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1. Full Text Genotype-phenotype correlations in neonatal epilepsies caused by mutations in the voltage sensor of K(v)7.2 potassium channel subunits
by Miceli, F and Soldovieri, MV and Ambrosino, P and Barrese, V and Migliore, M and Cilio, MR and Taglialatela, M
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, ISSN 0027-8424, 03/2013, Volume 110, Issue 11, pp. 4386 - 4391
Mutations in the K(v)7.2 gene encoding for voltage-dependent K+ channel subunits cause neonatal epilepsies with wide phenotypic heterogeneity. Two mutations... 
brain development | potassium channel gating | MULTIDISCIPLINARY SCIENCES | channelopathies | pi-stacking interaction | CONVULSIONS | SUPPRESSION | ENCEPHALOPATHY | SEIZURES | EXCITABILITY | KCNQ2 SUBUNITS | BENIGN | anticonvulsants | K+ CHANNEL | NEUTRALIZATION | CHARGE | Pyramidal Cells - metabolism | Cricetinae | Epilepsy, Benign Neonatal - metabolism | Cricetulus | KCNQ3 Potassium Channel - metabolism | Humans | Models, Molecular | Genotype | Epilepsy, Benign Neonatal - pathology | KCNQ3 Potassium Channel - genetics | Mutation, Missense | Anticonvulsants - pharmacology | KCNQ2 Potassium Channel - chemistry | Phenotype | Animals | Epilepsy, Benign Neonatal - genetics | KCNQ2 Potassium Channel - metabolism | KCNQ2 Potassium Channel - genetics | Pyramidal Cells - pathology | Phenylenediamines - pharmacology | Structural Homology, Protein | Amino Acid Substitution | CHO Cells | Carbamates - pharmacology
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2. Full Text Potent KCNQ2/3-specific channel activator suppresses in vivo epileptic activity and prevents the development of tinnitus
by Kalappa, Bopanna I and Soh, Heun and Duignan, Kevin M and Furuya, Takeru and Edwards, Scott and Tzingounis, Anastasios V and Tzounopoulos, Thanos
Journal of Neuroscience, ISSN 0270-6474, 2015, Volume 35, Issue 23, pp. 8829 - 8842
Voltage-gated Kv7 (KCNQ) channels are voltage-dependent potassium channels that are activated at resting membrane potentials and therefore provide a powerful... 
Epilepsy | KCNQ channels | Tinnitus | epilepsy | ANTICONVULSANT RETIGABINE | STIMULATION | PHENOTYPE | MUSCLE | DORSAL COCHLEAR NUCLEUS | NEUROSCIENCES | tinnitus | SPECTRUM | DIFFERENTIATION | KCNQ2 ENCEPHALOPATHY | K+ CHANNELS | POTASSIUM CHANNEL | Membrane Potentials - genetics | Phenylenediamines - therapeutic use | Humans | Male | Epilepsy - etiology | Tinnitus - prevention & control | Carbamates - chemistry | KCNQ2 Potassium Channel - agonists | KCNQ2 Potassium Channel - metabolism | HEK293 Cells | Tinnitus - etiology | Epilepsy - genetics | Female | Disease Models, Animal | Animals, Newborn | Membrane Potentials - drug effects | Anticonvulsants - therapeutic use | Rats | Transcription Factors - genetics | Mutation - genetics | Rats, Sprague-Dawley | Homeodomain Proteins - genetics | Mice, Inbred ICR | Mice, Knockout | Animals | Anticonvulsants - chemistry | Evoked Potentials, Auditory, Brain Stem - genetics | KCNQ2 Potassium Channel - genetics | Epilepsy - drug therapy | Mice | Carbamates - therapeutic use | In Vitro Techniques | Phenylenediamines - chemistry | KCNQ Potassium Channels - genetics
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3. Full Text Dominant‐negative effects of KCNQ2 mutations are associated with epileptic encephalopathy
by Orhan, Gökce and Bock, Merle and Schepers, Dorien and Ilina, Elena I and Reichel, Stephanie Nadine and Löffler, Heidi and Jezutkovic, Nicole and Weckhuysen, Sarah and Mandelstam, Simone and Suls, Arvid and Danker, Timm and Guenther, Elke and Scheffer, Ingrid E and Jonghe, Peter and Lerche, Holger and Maljevic, Snezana
Annals of Neurology, ISSN 0364-5134, 03/2014, Volume 75, Issue 3, pp. 382 - 394
Objective Mutations in KCNQ2 and KCNQ3, encoding the voltage-gated potassium channels K(V)7.2 and K(V)7.3, are known to cause benign familial neonatal seizures... 
PATHWAYS | ANTICONVULSANT RETIGABINE | POTASSIUM CHANNELS | BENIGN | PHENOTYPE | DISORDERS | VOLTAGE-DEPENDENT ACTIVATION | K+ CHANNEL | SUPPRESSION | NEUROSCIENCES | CLINICAL NEUROLOGY | FAMILIAL NEONATAL CONVULSIONS | Xenopus | Genetic Predisposition to Disease - genetics | Membrane Potentials - genetics | Potassium Channels, Voltage-Gated - physiology | Epilepsy, Benign Neonatal - physiopathology | Humans | KCNQ2 Potassium Channel - drug effects | Mutation, Missense | Oocytes | Animals | Epilepsy, Benign Neonatal - genetics | KCNQ2 Potassium Channel - genetics | Potassium Channels, Voltage-Gated - drug effects | Phenylenediamines - pharmacology | KCNQ2 Potassium Channel - physiology | Carbamates - pharmacology | Potassium Channels, Voltage-Gated - genetics | Potassium | Mutation
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4. Full Text Lack of correlation between surface expression and currents in epileptogenic AB-calmodulin binding domain Kv7.2 potassium channel mutants
by Alaimo, Alessandro and Etxeberria, Ainhoa and Gómez-Posada, Juan Camilo and Gomis-Perez, Carolina and Fernández-Orth, Juncal and Malo, Covadonga and Villarroel, Alvaro
Channels, ISSN 1933-6950, 01/2018, Volume 12, Issue 1, pp. 299 - 310
Heteromers of Kv7.2/Kv7.3 subunits constitute the main substrate of the neuronal M-current that limits neuronal hyper-excitability and firing frequency.... 
epilepsy | KCNQ | surface expression | Kv7 | channelopathy | Calmodulin | C-TERMINUS | BIOCHEMISTRY & MOLECULAR BIOLOGY | PHOSPHOLIPASE-C | BULLFROG SYMPATHETIC NEURONS | FAMILIAL NEONATAL CONVULSIONS | KCNQ2 K+ CHANNEL | MUTATION | VOLTAGE SENSOR | KCNQ2/KCNQ3 | MODULATION | Xenopus | KCNQ2 Potassium Channel - chemistry | Animals | Calmodulin - metabolism | KCNQ2 Potassium Channel - metabolism | Humans | Surface Properties | HEK293 Cells | KCNQ2 Potassium Channel - genetics | Protein Binding | Protein Domains
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5. Full Text Epilepsy-associated KCNQ2 channels regulate multiple intrinsic properties of layer 2/3 pyramidal neurons
by Niday, Zachary and Hawkins, Virginia E and Soh, Heun and Mulkey, Daniel K and Tzingounis, Anastasios V
Journal of Neuroscience, ISSN 0270-6474, 01/2017, Volume 37, Issue 3, pp. 576 - 586
KCNQ2 potassium channels are critical for normal brain function, as both loss-of-function and gain-of-function KCNQ2 variants can lead to various forms of... 
KCNQ3 | Sodium channels | Potassium channels | Epilepsy | KCNQ2 | Neocortex - physiology | Humans | Mice, Transgenic | Epilepsy - physiopathology | KCNQ2 Potassium Channel - deficiency | Mice, Knockout | Action Potentials - physiology | Animals | Pyramidal Cells - physiology | HEK293 Cells | KCNQ2 Potassium Channel - genetics | Epilepsy - genetics | KCNQ2 Potassium Channel - physiology | Mice | epilepsy | sodium channels | potassium channels
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6. Full Text Endoplasmic reticulum retention of KCNQ2 potassium channel mutants following temperature elevation
by Yu, Fang and Xu, Jian and Xiao, Zheman and Peng, Biwen and He, Xiaohua
Bio-Medical Materials and Engineering, ISSN 0959-2989, 2017, Volume 28, Issue 1, pp. S243 - S253
BACKGROUND: KCNQ2 plays a key role in the regulation of neuronal excitability. The R214W and Y284C mutants of KCNQ2 channels, which are associated with BFNC,... 
temperature | benign familial neonatal convulsions | febrile seizures | ion channels | KCNQ2 | MATERIALS SCIENCE, BIOMATERIALS | ENGINEERING, BIOMEDICAL | PROTEIN-KINASE CK2 | SURFACE EXPRESSION | TRAFFICKING | SODIUM-CHANNEL | FAMILIAL NEONATAL CONVULSIONS | INITIAL SEGMENT | EPILEPSY | KCNQ2/KCNQ3 | K+ CHANNELS | KCNQ2 Potassium Channel - analysis | Point Mutation | Temperature | Endoplasmic Reticulum - genetics | KCNQ2 Potassium Channel - metabolism | Humans | HEK293 Cells | KCNQ2 Potassium Channel - genetics | Endoplasmic Reticulum - metabolism | Hot Temperature | Protein Transport | Temperature dependence | Trafficking | Excitability | Fluorescence | High temperature | Confocal | Retention | Western blotting | Mutants | Elevation | Temperature effects | Ion channels | Potassium channels (voltage-gated) | Endoplasmic reticulum | Potassium | Fluorescence microscopy | KCNQ2 protein | Seizures
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7. Full Text A recurrent KCNQ2 pore mutation causing early onset epileptic encephalopathy has a moderate effect on M current but alters subcellular localization of Kv7 channels
by Abidi, Affef and Devaux, Jérôme J and Molinari, Florence and Alcaraz, Gisèle and Michon, François-Xavier and Sutera-Sardo, Julie and Becq, Hélène and Lacoste, Caroline and Altuzarra, Cécilia and Afenjar, Alexandra and Mignot, Cyril and Doummar, Diane and Isidor, Bertrand and Guyen, Sylvie N and Colin, Estelle and De La Vaissière, Sabine and Haye, Damien and Trauffler, Adeline and Badens, Catherine and Prieur, Fabienne and Lesca, Gaetan and Villard, Laurent and Milh, Mathieu and Aniksztejn, Laurent
Neurobiology of Disease, ISSN 0969-9961, 2015, Volume 80, pp. 80 - 92
Abstract Mutations in the KCNQ2 gene encoding the voltage-dependent potassium M channel Kv7.2 subunit cause either benign epilepsy or early onset epileptic... 
Neurology | Early epileptic encephalopathy | p.A294G mutation | Kv7 channels | Subcellular channel expression | p.A294V mutation | M-current | P.A294V mutation | P.A294G mutation | ANKYRIN-G | POTASSIUM CHANNELS | HIPPOCAMPAL PYRAMIDAL NEURONS | NEUROSCIENCES | FAMILIAL NEONATAL CONVULSIONS | SYNAPTIC INTEGRATION | EXCITABILITY | BENIGN | CALMODULIN | VOLTAGE SENSOR | K+ CHANNEL | Cricetulus | Brain - physiopathology | Humans | Cells, Cultured | Epilepsy - physiopathology | Epilepsy - diagnosis | Brain - metabolism | Hippocampus - metabolism | Phenotype | Animals | KCNQ2 Potassium Channel - metabolism | KCNQ2 Potassium Channel - genetics | Epilepsy - genetics | KCNQ2 Potassium Channel - physiology | Neurons - metabolism | Mutation | CHO Cells | Encephalopathy | Epilepsy | Genetic aspects | Life Sciences | Genetics
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8. Full Text Suppression of KCNQ/M (Kv7) potassium channels in dorsal root ganglion neurons contributes to the development of bone cancer pain in a rat model
by Zheng, Qin and Fang, Dong and Liu, Min and Cai, Jie and Wan, You and Han, Ji-Sheng and Xing, Guo-Gang
Pain, ISSN 0304-3959, 03/2013, Volume 154, Issue 3, pp. 434 - 448
Suppression of KCNQ/M channels in dorsal root ganglia neurons is associated with neuronal hyperexcitability and cancer-induced bone pain in rats. Bone cancer... 
KCNQ channel | M current | Retigabine | Hyperexcitability | Dorsal root ganglion | Bone cancer pain | XE-991 | SRC TYROSINE KINASE | M-CURRENT MODULATORS | SYMPATHETIC NEURONS | NERVE INJURY | NEUROSCIENCES | MEMBRANE-POTENTIAL OSCILLATIONS | SENSORY NEURONS | CLINICAL NEUROLOGY | NEUROPATHIC PAIN | NR2B-CONTAINING NMDA RECEPTORS | ANESTHESIOLOGY | MEDIATED INHIBITION | K+ CHANNELS | Neoplasm Transplantation | Phenylenediamines - therapeutic use | Nociception - physiology | Bone Neoplasms - secondary | Stress, Mechanical | Ganglia, Spinal - physiopathology | KCNQ3 Potassium Channel - physiology | Bone Neoplasms - pathology | KCNQ2 Potassium Channel - antagonists & inhibitors | Synaptic Transmission | Tibia - pathology | Sensory Receptor Cells - physiology | Bone Neoplasms - physiopathology | Mammary Neoplasms, Experimental - pathology | Pain - etiology | Female | KCNQ2 Potassium Channel - physiology | Sensory Receptor Cells - metabolism | Carcinoma - pathology | Potassium Channel Blockers - pharmacology | Carbamates - pharmacology | Carcinoma - secondary | KCNQ3 Potassium Channel - antagonists & inhibitors | Hot Temperature - adverse effects | Down-Regulation | Rats | KCNQ3 Potassium Channel - genetics | KCNQ2 Potassium Channel - biosynthesis | Rats, Sprague-Dawley | Anthracenes - pharmacology | Carcinoma - physiopathology | Hyperalgesia - physiopathology | KCNQ3 Potassium Channel - biosynthesis | Patch-Clamp Techniques | Animals | KCNQ2 Potassium Channel - genetics | Hyperalgesia - etiology | Phenylenediamines - pharmacology | Carbamates - therapeutic use | Cancer pain | Bone cancer | Neurosciences | Potassium channels | Ganglion | Neurons
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9. Full Text Pointed rhythmic theta waves: a unique EEG pattern in KCNQ2‐related neonatal epileptic encephalopathy
by Buttle, Sarah Grace and Sell, Erick and Dyment, David and Bulusu, Srinivas and Pohl, Daniela
Epileptic Disorders, ISSN 1294-9361, 09/2017, Volume 19, Issue 3, pp. 351 - 356
We report the case of an infant with KCNQ2‐related neonatal epileptic encephalopathy presenting with intractable seizures beginning on the second day of life,... 
mutation | neonatal seizure | epileptic encephalopathy | lidocaine | KCNQ2 | EEG marker | KCNQ2 mutation | SEIZURES | PHENOTYPE | KCNQ2 ENCEPHALOPATHY | CLINICAL NEUROLOGY | Spasms, Infantile - physiopathology | Brain - physiopathology | Humans | Anticonvulsants - therapeutic use | Carbamazepine - therapeutic use | Lidocaine - therapeutic use | Treatment Outcome | Electroencephalography | Spasms, Infantile - genetics | Spasms, Infantile - drug therapy | KCNQ2 Potassium Channel - genetics | Female | Infant, Newborn | Neonates | Basal ganglia | Weaning | Epilepsy | EEG | Theta rhythms | Rhythms | Antiepileptic agents | Waves | Carbamazepine | Ganglia | Genetic screening | Convulsions & seizures | Missense mutation | Sleep | Magnetic resonance imaging | Encephalopathy | Potassium channels (voltage-gated) | Lidocaine | KCNQ2 protein | Seizures
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10. Full Text Redistribution of Kv1 and Kv7 enhances neuronal excitability during structural axon initial segment plasticity
by Kuba, Hiroshi and Yamada, Rei and Ishiguro, Go and Adachi, Ryota
Nature Communications, ISSN 2041-1723, 11/2015, Volume 6, Issue 1, p. 8815
Structural plasticity of the axon initial segment (AIS), the trigger zone of neurons, is a powerful means for regulating neuronal activity. Here, we show that... 
ACTIVITY-DEPENDENT RELOCATION | PYRAMIDAL NEURONS | COCHLEAR NUCLEUS NEURONS | INTRINSIC EXCITABILITY | MULTIDISCIPLINARY SCIENCES | SPIKE INITIATION | MAGNOCELLULARIS | ACTION-POTENTIAL INITIATION | AUDITORY NEURONS | POTASSIUM CHANNEL SUBUNITS | K+ CHANNELS | Kv1.1 Potassium Channel - genetics | Kv1.1 Potassium Channel - chemistry | Kv1.1 Potassium Channel - metabolism | Neurons - chemistry | Axons - metabolism | Axons - chemistry | Protein Transport | KCNQ2 Potassium Channel - chemistry | Animals | KCNQ2 Potassium Channel - metabolism | Neuronal Plasticity | Chickens | KCNQ2 Potassium Channel - genetics | Neurons - metabolism | Kinetics
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11. Full Text The Kv7.2/Kv7.3 heterotetramer assembles with a random subunit arrangement
by Stewart, Andrew P and Gómez-Posada, Juan Camilo and McGeorge, Jessica and Rouhani, Maral J and Villarroel, Alvaro and Murrell-Lagnado, Ruth D and Edwardson, J. Michael
Journal of Biological Chemistry, ISSN 0021-9258, 04/2012, Volume 287, Issue 15, pp. 11870 - 11877
Voltage-gated K+ channels composed of Kv7.2 and Kv7.3 are the predominant contributors to the M-current, which plays a key role in controlling neuronal... 
DOMAIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | STOICHIOMETRY | KCNQ2 | KCNQ2/KCNQ3 POTASSIUM CHANNELS | FORCE MICROSCOPY REVEALS | RESIDUE | RECEPTORS | EXPRESSION | K+ CHANNELS | Cell Line | Protein Subunits | Recombinant Fusion Proteins - isolation & purification | KCNQ3 Potassium Channel - metabolism | Humans | Protein Multimerization | Recombinant Fusion Proteins - chemistry | Recombinant Fusion Proteins - metabolism | KCNQ2 Potassium Channel - chemistry | Microscopy, Confocal | KCNQ2 Potassium Channel - metabolism | KCNQ3 Potassium Channel - isolation & purification | Protein Structure, Quaternary | KCNQ3 Potassium Channel - chemistry | Microscopy, Atomic Force | Protein Binding | KCNQ2 Potassium Channel - isolation & purification | Membrane Proteins | Potassium Channels | Protein Structure and Folding | Ion Channels | Molecular Imaging | Atomic Force Microscopy | Protein Structure
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12. Full Text Retigabine, a Kv7.2/Kv7.3-channel opener, attenuates drug-induced seizures in knock-in mice harboring Kcnq2 mutations
by Ihara, Yukiko and Tomonoh, Yuko and Deshimaru, Masanobu and Zhang, Bo and Uchida, Taku and Ishii, Atsushi and Hirose, Shinichi
PLoS ONE, ISSN 1932-6203, 02/2016, Volume 11, Issue 2, p. e0150095
The hetero-tetrameric voltage-gated potassium channel Kv7.2/Kv7.3, which is encoded by KCNQ2 and KCNQ3, plays an important role in limiting network... 
Protein Structure, Tertiary | Seizures - genetics | Phenylenediamines - therapeutic use | KCNQ3 Potassium Channel - metabolism | Humans | Kainic Acid - pharmacology | Seizures - drug therapy | Models, Molecular | Seizures - metabolism | Gene Knock-In Techniques | Seizures - chemically induced | KCNQ2 Potassium Channel - chemistry | Animals | KCNQ2 Potassium Channel - metabolism | KCNQ2 Potassium Channel - genetics | Phenylenediamines - pharmacology | Mice | Mutation | Carbamates - therapeutic use | Carbamates - pharmacology | Ion Channel Gating - drug effects | Seizing | Neonates | Brain | Pediatrics | Firing pattern | Epilepsy | EEG | Excitability | Electroencephalography | Antiepileptic agents | Video recording | Medicine | Phenobarbital | KCNQ3 protein | Brain research | Coding | Encephalopathy | Potassium channels (voltage-gated) | Kainic acid | Potassium | KCNQ2 protein | Seizures
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13. Full Text Low expression of Kv7/M channels facilitates intrinsic and network bursting in the developing rat hippocampus
by Victoria F. Safiulina and Paola Zacchi and Maurizio Taglialatela and Yoel Yaari and Enrico Cherubini
The Journal of Physiology, ISSN 0022-3751, 11/2008, Volume 586, Issue 22, pp. 5437 - 5453
Early in development, network activity in the hippocampus is characterized by recurrent synchronous bursts, whose cellular correlates are giant depolarizing... 
PHYSIOLOGY | ANTICONVULSANT RETIGABINE | CA1 PYRAMIDAL CELLS | IMMUNOHISTOCHEMICAL ANALYSIS | SPIKE AFTERDEPOLARIZATION | NEURONAL M-CURRENT | SYMPATHETIC NEURONS | KCNQ2/KCNQ3 K+ CHANNELS | NEUROSCIENCES | NEUROTRANSMITTER RELEASE ENHANCER | KCNQ2 POTASSIUM CHANNEL | GIANT DEPOLARIZING POTENTIALS | Pyramidal Cells - metabolism | Sodium Potassium Chloride Symporter Inhibitors | Rats, Wistar | gamma-Aminobutyric Acid - metabolism | Hippocampus - drug effects | Sodium-Potassium-Chloride Symporters - metabolism | KCNQ2 Potassium Channel - antagonists & inhibitors | KCNQ2 Potassium Channel - agonists | Nerve Net - cytology | KCNQ2 Potassium Channel - metabolism | Indoles - pharmacology | Synaptic Transmission - drug effects | Pyramidal Cells - drug effects | Hippocampus - growth & development | Action Potentials - drug effects | Potassium Channel Blockers - pharmacology | Carbamates - pharmacology | Animals, Newborn | Nerve Net - growth & development | Rats | gamma-Aminobutyric Acid - pharmacology | Hippocampus - cytology | Hippocampus - metabolism | Animals | Solute Carrier Family 12, Member 2 | Nerve Net - metabolism | Phenylenediamines - pharmacology | Pyridines - pharmacology | Kinetics | In Vitro Techniques | GABA | Brain | Neurosciences | Neurons | Neuroscience
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14. Full Text Pharmacophore modeling, 3D-QSAR, and in silico ADME prediction of N-pyridyl and pyrimidine benzamides as potent antiepileptic agents
by Malik, Ruchi and Mehta, Pakhuri and Srivastava, Shubham and Choudhary, Bhanwar Singh and Sharma, Manish
Journal of Receptors and Signal Transduction, ISSN 1079-9893, 05/2017, Volume 37, Issue 3, pp. 259 - 266
Biological mechanism attributing mutations in KCNQ2/Q3 results in benign familial neonatal epilepsy (BFNE), a rare form of epilepsy and thus neglected. It... 
epilepsy | 3D-QSAR | Docking | KCNQ2/Q3 openers | ADME | BIOCHEMISTRY & MOLECULAR BIOLOGY | Q3 openers | ANTICONVULSANT | MECHANISMS | DISCOVERY | POTASSIUM CHANNEL OPENERS | CELL BIOLOGY | ACCURATE DOCKING | KCNQ2 | DRUGS | NEUROBIOLOGY | RETIGABINE | K+ CHANNELS | KCNQ3 Potassium Channel - antagonists & inhibitors | Humans | Anticonvulsants - therapeutic use | Models, Molecular | Epilepsy, Benign Neonatal - pathology | KCNQ3 Potassium Channel - genetics | Drug Discovery | KCNQ2 Potassium Channel - antagonists & inhibitors | Pyrimidines - chemistry | KCNQ2 Potassium Channel - chemistry | Epilepsy, Benign Neonatal - drug therapy | Benzamides - therapeutic use | Epilepsy, Benign Neonatal - genetics | Hydrogen Bonding | Anticonvulsants - chemistry | Computer Simulation | KCNQ2 Potassium Channel - genetics | Hydrophobic and Hydrophilic Interactions | KCNQ3 Potassium Channel - chemistry | Molecular Docking Simulation | Mutation | Binding Sites | Quantitative Structure-Activity Relationship | Benzamides - chemistry
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