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1. Full Text Effects of S906T polymorphism on the severity of a novel borderline mutation I692M in Na(v)1.4 cause periodic paralysis
by Fan, C and Mao, N and Lehmann-Horn, F and Burmann, J and Jurkat-Rott, K
CLINICAL GENETICS, ISSN 0009-9163, 06/2017, Volume 91, Issue 6, pp. 859 - 867
Hyperkalemic periodic paralysis (HyperPP) is a dominantly inherited muscle disease caused by mutations in SCN4A gene encoding skeletal muscle voltage gated... 
ACTIVATION | novel borderline mutation | IMPAIRED SLOW INACTIVATION | MECHANISM | founder effect | GENOTYPE | hyperkalemic periodic paralysis | GATED SODIUM-CHANNELS | MUSCLE | PHENOTYPE | Na(v)1 | NA+ CHANNEL | EXCITABILITY | FUNCTIONAL EXPRESSION | GENETICS & HEREDITY
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2. Full Text Characterization of specific allosteric effects of the Na+ channel beta 1 subunit on the Na(v)1.4 isoform
by Sanchez-Solano, A and Islas, AA and Scior, T and Paiz-Candia, B and Millan-PerezPena, L and Salinas-Stefanon, EM
EUROPEAN BIOPHYSICS JOURNAL WITH BIOPHYSICS LETTERS, ISSN 0175-7571, 07/2017, Volume 46, Issue 5, pp. 485 - 494
The mechanism of inactivation of mammalian voltage-gated Na+ channels involves transient interactions between intracellular domains resulting in direct pore... 
C-type | DOMAIN | Na(v)1.4 | SODIUM-CHANNELS | BETA-1-SUBUNIT | BLOCK | Loss of function | MECHANISMS | Inactivation | Allosteric | IFM | BIOPHYSICS | Sodium | FUNCTIONAL EXPRESSION | Mutant | PORE | Oocyte | BETA SUBUNIT | MODULATION
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3. Full Text The Role of Individual Disulfide Bonds of mu-Conotoxin GIIIA in the Inhibition of Na(V)1.4
by Han, PG and Wang, K and Dai, XD and Cao, Y and Liu, SY and Jiang, H and Fan, CX and Wu, WJ and Chen, JS
MARINE DRUGS, ISSN 1660-3397, 11/2016, Volume 14, Issue 11
mu-Conotoxin GIIIA, a peptide toxin isolated from Conus geographus, preferentially blocks the skeletal muscle sodium channel Na(V)1.4. GIIIA folds compactly to... 
THERAPEUTICS | PIIIA | CHEMISTRY, MEDICINAL | SUBTYPES | Na(V)1.4 | mu-conotoxin | MOLECULAR DETERMINANTS | PEPTIDE | ALPHA-CONOTOXINS | disulfide bond | electrophysiology | GIIIA | PORE | ANALGESICS | MUSCLE SODIUM-CHANNELS | BLOCKER
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4. Full Text The Effect of Lamotrigine on Na(v)1.4 Voltage-Gated Sodium Channels
by Nakatani, Y and Masuko, H and Amano, T
JOURNAL OF PHARMACOLOGICAL SCIENCES, ISSN 1347-8613, 10/2013, Volume 123, Issue 2, pp. 203 - 206
Lamotrigine (LTG) is an anticonvulsant drug used in the treatment of epilepsy and bipolar disorder and it has been known that LTG targets voltage-dependent... 
RAT HIPPOCAMPAL-NEURONS | SITE | Na(v)1.4 | PHENYTOIN | lamotrigine | voltage-clamp | LIDOCAINE | NA+ CHANNELS | PORE | CARBAMAZEPINE | PHARMACOLOGY & PHARMACY | BINDING | Dose-Response Relationship, Drug | Membrane Potentials - drug effects | Patch-Clamp Techniques | Triazines - pharmacology | Voltage-Gated Sodium Channels - drug effects | Animals | Humans | HEK293 Cells | Voltage-Gated Sodium Channel Blockers - pharmacology | Mice | Anticonvulsants - pharmacology | Lamotrigine
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5. Full Text Molecular Surface of JZTX-V (beta-Theraphotoxin-Cj2a) Interacting with Voltage-Gated Sodium Channel Subtype Na(V)1.4
by Luo, J and Zhang, YY and Gong, MT and Lu, SS and Ma, YF and Zeng, XZ and Liang, SP
TOXINS, ISSN 2072-6651, 07/2014, Volume 6, Issue 7, pp. 2177 - 2193
Voltage-gated sodium channels (VGSCs; Na(V)1.1-Na(V)1.9) have been proven to be critical in controlling the function of excitable cells, and human genetic... 
NERVOUS-SYSTEM | LOCALIZATION | spider toxin | ACTIVATION | ISOFORMS | RAT | Na(V)1.4 | TOXINS | NEURONS | TOXICOLOGY | voltage gated sodium channels | SPIDER-VENOM PEPTIDES | EXPRESSION | MODULATION | JZTX-V
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6. Full Text Isolation and characterization of two novel scorpion toxins: The alpha-toxin-like CeII8, specific for Na(v)1.7 channels and the classical anti-mammalian CeII9, specific for Na(v)1.4 channels
by Vandendriessche, T and Olamendi-Portugal, T and Zamudio, FZ and Possani, LD and Tytgat, J
TOXICON, ISSN 0041-0101, 09/2010, Volume 56, Issue 4, pp. 613 - 623
Scorpion beta-toxins represent a particular pharmacological group of voltage-gated sodium channel (VGSC) neurotoxins They typically shift the voltage... 
ENHANCED ACTIVATION | VENOM | Na(v)1.4 | CENTRUROIDES-ELEGANS | GATED SODIUM-CHANNEL | Scorpion beta-toxins | Scorpion alpha-toxins | SKELETAL-MUSCLE | Centruroides elegans | DOMAIN-II | PHARMACOLOGY & PHARMACY | K+-CHANNELS | BETA-TOXINS | TOXICOLOGY | VOLTAGE-SENSOR | Na(v)1.7 | MODULATION | Two-electrode voltage-clamp technique | Protein Structure, Tertiary | Xenopus | Amino Acid Sequence | Neurotoxins - chemistry | Chromatography, Ion Exchange | Models, Molecular | Molecular Sequence Data | Neurotoxins - toxicity | Chromatography, High Pressure Liquid | Neurotoxins - isolation & purification | Scorpion Venoms - toxicity | Sequence Alignment | Animals | Scorpion Venoms - chemistry | Sodium Channels - chemistry | Chemical Fractionation | Mass Spectrometry | Mice | Binding Sites | Scorpion Venoms - isolation & purification | Index Medicus
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7. Full Text Ranolazine block of human Na(v)1.4 sodium channels and paramyotonia congenita mutants
by El-Bizri, N and Kahlig, KM and Shryock, JC and George, AL and Belardinelli, L and Rajamani, S
CHANNELS, ISSN 1933-6950, 03/2011, Volume 5, Issue 2, pp. 161 - 172
The antianginal drug ranolazine exerts voltage- and use-dependent block (UDB) of several Na+ channel isoforms, including Na(v)1.4. We hypothesized that... 
DEPENDENT BLOCK | PERSISTENT CURRENT | angina | BIOCHEMISTRY & MOLECULAR BIOLOGY | NA+ CHANNELS | Na channels | Markov model | HYPERKALEMIC PERIODIC PARALYSIS | action potential | HUMAN SKELETAL-MUSCLE | paramyotonia congenita | INACTIVATION | excitability | MEXILETINE | LIDOCAINE | SCN4A | NONDYSTROPHIC MYOTONIAS | MUTATIONS | skeletal muscle
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8. Full Text Structure of the Nav1.4-β1 Complex from Electric Eel
by Yan, Zhen and Yan, Nieng and Zhou, Qiang and Wang, Lin and Wu, Jianping and Zhao, Yanyu and Huang, Gaoxingyu and Peng, Wei and Shen, Huaizong and Lei, Jianlin
Cell, ISSN 0092-8674, 07/2017, Volume 170, Issue 3, pp. 470 - 482.e11
Voltage-gated sodium (Na ) channels initiate and propagate action potentials. Here, we present the cryo-EM structure of EeNa 1.4, the Na channel from electric... 
Nav1.4 | electromechanical coupling | Nav channels | structural biology | the beta-1 subunit | voltage-gated sodium channels | cryo-EM | fast inactivation | Na(v) channels | Na | Na(v)1.4 | channels | Cryo-EM | 1.4 | The beta-1 subunit | Fast inactivation | Electromechanical coupling | Structural biology | Voltage-gated sodium channels
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9. Full Text State-dependent block of rat Na(v)1.4 sodium channels expressed in Xenopus oocytes by pyrazoline-type insecticides
by Silver, K and Soderlund, DM
NEUROTOXICOLOGY, ISSN 0161-813X, 06/2005, Volume 26, Issue 3, pp. 397 - 406
Insecticidal pyrazolines inhibit voltage-sensitive sodium channels of both insect and mammalian neurons ill a voltage-dependent manner: Studies on the effects... 
Na(v)1.4 | ROOT GANGLION NEURONS | OXADIAZINE INSECTICIDE | insecticide | N-DECARBOMETHOXYLATED METABOLITE | MOLECULAR DETERMINANTS | NEUROSCIENCES | LOCAL-ANESTHETIC RECEPTOR | DIHYDROPYRAZOLE INSECTICIDES | RESISTANT | DCJW | oocyte | PHARMACOLOGY & PHARMACY | TOXICOLOGY | indoxacarb | RH 3421 | GATED NA+ CHANNELS | BRAIN
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10. Full Text Prolonged attacks of weakness with hypokalemia in SCN4A-related paramyotonia congenita
by Osch, T. van and Stunnenberg, B.C and Sternberg, Damien and Kerklaan, Bertjan J
Muscle and Nerve, ISSN 0148-639X, 2018, Volume 58, Issue 4, pp. E27 - E28
paramyotonia congenita | SCN4A | Nav1.4 | sodium channelopathy | hypokalemic periodic paralysis | 1.4 | SKELETAL-MUSCLE | PARALYSIS | Na(v)1.4 | FAMILIES | MUTATION | NEUROSCIENCES | CLINICAL NEUROLOGY | CHANNELOPATHIES | Paralysis | Hypokalemia | Sodium channels
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11. Full Text Investigation of the selectivity of one type of small-molecule inhibitor for three Na v channel isoforms based on the method of computer simulation
by Zhao, Fan and Jin, Wei and Ma, Lin and Zhang, Jian-Ye and Wang, Jin-Long and Zhang, Jing-Hai and Song, Yong-Bo
Journal of Biomolecular Structure and Dynamics, ISSN 0739-1102, 02/2019, Volume 37, Issue 3, pp. 702 - 713
Voltage-gated sodium (Na-v) channels play a pivotal role for the changes in membrane potential and belong to large membrane proteins that compose four voltage... 
1.5 | 1.7 | sodium channel inhibitor | VSD4 | molecular dynamics simulation | 1.4 | Na(v)1.4 | BIOPHYSICS | EFFICACY | BIOCHEMISTRY & MOLECULAR BIOLOGY | SCN9A | VOLTAGE SENSOR | Na(v)1.5 | Na(v)1.7 | ACCURACY
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12. Full Text Enhanced closed-state inactivation of mutant cardiac sodium channels (SCN5A N1541D and R1632C) through different mechanisms
by Dharmawan, Tommy and Nakajima, Tadashi and Iizuka, Takashi and Tamura, Shuntaro and Matsui, Hiroki and Kaneko, Yoshiaki and Kurabayashi, Masahiko
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 05/2019, Volume 130, pp. 88 - 95
variants can be associated with overlapping phenotypes such as Brugada syndrome (BrS), sinus node dysfunction and supraventricular tachyarrhythmias. Our... 
Sinus node dysfunction | SCN5A | Brugada syndrome | Sodium currents | Supraventricular tachyarrhythmias | Closed-state inactivation | MOLECULAR-MECHANISM | CARDIAC & CARDIOVASCULAR SYSTEMS | MUTATION | NA(V)1.4 | CELL BIOLOGY | Tachycardia | Analysis
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13. Full Text Loss-of-function mutations in SCN4A cause severe foetal hypokinesia or 'classical' congenital myopathy
by Zaharieva, I.T and Thor, M.G and Oates, E.C and Karnebeek, C. van and Hendson, G and Blom, E and Witting, N and Rasmussen, M and Gabbett, M.T and Ravenscroft, G and Sframeli, M and Suetterlin, K and Sarkozy, A and D'Argenzio, L and Hartley, L and Matthews, E and Pitt, M and Vissing, J and Ballegaard, M and Krarup, C and Slordahl, A and Halvorsen, H and Ye, X.C and Zhang, L.H and Lokken, N and Werlauff, U and Abdelsayed, M and Davis, M.R and Feng, L and Phadke, R and Sewry, C.A and Morgan, J.E and Laing, N.G and Vallance, H and Ruben, P and Hanna, M.G and Lewis, S and Kamsteeg, E.J and Mannikko, R and Muntoni, F
Brain, ISSN 0006-8950, 2016, Volume 139, Issue 3, pp. 674 - 691
See Cannon (doi:10.1093/brain/awv400) for a scientific commentary on this article.Congenital myopathies are a clinically and genetically heterogeneous group of... 
Foetal akinesia | Loss-of-function mutation | Congenital myopathy | Foetal hypokinesia | SCN4A | PERIODIC PARALYSIS | MYASTHENIC SYNDROME | SODIUM-CHANNEL | NEUROSCIENCES | NA(V)1.4 | CLINICAL NEUROLOGY | PATHOPHYSIOLOGY | INACTIVATION | SKELETAL-MUSCLE | foetal hypokinesia | GENETICS | loss-of-function mutation | foetal akinesia | EXPRESSION | congenital myopathy | CHANNELOPATHIES | Severity of Illness Index | NAV1.4 Voltage-Gated Sodium Channel - genetics | Humans | Xenopus laevis | Child, Preschool | Male | Myopathies, Structural, Congenital - genetics | Mutation - genetics | Animals | Pedigree | Hypokinesia - diagnosis | Adolescent | HEK293 Cells | Hypokinesia - genetics | Adult | Female | Myopathies, Structural, Congenital - diagnosis | Child | Infant, Newborn | Original
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14. Full Text Role of the voltage sensor module in Na-v domain IV on fast inactivation in sodium channelopathies: The implication of closed-state inactivation
by Nakajima, T and Kaneko, Y and Dharmawan, T and Kurabayashi, M
CHANNELS, ISSN 1933-6950, 01/2019, Volume 13, Issue 1, pp. 331 - 343
The segment 4 (S4) voltage sensor in voltage-gated sodium channels (Na(v)s) have domain-specific functions, and the S4 segment in domain DIV (DIVS4) plays a... 
MOLECULAR-MECHANISM | PERIODIC PARALYSIS | sodium channelopathies | voltage sensor | BIOCHEMISTRY & MOLECULAR BIOLOGY | SCN5A MUTATIONS | CAUSES PARAMYOTONIA | voltage-gated sodium channel | CONGENITA | NA(V)1.4 | Closed-state inactivation | fast inactivation | BRUGADA-SYNDROME | GATING PORE CURRENTS | CHANNEL MUTATIONS | SPECTRUM
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15. Full Text Depolarization-Activated Gating Pore Current Conducted by Mutant Sodium Channels in Potassium-Sensitive Normokalemic Periodic Paralysis
by Stanislav Sokolov and Todd Scheuer and William A. Catterall
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2008, Volume 105, Issue 50, pp. 19980 - 19985
Some inherited periodic paralyses are caused by mutations in skeletal muscle ${\rm Na}_{{\rm V}}1.4$ sodium channels that alter channel gating and impair... 
Depolarization | Electric potential | Sodium channels | Action potentials | Sodium | Sensors | Paralysis | Electric current | Potassium | Skeletal muscle | Gating charge | Voltage sensor | 1.4 | ENHANCED INACTIVATION | Na-v 1.4 | CHARGE MOVEMENT | voltage sensor | MULTIDISCIPLINARY SCIENCES | gating charge | DEPENDENT K+ CHANNEL | SKELETAL-MUSCLE | PARAMYOTONIA-CONGENITA | FUNCTIONAL EXPRESSION | SLOW INACTIVATION | ION-CHANNEL | MUTATIONS | skeletal muscle | VOLTAGE-SENSOR | Potassium - metabolism | Xenopus | Paralyses, Familial Periodic - physiopathology | Rats | Sodium Channels - physiology | Sodium - metabolism | Oocytes | Muscle Proteins - genetics | Muscle Proteins - agonists | Sodium Channel Agonists | Animals | Ion Channel Gating - genetics | Membrane Potentials | Muscle, Skeletal - physiopathology | Sodium Channels - genetics | Muscle, Skeletal - pathology | Mutation | Muscle Proteins - physiology | Paralyses, Familial Periodic - genetics | Polarization (Electricity) | Muscles | Influence | Research | Properties | Mutation (Biology) | Nav 1.4 | Biological Sciences
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16. Full Text A novel Ile1455Thr variant in the skeletal muscle sodium channel alpha-subunit in a patient with a severe adult-onset proximal myopathy with electrical myotonia and a patient with mild paramyotonia phenotype
by Bednarz, Marcin and Stunnenberg, Bas C and Kusters, Benno and Kamsteeg, Erik-Jan and Saris, Christiaan G and Groome, James and Winston, Vern and Meola, Giovanni and Jurkat-Rott, Karin and Voermans, Nicol C
Neuromuscular Disorders, ISSN 0960-8966, 2016, Volume 27, Issue 2, pp. 175 - 182
Highlights • Novel p.Ile1455Thr in IVS4 variant with varying phenotype. • Loss-of-function feature of the variant conduces to progressive myopathy in patient... 
Neurology | Paramyotonia congenita | Whole-cell recording | NaV1.4 voltage-gated sodium channel | Myopathy | 1.4 voltage-gated sodium channel | DIAGNOSIS | Na(v)1.4 voltage-gated sodium channel | WEAKNESS | NEUROSCIENCES | FAST INACTIVATION | NA(V)1.4 | CLINICAL NEUROLOGY | MUTATION | HYPOKALEMIC PERIODIC PARALYSIS | GATING PORE CURRENTS | SCN4A | CONGENITAL MYASTHENIC SYNDROME | VOLTAGE-SENSOR | Myotonic Dystrophy - physiopathology | Patch-Clamp Techniques | NAV1.4 Voltage-Gated Sodium Channel - genetics | Humans | Middle Aged | Myotonic Dystrophy - genetics | Adult | Female | Male | Myotonia Congenita - physiopathology | Myotonia Congenita - genetics | Muscles | Genetic aspects | Molecular dynamics
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17. Full Text Predictably Convergent Evolution of Sodium Channels in the Arms Race between Predators and Prey
by Brodie III, Edmund D and Brodie Jr, Edmund D
Brain, Behavior and Evolution, ISSN 0006-8977, 09/2015, Volume 86, Issue 1, pp. 48 - 57
Evolution typically arrives at convergent phenotypic solutions to common challenges of natural selection. However, diverse molecular and physiological... 
Original Paper | Newt | Tetrodotoxin | Snake | Thamnophis | Coevolution | Na V 1.4 | Voltage-gated sodium channel | DANGEROUS PREY | Na(v)1.4 | NA+ CHANNELS | TETRODOTOXIN-BINDING-PROTEIN | NEUROSCIENCES | ZOOLOGY | OUTER VESTIBULE | ADAPTATION | RESISTANCE | BEHAVIORAL SCIENCES | TARICHA-GRANULOSA | GARTER SNAKES | ADAPTIVE EVOLUTION | Adaptation, Physiological | Biological Evolution | Predatory Behavior - physiology | Animals | Muscle, Skeletal - drug effects | Selection, Genetic | Models, Molecular | Muscle, Skeletal - metabolism | Sodium Channel Blockers - pharmacology | Sodium Channels - genetics | Sodium Channels - physiology | Tetrodotoxin - pharmacology | Index Medicus
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18. Full Text Congenital myopathy with "corona" fibres, selective muscle atrophy, and craniosynostosis associated with novel recessive mutations in SCN4A
by Gonorazky, HD and Marshall, CR and Al-Murshed, M and Hazrati, LN and Thor, MG and Hanna, MG and Mannikko, R and Ray, PN and Yoon, G
NEUROMUSCULAR DISORDERS, ISSN 0960-8966, 06/2017, Volume 27, Issue 6, pp. 574 - 580
We describe two brothers with lower facial weakness, highly arched palate, scaphocephaly due to synostosis of the sagittal and metopic sutures, axial... 
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