiological conditions where expression of ?3 and Na(v)1.3 are both enhanced...
Patterned electrical activity modulates sodium channel expression in sensory neuronsJoshua P Klein
Department of Neurology and PVA EPVA Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA
J Neurosci Res 74:192-8. 2003..These results show that a change in neuronal activity can alter the expression of sodium channel genes in a subtype-specific manner, via a mechanism independent of NGF withdrawal...
Expression of voltage-gated sodium channel alpha subunit in human ovarian cancerRui Gao
Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, P R China
Oncol Rep 23:1293-9. 2010..Our findings suggested that abnormal expression of Nav1.5 could be an integral component of the metastatic process in human ovarian cancer and might serve as a therapeutic target in ovarian cancer treatment...
Familial neonatal seizures with intellectual disability caused by a microduplication of chromosome 2q24.3Sarah E Heron
SA Pathology at Women s and Children s Hospital, Adelaide, South Australia, Australia
Epilepsia 51:1865-9. 2010..Characterization revealed a 1.57 Mb duplication at 2q24.3 containing eight genes including SCN2A, SCN3A, and the 3¢ end of SCN1A...
Comparative study of the distribution of the alpha-subunits of voltage-gated sodium channels in normal and axotomized rat dorsal root ganglion neuronsTetsuo Fukuoka
Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo 663 8501, Japan
J Comp Neurol 510:188-206. 2008..3 induction was independent of either TrkA or GFRalpha1 expression, suggesting that the induction of Nav1.3 may be one of the common responses of axotomized DRG neurons without a direct relationship to NGF/GDNF supply...
Molecular and functional characterization of voltage-gated sodium channels in human spermFrancisco M Pinto
Instituto de Investigaciones Quimicas, CSIC, Sevilla, Spain
Reprod Biol Endocrinol 7:71. 2009..We have investigated the expression of voltage-gated sodium channels in human spermatozoa and characterized their role in sperm motility...
Increased late sodium currents are related to transcription of neuronal isoforms in a pressure-overload modelYutao Xi
Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi an Jiaotong University, 277 West Yanta Road, Xi an, Shaanxi, China
Eur J Heart Fail 11:749-57. 2009..However, the underlying mechanism of late I(Na) (I(NaL)) production remains uncertain. We hypothesized that transcriptional alteration among sodium channel (NaCh) isoforms may contribute to I(NaL) in failing cardiomyocytes...
Multidrug resistance in epilepsy and polymorphisms in the voltage-gated sodium channel genes SCN1A, SCN2A, and SCN3A: correlation among phenotype, genotype, and mRNA expressionPatrick Kwan
Division of Neurology, Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, China
Pharmacogenet Genomics 18:989-98. 2008..We investigated the association of AED responsiveness with genetic polymorphisms and correlated any association with mRNA expression of the neuronal sodium channels...
Increased peripheral nerve excitability and local NaV1.8 mRNA up-regulation in painful neuropathyDevang Kashyap Thakor
Division of Oral Biology and Medicine, School of Dentistry, University of California, Los Angeles, CA 90095 1668, USA
Mol Pain 5:14. 2009..We have hypothesized that altered local expression of NaV1.8 in the peripheral axons of DRG neurons could facilitate nociceptive signal generation and propagation after neuropathic injury...
Mutation of sodium channel SCN3A in a patient with cryptogenic pediatric partial epilepsyKatherine D Holland
Division of Neurology, Cincinnati Children s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
Neurosci Lett 433:65-70. 2008Mutations in the sodium channel genes SCN1A and SCN2A have been identified in monogenic childhood epilepsies, but SCN3A has not previously been investigated as a candidate gene for epilepsy...
Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant miceMohammed A Nassar
Molecular Nociception Group, Department of Biology, University College London WC1E 6BT, UK
Mol Pain 2:33. 2006..Furthermore, ectopic discharges from damaged nerves were unaffected by the absence of Nav1.3 in global knock-out mice. Our data demonstrate that Nav1.3 is neither necessary nor sufficient for the development of nerve-injury related pain...
Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromasJoel 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...
Neuropathic pain: emerging treatmentsA Dray
AstraZeneca Research and Development, 7171 Frederick Banting Street, Montreal, Canada
Br J Anaesth 101:48-58. 2008..Finally of note is the emergence of biological approaches, for example, antibodies, siRNA, gene therapy, offering powerful therapeutic additions with which to redress the neurological disease imbalances causing neuropathic pain...
Sodium channel activity modulates multiple functions in microgliaJoel 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...
Ralfinamide administered orally before hindpaw neurectomy or postoperatively provided long-lasting suppression of spontaneous neuropathic pain-related behavior in the ratShi Hong Zhang
Department of Pharmacology, School of Medicine, Zhejiang University, Hangzhou, PR China
Pain 139:293-305. 2008..3, Nav1.7, Nav1.8, and Cav2.2 channels in rat DRG neurons, inhibition of substance P release from spinal cord synaptosomes, NMDA receptor antagonism and neuroprotection...
Proteomic profiling of neuromas reveals alterations in protein composition and local protein synthesis in hyper-excitable nervesHong Lei Huang
Molecular Nociception Group, NPP Department, UCL, Gower Street, London WC1E6BT, UK
Mol Pain 4:33. 2008..An altered repertoire of protein expression, local protein synthesis and topological re-arrangements of ion channels may all play important roles in neuroma hyper-excitability...
Altered expression of sodium channel distribution in the dorsal root ganglion after gradual elongation of rat sciatic nervesKatsunori Ohno
Department of Orthopedic Surgery, Osaka Medical College, 2 7, Daigaku machi, Takatsuki 569 8686, Japan
J Orthop Res 28:481-6. 2010..Our findings indicate that Nav1.8 downregulation may be one of the pathophysiological mechanisms involved in limb lengthening-induced neuropathy...
Astrocytes within multiple sclerosis lesions upregulate sodium channel Nav1.5Joel A Black
Neuroscience Research Centre Bldg 34, VA Connecticut Healthcare System 127A, 950 Campbell Avenue, West Haven, CT 06516, USA
Brain 133:835-46. 2010..Our observations suggest that the upregulated expression of Nav1.5 in astrocytes may provide a compensatory mechanism, which supports sodium/potassium pump-dependent ionic homoeostasis in areas of central nervous system injury...
Molecular differential expression of voltage-gated sodium channel ? and ? subunit mRNAs in five different mammalian cell linesDebora Baroni
Istituto di Biofisica, CNR, Via De Marini, 6, 16149, Genoa, Italy
J Bioenerg Biomembr 43:729-38. 2011..This data provide a standard for the study of the modulation of the sodium channel expression in mammalian excitable tissues...
Re-evaluation of the phenotypic changes in L4 dorsal root ganglion neurons after L5 spinal nerve ligationTetsuo Fukuoka
Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
Pain 153:68-79. 2012..Because neuropathic pain behaviors were developed by rats with SNL but not the sham-operation, the small number of injured L4 neurons likely do not contribute to the pathomechanisms of neuropathic pain...
Infantile epilepsy associated with mosaic 2q24 duplication including SCN2A and SCN3AMarilena Vecchi
Pediatric Neurology and Clinical Neurophysiology Unit, Department of Pediatrics, University of Padova, Italy
Seizure 20:813-6. 2011..3q24.3 involving SCN2A and SCN3A genes. Additional analyses (radiolabeled RFLP and quantitative PCR) confirmed the mosaicism of the duplication...
Propranolol blocks cardiac and neuronal voltage-gated sodium channelsDao W Wang
Department of Medicine, Vanderbilt University School of Medicine Nashville, TN, USA
Front Pharmacol 1:144. 2010..5 channels. Our findings establish sodium channels as targets for propranolol and may help explain some beneficial effects of the drug in treating cardiac arrhythmias, and may explain certain adverse central nervous system effects...
Refractory neonatal epilepsy with a de novo duplication of chromosome 2q24.2q24.3Akihisa Okumura
Department of Pediatrics, Juntendo University Faculty of Medicine, 2 1 1 Hongo, Bunkyo ku, Tokyo, Japan
Epilepsia 52:e66-9. 2011..3-Mb duplication of 2q24.2q24.3, where at least 22 genes including a cluster of voltage-gated sodium channel genes (SCN1A, SCN2A, SCN3A, SCN7A, and SCN9A) and one noncoding RNA are located.
Intrathecal lidocaine pretreatment attenuates immediate neuropathic pain by modulating Nav1.3 expression and decreasing spinal microglial activationKuang I Cheng
Division of Plastic and Reconstructive Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
BMC Neurol 11:71. 2011..Intrathecal lidocaine reverses tactile allodynia after nerve injury, but whether neuropathic pain is attenuated by intrathecal lidocaine pretreatment is uncertain...
[Role of voltage-sodium channels in neuropathic pain]Wen ting Shou
Key Laboratory of Medical Neurobiology of Ministry of Health of China, China
Zhejiang Da Xue Xue Bao Yi Xue Ban 40:217-21. 2011..Here we reviewed the roles of sodium channels in neuropathic pain, which may be applicable for the development of new drugs with enhanced efficacy for neuropathic pain treatment...
Neuropathic Nav1.3-mediated sensitization to P2X activation is regulated by protein kinase CGary Mo
Montreal Neurological Institute and The Alan Edwards Centre for Research on Pain, Department of Neurology and Neurosurgery, McGill University, Montreal, Canada
Mol Pain 7:14. 2011..Here we demonstrate the contribution of PKC to P2X-evoked VGSC activation in dorsal root ganglion (DRG) neurons in neuropathic conditions...
Promoter analysis of mouse Scn3a gene and regulation of the promoter activity by GC box and CpG methylationGuang Fei Deng
Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and The Ministry of Education of China, Institute of Neuroscience and The Second Affiliated Hospital of GuangZhou Medical University, 250 Chang gang dong Road, Guangzhou, China
J Mol Neurosci 44:115-21. 2011..The expression of mouse Scn3a product (Na(v)1.3) mainly occurs in embryonic and early postnatal brain but not in adult brain...
Disruption of the SCN2A and SCN3A genes in a patient with mental retardation, neurobehavioral and psychiatric abnormalities, and a history of infantile seizuresM Bartnik
Department of Medical Genetics, Institute of Mother and Child, Warsaw, Poland
Clin Genet 80:191-5. 2011..aCGH), we have identified a de novo ~110-kb deletion involving exons 1-2 of SCN2A and non-coding exon 1a of SCN3A in a 25-year-old female with mental retardation, neurobehavioral and psychiatric abnormalities, and a history of ..
Laminae-specific distribution of alpha-subunits of voltage-gated sodium channels in the adult rat spinal cordT Fukuoka
Department of Anatomy and Neuroscience, Hyogo College of Medicine, 1 1 Mukogawa cho, Nishinomiya, Hyogo 663 8501, Japan
Neuroscience 169:994-1006. 2010..Comparison with our previous data concerning the subpopulation-specific distribution of Nav transcripts in primary afferent neurons provides potentially specific targets for local analgesics at the peripheral nerve and spinal levels...
A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neuronsMark Estacion
Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
Exp Neurol 224:362-8. 2010..b>SCN3A, the gene which encodes Na(V)1.3, is part of this cluster, but until recently was not associated with any mutation...
Sodium channel gene family: epilepsy mutations, gene interactions and modifier effectsMiriam H Meisler
Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109 5618, USA
J Physiol 588:1841-8. 2010..A small number of mutations have been found in SCN2A, SCN3A and SCN9A, and studies in the mouse suggest that SCN8A may also contribute to seizure disorders...
Array-CGH detection of a de novo 2.8 Mb deletion in 2q24.2-->q24.3 in a girl with autistic features and developmental delayChih Ping Chen
Department of Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei, Taiwan
Eur J Med Genet 53:217-20. 2010..8 Mb de novo deletion of chromosome 2q24.2-->q24.3 detected by array-CGH. This region contains two neuronal voltage-gated sodium channel genes SCN2A and SCN3A.
Upregulation of Nav1.3 Channel Induced by rrTNF in Cultured Adult Rat DRG Neurons via p38 MAPK and JNK PathwaysYing Zang
Pain Research Center and Department of Physiology, Zhongshan Medical School, Sun Yat Sen University, Guangzhou 510080, Guangdong, People s Republic of China
Chin J Physiol 54:241-6. 2011..3 completely (P<0.001). These data show that the activation of both p38 MAPK and JNK in DRG neurons was involved in the re-expression of Nav1.3 channel triggered by TNF-?, which might contribute to neuropathic pain...
Voltage-gated sodium channel Nav1.1, Nav1.3 and beta1 subunit were up-regulated in the hippocampus of spontaneously epileptic ratFeng Guo
Department of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang 110001, China
Brain Res Bull 75:179-87. 2008..The results of this study may be of value in revealing components of the molecular mechanisms of hippocampal excitation that are related to genetic epilepsy...
SCN1A mutations and epilepsyJohn C Mulley
Department of Genetic Medicine, Women s and Children s Hospital, North Adelaide, South Australia, Australia
Hum Mutat 25:535-42. 2005SCN1A is part of the SCN1A-SCN2A-SCN3A gene cluster on chromosome 2q24 that encodes for alpha pore forming subunits of sodium channels. The 26 exons of SCN1A are spread over 100 kb of genomic DNA...
Three brain sodium channel alpha-subunit genes are clustered on the proximal segment of mouse chromosome 2D Malo
Department of Biochemistry, McGill University, Montreal, Canada
Genomics 10:666-72. 1991..Physical mapping by pulsed-field gel electrophoresis has established that Scn2a and Scn3a (genes encoding type II and type III sodium channel alpha-subunit isoforms) are physically linked and are ..
Molecular diversity of voltage-gated sodium channel alpha subunits expressed in neuronal and non-neuronal excitable cellsI Mechaly
I N S E R M U583, Institut des Neurosciences de Montpellier Hôpital St Eloi, 80, rue Augustin Fliche, 34295 Montpellier Cedex 5, France
Neuroscience 130:389-96. 2005....
Voltage-gated sodium channels and pain pathwaysJohn N Wood
Molecular Nociception Group, Department of Biology, University College, Gower Street, London WC1E 6BT, UK
J Neurobiol 61:55-71. 2004..Taken together, these data suggest that isotype-specific sodium channel blockers could be useful analgesics...
Contactin associates with sodium channel Nav1.3 in native tissues and increases channel density at the cell surfaceBhaval S Shah
Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
J Neurosci 24:7387-99. 2004..We propose that the upregulation of contactin and its colocalization with Na(v)1.3 in axotomized DRG neurons may contribute to the hyper-excitablity of the injured neurons...
Requirement of neuronal- and cardiac-type sodium channels for murine sinoatrial node pacemakingMing Lei
University Laboratory of Physiology, University of Oxford, OX1 3PT, UK
J Physiol 559:835-48. 2004..1) and cardiac Nav1.5 isoforms are involved in pacemaking, although the cardiac Nav1.5 isoform alone is involved in the propagation of the action potential from the SA node to the surrounding atrial muscle...
Expression of the sodium channel beta3 subunit in injured human sensory neuronsMaria A Casula
Peripheral Neuropathy Unit, Imperial College London, Area A, Ground Floor, Hammersmith Hospital, Du Cane Rd, London W12 0NN, UK
Neuroreport 15:1629-32. 2004..beta3-subunit expression may thus be regulated differently from beta1, beta2 and Nav1.8. Targeting beta3 interactions with key alpha-subunits, particularly Nav1.3 and Nav1.8, may provide novel selective analgesics...
Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injuryBryan C Hains
Department of Neurology and Paralyzed Veterans of America Eastern Paralyzed Veterans Association Neuroscience Research Center, Yale University School of Medicine, New Haven, Connecticut 06510, USA
J Neurosci 23:8881-92. 2003..3 expression and neuronal hyperexcitability associated with central neuropathic pain...
Sodium channels SCN1A, SCN2A and SCN3A in familial autismL A Weiss
Department of Human Genetics, University of Michigan, 4708 Medical Science II, Ann Arbor, MI 48109 0618, USA
Mol Psychiatry 8:186-94. 2003..SNP density was 1/kb in the genomic sequence screened. We report 38 sodium channel SNPs that will be useful in future association and linkage studies...
Functional modulation of human brain Nav1.3 sodium channels, expressed in mammalian cells, by auxiliary beta 1, beta 2 and beta 3 subunitsL S Meadows
Montreal Neurological Institute, McGill University, Montreal, QC, Canada
Neuroscience 114:745-53. 2002..The results of this study support the hypothesis that Na(v)1.3 may mediate this fast sodium current...
Changes in the mRNAs encoding voltage-gated sodium channel types II and III in human epileptic hippocampusW R Whitaker
Department of Neurobiology, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK
Neuroscience 106:275-85. 2001..However, it is likely that such changes would affect the intrinsic excitability of hippocampal neurones...
Genomic structures of SCN2A and SCN3A - candidate genes for deafness at the DFNA16 locusN Kasai
Department of Otolaryngology, Okayama University Medical School, 700 8558, Okayama, Japan
Gene 264:113-22. 2001..members of the voltage-gated sodium channel family, the type 2 alpha subunit (SCN2A) and the type 3 alpha subunit (SCN3A)...
Cloning, distribution and functional analysis of the type III sodium channel from human brainY H Chen
Molecular Pharmacology Unit, GlaxoWellcome, Medicines Research Centre, Gunnels Wood Road, Stevenage SG1 2NY, UK
Eur J Neurosci 12:4281-9. 2000..The distinct properties of the channel, together with its wide distribution in adult brain, suggest that in humans, type III may have important physiological roles under normal, and perhaps also pathological conditions...
A second locus for familial generalized epilepsy with febrile seizures plus maps to chromosome 2q21-q33S Baulac
INSERM U289, Hopital de la Salpetriere, Paris Cedex, France
Am J Hum Genet 65:1078-85. 1999..Four genes coding for different isoforms of the alpha-subunit voltage-gated sodium channels (SCN1A, SCN2A1, SCN2A2, and SCN3A) located in this region are strong candidates for the disease gene.
Isolation of a human-brain sodium-channel gene encoding two isoforms of the subtype III alpha-subunitC M Lu
Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, USA
J Mol Neurosci 10:67-70. 1998..that this transcript represents the two isoforms (neonatal and adult) of the human brain sodium channel gene, SCN3A (GenBank accession numbers AF035685 and AF035686)...
A new sodium channel alpha-subunit gene (Scn9a) from Schwann cells maps to the Scn1a, Scn2a, Scn3a cluster of mouse chromosome 2M C Beckers
Department of Biochemistry, McGill University, Montreal, H3G 1Y6, Canada
Genomics 36:202-5. 1996....
Targeted gene walking by low stringency polymerase chain reaction: assignment of a putative human brain sodium channel gene (SCN3A) to chromosome 2q24-31M S Malo
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139
Proc Natl Acad Sci U S A 91:2975-9. 1994..assign this sequence as a part of a gene coding the alpha-subunit of a human brain type III sodium channel (SCN3A)...
Contactin regulates the current density and axonal expression of tetrodotoxin-resistant but not tetrodotoxin-sensitive sodium channels in DRG neuronsAnthony M Rush
Department of Neurology, Yale School of Medicine, LCI 707, 333 Cedar St, New Haven, CT 06510, USA
Eur J Neurosci 22:39-49. 2005....
Sodium channels and nociception: recent concepts and therapeutic opportunitiesDouglas S Krafte
Icagen Inc, P O Box 14487, Research Triangle Park, NC 27709, USA
Curr Opin Pharmacol 8:50-6. 2008..All of these data are converging to suggest next generation sodium channel blockers may offer the potential for novel pain therapies in the future...
The voltage-gated sodium channel Scn8a is a genetic modifier of severe myoclonic epilepsy of infancyMelinda S Martin
Department of Human Genetics, Emory University, Atlanta, GA 30322, USA
Hum Mol Genet 16:2892-9. 2007..four voltage-gated sodium channel genes that are primarily expressed in the central nervous system: SCN1A, SCN2A, SCN3A and SCN8A...
Expression of Nav1.1 in rat retinal AII amacrine cellsYuko Kaneko
Department of Physiology, Faculty of Medicine, Saitama Medical University, 38 Morohongo, Moroyama, Iruma gun, Saitama 350 0495, Japan
Neurosci Lett 424:83-8. 2007..Therefore, we combined ISH with immunohistochemistry and discovered that most of the PV-immunoreactive cells located at the INL/IPL border express Nav1.1. Our results show that AII amacrine cells express Nav1.1...
Functional and molecular characterization of voltage-gated sodium channels in uteri from nonpregnant ratsMarian Seda
Instituto de Investigaciones Quimicas, 41092 Sevilla, Spain
Biol Reprod 77:855-63. 2007..Using end-point and real-time quantitative RT-PCR, we detected the presence of the VGSC alpha subunits Scn2a1, Scn3a, Scn5a, and Scn8a in the cDNA from longitudinal muscle...
Sodium channel expression and the molecular pathophysiology of pain after SCIBryan C Hains
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, and Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, CT 06516, USA
Prog Brain Res 161:195-203. 2007..3 dysregulation contributes to post-SCI chronic pain. If proven to be similar in humans, targeting of this system after SCI may offer hope for treatment of clinical pain...
Differentiated pattern of sodium channel expression in dissociated Purkinje neurons maintained in long-term cultureMark Fry
Department of Physiology, Queen s University, Kingston, Ontario, Canada
J Neurochem 101:737-48. 2007..4, Nav 1.5 or Nav1.8 Na+ channel alpha subunit gene expression in cultured Purkinje neurons, as observed in vivo. Together, the results indicate that key aspects of Na+ channel expression in mature Purkinje neurons in vivo occur in vitro...
Downregulation of neuronal sodium channel subunits Nav1.1 and Nav1.6 in the sinoatrial node from volume-overloaded heart failure ratYuan 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...
Isolation and structure-activity of mu-conotoxin TIIIA, a potent inhibitor of tetrodotoxin-sensitive voltage-gated sodium channelsRichard J Lewis
Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia
Mol Pharmacol 71:676-85. 2007..TIIIA and analogs provide new biochemical probes as well as insights into the structure-activity of mu-conotoxins...
Sodium channel expression in the ventral posterolateral nucleus of the thalamus after peripheral nerve injuryPeng Zhao
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
Mol Pain 2:27. 2006..3 sodium channel increases the excitability of VPL neurons injury, contributing to neuropathic pain...
Immunolocalization of NaV1.2 channel subtypes in rat and cat brain and spinal cord with high affinity antibodiesMiranda Jarnot
Department of Neuroscience, Cell Biology and Physiology, Wright State University, 3640 Col Glenn Highway, Dayton, OH 45435, USA
Brain Res 1107:1-12. 2006..Specific staining was limited to fibers located in the granule and molecular layer, in an orientation consistent with granule cell unmyelinated axon labeling...
Identification of functional voltage-gated Na(+) channels in cultured human pulmonary artery smooth muscle cellsOleksandr Platoshyn
Division of Pulmonary and Critical Care Medicine, Department of Medicine, School of Medicine, University of California, 9500 Gilman Drive, MC 0725, San Diego, La Jolla, CA 92093 0725, USA
Pflugers Arch 451:380-7. 2005..Whether their expression and/or activity are heightened in the pathological state is discussed...
Functional and molecular identification of sodium-coupled dicarboxylate transporters in rat primary cultured cerebrocortical astrocytes and neuronsEtsuo Yodoya
Department of Biopharmaceutics, Kyoto Pharmaceutical University, Yamashina ku, Kyoto, Japan
J Neurochem 97:162-73. 2006..Of these transporters, NaC3 (formerly known as Na+-coupled dicarboxylate transporter 3, NaDC3/SDCT2) and NaC2 (formerly known as Na+-coupled ..
Fire and phantoms after spinal cord injury: Na+ channels and central painStephen G Waxman
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
Trends Neurosci 29:207-15. 2006....
Changes in electrophysiological properties and sodium channel Nav1.3 expression in thalamic neurons after spinal cord injuryBryan C Hains
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
Brain 128:2359-71. 2005....
International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channelsWilliam 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...
Interactions of the low density lipoprotein receptor gene family with cytosolic adaptor and scaffold proteins suggest diverse biological functions in cellular communication and signal transductionM Gotthardt
Department of Molecular Genetics and Pathology, University of Texas Southwestern Medical Center, Dallas 75390-9046, USA
J Biol Chem 275:25616-24. 2000..They form the basis for the elucidation of the molecular pathways by which cells respond to the diversity of ligands that bind to these multifunctional receptors on the cell surface...
Characterization of 5' untranslated regions of the voltage-gated sodium channels SCN1A, SCN2A, and SCN3A and identification of cis-conserved noncoding sequencesMelinda S Martin
Department of Human Genetics, Emory University, Atlanta, GA 30322, USA
Genomics 90:225-35. 2007The human voltage-gated sodium channel gene cluster on chromosome 2q24 contains three paralogs, SCN1A, SCN2A, and SCN3A, which are expressed in the central nervous system...
Distribution and functional characterization of human Nav1.3 splice variantsR Thimmapaya
Neuroscience Research, Abbott Laboratories, Abbott Park, IL 60064, USA
Eur J Neurosci 22:1-9. 2005..This study has demonstrated that all four human splice variants of the Nav1.3 channel alpha subunit are widely expressed and generate functional TTX-sensitive Na+ channels that likely modulate cellular excitability...
Research Grants
- Trigeminal Neuropathic Pain MechanismsMichael Henry; Fiscal Year: 2006..Identification of specific sodium channel alterations after injury may help develop more selective treatments for neuropathic pain. ..
- Scn8a and Seizure ResistanceAlan L Goldin; Fiscal Year: 2010..in the sodium channel SCN1A are a major cause of GEFS+ and SMEI, even though three other sodium channels (SCN2A, SCN3A, and SCN8A) are expressed in the central nervous system (CNS)...
- HEREDITARY DEFECTS IN HUMAN SODIUM CHANNELSAlfred L George; Fiscal Year: 2010..The experimental sequence begins with studies to elucidate the functional consequences of novel SCN3A mutations associated with genetic epilepsy syndromes (Specific Aim 1)...
- Molecular Properties of Voltage-Sensitive Calcium ChannelsWilliam A Catterall; Fiscal Year: 2010....
- CELL BIOLOGY OF THE NEURONAL SODIUM CHANNELWilliam Catterall; Fiscal Year: 2001..These results will be essential for understanding the molecular basis of expression and localization of sodium channels. ..
- CELL BIOLOGY OF THE NEURONAL SODIUM CHANNELWilliam A Catterall; Fiscal Year: 2010..This project will use a mouse genetic model of this disease to determine how this gene defect causes epilepsy and to test new drug combinations for control of this intractable epilepsy syndrome. ..
- Regulation of Cardiac Calcium Channels by an Autoinhibitory Signaling ComplexWilliam A Catterall; Fiscal Year: 2010..This information will provide the essential basic science background for translational research aimed at preventing and treating cardiovascular disease. ..
- Receptor Sites and Antagonists for Paralytic NeurotoxinsWilliam Catterall; Fiscal Year: 2007....
- VOLTAGE SENSITIVE SODIUM CHANNELS IN BRAINWilliam Catterall; Fiscal Year: 2007..These proposed studies will give new insight into the molecular mechanisms of sodium channel gating and its modification by second messenger-activated protein phosphorylation. ..
- Gene interaction in development and diseaseMIRIAM MEISLER; Fiscal Year: 2007..Because of the high level of alternative splicing in the nervous system, variation in SCNM1 may be of particular significance for neurological disease. ..
- CELL BIOLOGY OF THE NEURONAL SODIUM CHANNELWilliam Catterall; Fiscal Year: 2006..Our results will add substantially to understanding of the cell biology of the Na channel and the functional significance of Na channel signaling complexes. ..
- Functional Genetics of the Neuronal Sodium Channel Gene SCN8AMIRIAM MEISLER; Fiscal Year: 2009..This project will characterize the neurological and behavioral effects of specific changes in sodium channel genes, using mouse models of human mutations. ..
- VOLTAGE-SENSITIVE SODIUM CHANNELS IN BRAINWilliam Catterall; Fiscal Year: 1991..These studies will provide essential information to understanding the molecular basis of electrical excitability...
- GENETIC REGULATION OF MOUSE ENZYMESMIRIAM MEISLER; Fiscal Year: 1991..These investigations will contribute to our understanding of the molecular basis of tissue-specific and hormonal regulation of mammalian gene expression...
- MOLECULAR PROPERTIES OF VOLTAGE-SENSITIVE CA++ CHANNELSWilliam Catterall; Fiscal Year: 1990..These results will provide a basis for analysis of the molecular basis of calcium channel function and physiological regulation...
- VOLTAGE-SENSITIVE SODIUM CHANNELS IN BRAINWilliam Catterall; Fiscal Year: 1980..These experiments will greatly enhance knoledge of the basic molecular mechanisms responsible for electrical excitability...
- TRAINING IN MOLECULAR NEUROBIOLOGYWilliam Catterall; Fiscal Year: 2007..The training program will integrate the substantial expertise of this group of faculty in a coordinated pre-doctoral and post-doctoral training effort. ..
- CELL BIOLOGY OF THE NEURONAL SODIUM CHANNELWilliam Catterall; Fiscal Year: 1992..The results will define the functional roles of these proteins in the development and maintenance of normal electrical excitability in central neurons...
- CELL BIOLOGY OF THE NEURONAL SODIUM CHANNELWilliam Catterall; Fiscal Year: 1993..Together, these experiments will provide important new information on the mechanisms used by central neurons to control the localization, cell surface density, and functional activity of sodium channels...
- MOLECULAR PROPERTIES OF VOLTAGE SENSITIVE CA++ CHANNELSWilliam Catterall; Fiscal Year: 2003..abstract_text> ..
- VOLTAGE SENSITIVE SODIUM CHANNELS IN BRAINWilliam Catterall; Fiscal Year: 2004..These proposed studies will give new insight into the molecular mechanisms of sodium channel gating and its modification by second messenger-activated protein phosphorylation and by drugs and neurotoxins. ..
- VOLTAGE-SENSITIVE SODIUM CHANNELS IN BRAINWilliam Catterall; Fiscal Year: 1993....
