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humans (20) 20
epilepsy (13) 13
index medicus (12) 12
nerve tissue proteins - genetics (9) 9
animals (8) 8
mutation (8) 8
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article (5) 5
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inhibition (3) 3
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epilepsies, myoclonic - genetics (2) 2
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1. Early somatic mosaicism is a rare cause of long-QT syndrome
by James Rush Priest and Charles Gawad and Kristopher M Kahlig and Joseph K Yu and Thomas O'Hara and Patrick M Boyle and Sridharan Rajamani and Michael J Clark and Sarah T K Garcia and Scott Ceresnak and Jason Harris and Sean Boyle and Frederick E Dewey and Lindsey Malloy-Walton and Kyla Dunn and Megan Grove and Marco V Perez and Norma F Neff and Richard Chen and Katsuhide Maeda and Anne Dubin and Luiz Belardinelli and John West and Christian Antolik and Daniela Macaya and Thomas Quertermous and Natalia A Trayanova and Stephen R Quake and Euan A Ashley
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2016, Volume 113, Issue 41, p. 11555
  Somatic mosaicism, the occurrence and propagation of genetic variation in cell lineages after fertilization, is increasingly recognized to play a causal role... 
Babies | Genotype & phenotype | Simulation | Genomes | Mutation | Cells
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2. Full Text Mutations in SCN10A Are Responsible for a Large Fraction of Cases of Brugada Syndrome
by Hu, Dan, MD, PhD and Barajas-Martínez, Hector, PhD and Pfeiffer, Ryan, BSc and Dezi, Fabio, MS and Pfeiffer, Jenna, AS and Buch, Tapan, MS and Betzenhauser, Matthew J., PhD and Belardinelli, Luiz, PhD and Kahlig, Kristopher M., PhD and Rajamani, Sridharan, PhD and DeAntonio, Harry J., DO and Myerburg, Robert J., MD and Ito, Hiroyuki, MD and Deshmukh, Pramod, MD and Marieb, Mark, MD and Nam, Gi-Byoung, MD, PhD and Bhatia, Atul, MD and Hasdemir, Can, MD and Haïssaguerre, Michel, MD and Veltmann, Christian, MD and Schimpf, Rainer, MD and Borggrefe, Martin, MD and Viskin, Sami, MD and Antzelevitch, Charles, PhD
JACC (Journal of the American College of Cardiology), ISSN 0735-1097, 2014, Volume 64, Issue 1, pp. 66 - 79
Abstract Background BrS is an inherited sudden cardiac death syndrome. Less than 35% of BrS probands have genetically identified pathogenic variants. Recent... 
Cardiovascular | Internal Medicine | genetics | sudden cardiac death | Brugada syndrome | electrophysiology | cardiac conduction disease | cardiac arrhythmias | COMMON VARIANTS | CARDIAC & CARDIOVASCULAR SYSTEMS | GENOME | GENETIC-VARIATION | NA(V)1.8 | CHANNELS | EPILEPSY | Brugada Syndrome - genetics | Young Adult | Brugada Syndrome - diagnosis | Humans | Middle Aged | Adult | Female | Male | Aged | Genetic Variation - genetics | Mutation, Missense - genetics | NAV1.8 Voltage-Gated Sodium Channel - genetics | Heart | Sects | Medical colleges | Genetic aspects | Electric properties
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3. Full Text SCN1A splice variants exhibit divergent sensitivity to commonly used antiepileptic drugs
: SCN1A Splice Variant Pharmacology
by Thompson, Christopher H and Kahlig, Kristopher M and George Jr, Alfred L
Epilepsia, ISSN 0013-9580, 05/2011, Volume 52, Issue 5, pp. 1000 - 1009
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4. Febrile temperatures unmask biophysical defects in Na^sub v^1.1 epilepsy mutations supportive of seizure initiation
by Linda Volkers and Kristopher M Kahlig and Joost HG Das and Marjan JA van Kempen and Dick Lindhout and Bobby PC Koeleman and Martin B Rook
The Journal of General Physiology, ISSN 0022-1295, 12/2013, Volume 142, Issue 6, p. 641
  Generalized epilepsy with febrile seizures plus (GEFS+) is an early onset febrile epileptic syndrome with therapeutic responsive (a)febrile seizures... 
Genotype & phenotype | Convulsions & seizures | Epilepsy | Mutation | Biophysics | Fever
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5. Full Text Ranolazine selectively blocks persistent current evoked by epilepsy-associated Na V1.1 mutations
by Kahlig, Kristopher M and Lepist, Irene and Leung, Kwan and Rajamani, Sridharan and George, Alfred L
British Journal of Pharmacology, ISSN 0007-1188, 11/2010, Volume 161, Issue 6, pp. 1414 - 1426
Sodium channel | Antiepileptic drugs | Epilepsy | Migraine | Ranolazine
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6. Full Text Blockade of na+ channels in pancreatic α-cells has antidiabetic effects
by Dhalla, Arvinder K and Yang, Ming and Ning, Yun and Kahlig, Kristopher M and Krause, Michael and Rajamani, Sridharan and Belardinelli, Luiz
Diabetes, ISSN 0012-1797, 10/2014, Volume 63, Issue 10, pp. 3545 - 3556
Pancreatic alpha-cells express voltage-gated Na+ channels (NaChs), which support the generation of electrical activity leading to an increase in intracellular... 
INSULIN | HYPERGLUCAGONEMIA | INACTIVATION | LATE SODIUM CURRENT | RANOLAZINE | ENDOCRINOLOGY & METABOLISM | POSTPRANDIAL HYPERGLYCEMIA | RECEPTOR | GLUCAGON SUPPRESSION | MICE | CONTRIBUTES | Hypoglycemic Agents - therapeutic use | Islets of Langerhans - drug effects | Acetanilides - pharmacology | Diabetes Mellitus, Experimental - drug therapy | Humans | Rats | Male | Sodium Channel Blockers - pharmacology | Piperazines - therapeutic use | Piperazines - pharmacology | Rats, Sprague-Dawley | Exocytosis - drug effects | NAV1.3 Voltage-Gated Sodium Channel - metabolism | Hypoglycemic Agents - pharmacology | Ranolazine | Glucagon-Secreting Cells - drug effects | Animals | Islets of Langerhans - metabolism | Glucagon-Secreting Cells - metabolism | Acetanilides - therapeutic use | Glucagon - metabolism | Diabetes Mellitus, Experimental - metabolism
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7. Impaired Na sub(V)1.2 function and reduced cell surface expression in benign familial neonatal-infantile seizures
by Misra, Sunita N and Kahlig, Kristopher M and George, Alfred L
Epilepsia, ISSN 0013-9580, 09/2008, Volume 49, Issue 9, pp. 1535 - 1545
Purpose: Mutations in SCN2A, the gene encoding the brain voltage-gated sodium channel alpha -subunit Na sub(V)1.2, are associated with inherited epilepsies... 
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8. Full Text Impaired Na.sub.V1.2 function and reduced cell surface expression in benign familial neonatal-infantile seizures
by Misra, Sunita N and Kahlig, Kristopher M and George, Alfred L
Epilepsia, ISSN 0013-9580, 09/2008, Volume 49, Issue 9, p. 1535
Genetic aspects | Seizures (Medicine)
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9. Multiplexed transposon-mediated stable gene transfer in human cells
by Kristopher M Kahlig and Sai K Saridey and Aparna Kaja and Melissa A Daniels and Alfred L George Jr and Matthew H Wilson
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 01/2010, Volume 107, Issue 4, p. 1343
  Generation of cultured human cells stably expressing one or more recombinant gene sequences is a widely used approach in biomedical research, biotechnology,... 
Cell culture | Biotechnology | Biomedical research | Genes | Cells | Deoxyribonucleic acid--DNA
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10. Full Text Early somatic mosaicism is a rare cause of long-QT syndrome
by James Rush Priest and Charles Gawad and Kristopher M. Kahlig and Joseph K. Yu and Thomas O’Hara and Patrick M. Boyle and Sridharan Rajamani and Michael J. Clark and Sarah T. K. Garcia and Scott Ceresnak and Jason Harris and Sean Boyle and Frederick E. Dewey and Lindsey Malloy-Walton and Kyla Dunn and Megan Grove and Marco V. Perez and Norma F. Neff and Richard Chen and Katsuhide Maeda and Anne Dubin and Luiz Belardinelli and John West and Christian Antolik and Daniela Macaya and Thomas Quertermous and Natalia A. Trayanova and Stephen R. Quake and Euan A. Ashley
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2016, Volume 113, Issue 41, pp. 11555 - 11560
Somatic mosaicism, the occurrence and propagation of genetic variation in cell lineages after fertilization, is increasingly recognized to play a causal role... 
Single cell | Mosaicism | Arrhythmia | Computational modeling | Genomics | ARRHYTHMIAS | DIAGNOSIS | MANAGEMENT | MULTIDISCIPLINARY SCIENCES | DILATED CARDIOMYOPATHY | MATERNAL MOSAICISM | MODEL | COMPUTATIONAL TECHNIQUES | single cell | CARDIAC SODIUM-CHANNEL | arrhythmia | mosaicism | genomics | CONDUCTION | MUTATIONS | computational modeling | Biological Sciences
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11. Full Text Regulation of dopamine transporter function and plasma membrane expression by dopamine, amphetamine, and cocaine
by Kahlig, Kristopher M and Galli, Aurelio
European Journal of Pharmacology, ISSN 0014-2999, 2003, Volume 479, Issue 1, pp. 153 - 158
Pharmacological alterations in dopamine transporter (DAT) function not only modulate dopamine reuptake, but they can induce rapid changes in the plasmalemmal... 
Dopamine transporter | Cocaine | Amphetamine | Trafficking | PROTEIN-KINASE-C | EXCHANGE DIFFUSION | RAT STRIATUM | cocaine | amphetamine | TRANSFECTED CELLS | HUMAN NOREPINEPHRINE TRANSPORTER | MICE LACKING | IN-VITRO | dopamine transporter | CARRIER-MEDIATED RELEASE | PHARMACOLOGY & PHARMACY | XENOPUS OOCYTES | trafficking | REVERSE TRANSPORT | Nerve Tissue Proteins - antagonists & inhibitors | Cocaine - metabolism | Humans | Nerve Tissue Proteins - agonists | Amphetamine - pharmacology | Dopamine - pharmacology | Amphetamine - metabolism | Membrane Transport Proteins - agonists | Membrane Transport Modulators | Gene Expression Regulation - drug effects | Nerve Tissue Proteins - metabolism | Cocaine - pharmacology | Animals | Membrane Transport Proteins - antagonists & inhibitors | Membrane Transport Proteins - metabolism | Cell Membrane - metabolism | Membrane Glycoproteins | Cell Membrane - drug effects | Dopamine - metabolism | Dopamine Plasma Membrane Transport Proteins
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12. Full Text Amphetamine Induces Dopamine Efflux through a Dopamine Transporter Channel
by Kristopher M. Kahlig and Francesca Binda and Habibeh Khoshbouei and Randy D. Blakely and Douglas G. McMahon and Jonathan A. Javitch and Aurelio Galli and Susan G. Amara
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2005, Volume 102, Issue 9, pp. 3495 - 3500
Drugs of abuse, including cocaine, amphetamine (AMPH), and heroin, elevate extracellular dopamine (DA) levels in the brain, thereby altering the... 
Electric potential | Molecules | Biological Sciences | Ratios | Carbon fibers | Neurons | Ion currents | Cocaine | Cell membranes | Pipettes | Electric current | Amperometry | Patch clamp | patch clamp | CHROMAFFIN CELLS | MECHANISM | MULTIDISCIPLINARY SCIENCES | COCAINE | RELEASE | CURRENTS | SEROTONIN TRANSPORTERS | amperometry | NOREPINEPHRINE TRANSPORTERS | VOLTAGE-DEPENDENT UPTAKE | NEURONS | RETINA | Brain - drug effects | Brain - metabolism | Cell Line | Microscopy, Confocal | Patch-Clamp Techniques | Biological Transport | Humans | Amphetamine - pharmacology | Dopamine - metabolism | Amphetamines | Drug abuse | Research
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13. Full Text SCN1A splice variants exhibit divergent sensitivity to commonly used antiepileptic drugs
by Thompson, Christopher H and Kahlig, Kristopher M and George Jr, Alfred L
Epilepsia, ISSN 0013-9580, 05/2011, Volume 52, Issue 5, pp. 1000 - 1009
Summary Purpose:  A common genetic variant (rs3812718) in a splice donor consensus sequence within the neuronal sodium channel gene SCN1A (encoding NaV1.1)... 
Alternative splicing | Antiepileptic drugs | Ion channel gene defects | GATED SODIUM-CHANNELS | CARBAMAZEPINE | POLYMORPHISM | CLINICAL NEUROLOGY | RAT HIPPOCAMPAL-NEURONS | INHIBITION | PHENYTOIN | GENE | EPILEPSY | NA+-CHANNELS | BINDING | Triazines | NAV1.1 Voltage-Gated Sodium Channel | Alternative Splicing | Humans | Protein Isoforms | Anticonvulsants - therapeutic use | Epilepsy - drug therapy | Epilepsy - genetics | Sodium Channels - genetics | Anticonvulsants - pharmacology | Nerve Tissue Proteins - genetics | Phenytoin | Exhibitions | Anopheles | Carbamazepine | Rodents | Mutation | Sodium channels | Conserved sequence | Pharmacogenetics | Exons | lamotrigine | Epilepsy | Sodium channels (voltage-gated) | Pharmacology | Antiepileptic agents | alternative splicing | antiepileptic drugs | ion channel gene defects
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14. Full Text Impaired NaV1.2 function and reduced cell surface expression in benign familial neonatal‐infantile seizures
by Misra, Sunita N and Kahlig, Kristopher M and George, Alfred L
Epilepsia, ISSN 0013-9580, 09/2008, Volume 49, Issue 9, pp. 1535 - 1545
Summary Purpose: Mutations in SCN2A, the gene encoding the brain voltage‐gated sodium channel α‐subunit Na V 1.2, are associated with inherited epilepsies... 
NaV1.2 | Sodium channel | Inherited epilepsy | SCN2A | Basic electrophysiology | 1.2 | Point Mutation - genetics | Patch-Clamp Techniques | Biotinylation | Epithelial Sodium Channels - genetics | Epilepsy, Benign Neonatal - genetics | DNA Mutational Analysis | Epilepsy, Benign Neonatal - physiopathology | Humans | DNA, Complementary - genetics | Cell Membrane - physiology | Electrophysiology - instrumentation | Infant, Newborn | Inherited Epilepsy | Basic Electrophysiology | Sodium Channel
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15. Full Text Eleclazine, a new selective cardiac late sodium current inhibitor, confers concurrent protection against autonomically induced atrial premature beats, repolarization alternans and heterogeneity, and atrial fibrillation in an intact porcine model
by Fuller, Henrique, BS and Justo, Fernanda, BS and Nearing, Bruce D., PhD and Kahlig, Kristopher M., PhD and Rajamani, Sridharan, PhD and Belardinelli, Luiz, MD and Verrier, Richard L., PhD, FHRS
Heart Rhythm, ISSN 1547-5271, 2016, Volume 13, Issue 8, pp. 1679 - 1686
Background The cardiac late sodium current (INa ) has been increasingly implicated in the initiation of atrial fibrillation (AF). Eleclazine (formerly known as... 
Cardiovascular | Epinephrine | Repolarization | Heterogeneity | Atrial fibrillation | Atrial premature beats | Acetylcholine | Late sodium current | Alternans | ARRHYTHMIAS | NERVOUS-SYSTEM | CARDIAC & CARDIOVASCULAR SYSTEMS | HEARTS | VENTRICULAR-TACHYCARDIA | VULNERABILITY | GS-458967 | POTENT | T-WAVE ALTERNANS | Atrial Premature Complexes - physiopathology | Atrial Premature Complexes - drug therapy | Heart Atria - drug effects | Atrial Fibrillation - drug therapy | Autonomic Nervous System - drug effects | Male | Atrial Fibrillation - physiopathology | Autonomic Nervous System - physiopathology | Oxazepines - pharmacology | Animals | Heart Ventricles - physiopathology | Swine | Electrocardiography | Heart Atria - physiopathology | Disease Models, Animal | Heart Ventricles - drug effects | Heart | Medical colleges | Analysis
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16. Full Text The novel late Na+ current inhibitor, GS‐6615 (eleclazine) and its anti‐arrhythmic effects in rabbit isolated heart preparations
by Rajamani, Sridharan and Liu, Gongxin and El‐Bizri, Nesrine and Guo, Donglin and Li, Cindy and Chen, Xiao‐Liang and Kahlig, Kristopher M and Mollova, Nevena and Elzein, Elfatih and Zablocki, Jeff and Belardinelli, Luiz
British Journal of Pharmacology, ISSN 0007-1188, 11/2016, Volume 173, Issue 21, pp. 3088 - 3098
Background and Purpose Enhanced late Na+ current (late INa) in the myocardium is pro‐arrhythmic. Inhibition of this current is a promising strategy to... 
ARRHYTHMIAS | LATE SODIUM CURRENT | FLECAINIDE | TORSADE-DE-POINTES | PHARMACOLOGY | RANOLAZINE | PHARMACOLOGY & PHARMACY | CURRENT BLOCKERS | LONG-QT SYNDROME | VENTRICULAR MYOCYTES | REPOLARIZATION | Rabbits | Animals | Anti-Arrhythmia Agents - pharmacology | Sodium Channels - metabolism | Heart - drug effects | Sodium Channel Blockers - pharmacology | Molecular Structure | Sodium Channel Blockers - chemistry | Anti-Arrhythmia Agents - chemistry | Long QT Syndrome - drug therapy | Oxazepines - pharmacology | Oxazepines - chemistry | Anti-arrhythmia drugs | Research Papers | Research Paper
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17. The novel late Na super(+) current inhibitor, GS-6615 (eleclazine) and its anti-arrhythmic effects in rabbit isolated heart preparations
by Rajamani, Sridharan and Liu, Gongxin and El-Bizri, Nesrine and Guo, Donglin and Li, Cindy and Chen, Xiao-Liang and Kahlig, Kristopher M and Mollova, Nevena and Elzein, Elfatih and Zablocki, Jeff and Belardinelli, Luiz
British Journal of Pharmacology, ISSN 0007-1188, 11/2016, Volume 173, Issue 21, pp. 3088 - 3098
Background and Purpose Enhanced late Na super(+) current (late I sub(Na)) in the myocardium is pro-arrhythmic. Inhibition of this current is a promising... 
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18. Full Text The novel late Na+current inhibitor, GS-6615 (eleclazine) and its anti-arrhythmic effects in rabbit isolated heart preparations
: Cardiac late INainhibitor
by Rajamani, Sridharan and Liu, Gongxin and El-Bizri, Nesrine and Guo, Donglin and Li, Cindy and Chen, Xiao-Liang and Kahlig, Kristopher M and Mollova, Nevena and Elzein, Elfatih and Zablocki, Jeff and Belardinelli, Luiz
British Journal of Pharmacology, ISSN 0007-1188, 11/2016, Volume 173, Issue 21, pp. 3088 - 3098
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19. Full Text Multiplexed Transposon-Mediated Stable Gene Transfer in Human Cells
by Kristopher M. Kahlig and Sal K. Saridey and Aparna Kaja and Melissa A. Daniels and Alfred L. George and Matthew H. Wilson and David E. Clapham
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2010, Volume 107, Issue 4, pp. 1343 - 1348
Generation of cultured human cells stably expressing one or more recombinant gene sequences is a widely used approach in biomedical research, biotechnology,... 
Genetic transposition | Sodium channels | Transposons | Sodium | Genomics | Cell lines | Stem cells | Transgenes | Pluripotent stem cells | Electric current | Sodium channel | piggyBac | SCN1B | SCN1A | SCN2B | TRANSFORMATION | STEM-CELLS | MULTIDISCIPLINARY SCIENCES | INDUCTION | FIBROBLASTS | LINES | sodium channel | ASSAYS | GENERATION | EXCISION | BACULOVIRUS GENOME | Cell Line | Gene Expression | Humans | Open Reading Frames | Genetic Markers | Nerve Tissue Proteins - genetics | DNA Transposable Elements | Nerve Tissue Proteins - metabolism | NAV1.1 Voltage-Gated Sodium Channel | Sodium Channels - metabolism | Protein Binding | Sodium Channels - genetics | Human cytogenetics | Genetic transformation | Research | Properties | Methods | Biological Sciences
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20. Full Text Divergent Sodium Channel Defects in Familial Hemiplegic Migraine
by Kristopher M. Kahlig and Thomas H. Rhodes and Michael Pusch and Tobias Freilinger and José M. Pereira-Monteiro and Michel D. Ferrari and Arn M. J. M. van den Maagdenberg and Martin Dichgans and Alfred L. George
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2008, Volume 105, Issue 28, pp. 9799 - 9804
Familial hemiplegic migraine type 3 (FHM3) is a severe autosomal dominant migraine disorder caused by mutations in the voltage-gated sodium channel ${\rm... 
Sodium channels | Electric potential | Brain | Sodium | HEK293 cells | Neurons | Migraine | Epilepsy | Genetic mutation | Membrane proteins | FHM3 | 1.1 | SCN1A | epilepsy | Na(v)1.1 | MULTIDISCIPLINARY SCIENCES | SPREADING DEPRESSION | SEIZURES | MOUSE MODEL | SEVERE MYOCLONIC EPILEPSY | ION CHANNELS | MUTATIONS | DOPAMINE UPTAKE | INFANCY | Cell Line | NAV1.1 Voltage-Gated Sodium Channel | Humans | Electrophysiology | Epilepsy - genetics | Family | Sodium Channels - genetics | Migraine with Aura - genetics | Mutation, Missense | Sodium - metabolism | Nerve Tissue Proteins - genetics | Physiological aspects | Evaluation | Properties | Biological transport, Active | Biological Sciences | NaV1.1
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