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1. 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
The Journal of neuroscience, ISSN 0270-6474, 01/2017, Volume 37, Issue 3, pp. 576 - 586
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 | Index Medicus | epilepsy | s | sodium channels | potassium channels
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2. Full Text Reduced axonal surface expression and phosphoinositide sensitivity in K v 7 channels disrupts their function to inhibit neuronal excitability in Kcnq2 epileptic encephalopathy
by Kim, Eung Chang and Zhang, Jiaren and Pang, Weilun and Wang, Shuwei and Lee, Kwan Young and Cavaretta, John P and Walters, Jennifer and Procko, Erik and Tsai, Nien-Pei and Chung, Hee Jung
Neurobiology of disease, ISSN 0969-9961, 10/2018, Volume 118, pp. 76 - 93
7 channels | Epileptic encephalopathy | Phosphoinositide | Surface expression | Excitability | Kcnq2 | Mutation | Current | Calmodulin | Epilepsy, Generalized - genetics | Phosphatidylinositols - genetics | Amino Acid Sequence | Brain Diseases - metabolism | Neurons - pathology | Gene Expression | Protein Structure, Secondary | Humans | Brain Diseases - genetics | Axons - metabolism | Rats | Epilepsy, Generalized - pathology | Phosphatidylinositols - biosynthesis | KCNQ2 Potassium Channel - biosynthesis | KCNQ2 Potassium Channel - chemistry | Animals | Brain Diseases - pathology | Epilepsy, Generalized - metabolism | Axons - pathology | HEK293 Cells | KCNQ2 Potassium Channel - genetics | Neurons - metabolism
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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
Neurosciences | Clinical Neurology | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | 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 | Index Medicus
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4. 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, pp. 8815 - 8815
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | 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 | Resistance | Homeostasis | Cochlea | Neurons | Channels | Elongation | Index Medicus
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5. 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
Neurology | Early epileptic encephalopathy | p.A294G mutation | Kv7 channels | Subcellular channel expression | p.A294V mutation | M-current | P.A294V mutation | P.A294G mutation | Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | 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 | Index Medicus | Life Sciences | Genetics
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6. Full Text Homomeric Kv7.2 current suppression is a common feature in KCNQ2 epileptic encephalopathy
by Gomis‐Pérez, Carolina and Urrutia, Janire and Marcé‐Grau, Anna and Malo, Covadonga and López‐Laso, Eduardo and Felipe‐Rucián, Ana and Raspall‐Chaure, Miquel and Macaya, Alfons and Villarroel, Alvaro
Epilepsia (Copenhagen), ISSN 0013-9580, 01/2019, Volume 60, Issue 1, pp. 139 - 148
epilepsy | PIP 2 | M‐current | early infantile epileptic encephalopathies | KCNQ2 | PIP | M-current | Clinical Neurology | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Epilepsy, Generalized - genetics | Amino Acid Sequence | Protein Structure, Secondary | Brain Diseases - diagnosis | Humans | Brain Diseases - genetics | Child, Preschool | Infant | Male | KCNQ2 Potassium Channel - chemistry | Pedigree | KCNQ2 Potassium Channel - genetics | Female | Epilepsy, Generalized - diagnosis | Child | Phosphatidylinositol | Phenotypes | Epilepsy | Encephalopathy | Potassium channels (voltage-gated) | Mutation | Phosphatidylinositol 4,5-diphosphate | KCNQ2 protein | Genotypes | Index Medicus
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7. 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 (Amsterdam), ISSN 0304-3959, 03/2013, Volume 154, Issue 3, pp. 434 - 448
KCNQ channel | M current | Retigabine | Hyperexcitability | Dorsal root ganglion | Bone cancer pain | XE-991 | Neurosciences | Clinical Neurology | Anesthesiology | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Biological and medical sciences | Medical sciences | Diseases of the osteoarticular system | Tumors of striated muscle and skeleton | 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 | Potassium channels | Ganglion | Neurons | Index Medicus
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8. Full Text Role of Kv7.2/Kv7.3 and M-1 muscarinic receptors in the regulation of neuronal excitability in hiPSC-derived neurons
by Kreir, Mohamed and De Bondt, An and Van den Wyngaert, Ilse and Teuns, Greet and Lu, Hua Rong and Gallacher, David J
European journal of pharmacology, ISSN 0014-2999, 09/2019, Volume 858, p. 172474
Life Sciences & Biomedicine | Pharmacology & Pharmacy | Science & Technology | KCNQ3 Potassium Channel - antagonists & inhibitors | KCNQ3 Potassium Channel - metabolism | Humans | Rats | Neurons - cytology | Receptor, Muscarinic M1 - antagonists & inhibitors | KCNQ3 Potassium Channel - genetics | KCNQ2 Potassium Channel - antagonists & inhibitors | KCNQ2 Potassium Channel - agonists | Gene Expression Regulation - drug effects | Receptor, Muscarinic M1 - agonists | Animals | KCNQ2 Potassium Channel - metabolism | Muscarinic Antagonists - pharmacology | KCNQ2 Potassium Channel - genetics | Neurons - metabolism | KCNQ3 Potassium Channel - agonists | Induced Pluripotent Stem Cells - cytology | Neurons - drug effects | Potassium Channel Blockers - pharmacology | Receptor, Muscarinic M1 - metabolism | Electrophysiological Phenomena - drug effects
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9. 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
The Journal of neuroscience, ISSN 0270-6474, 2015, Volume 35, Issue 23, pp. 8829 - 8842
Epilepsy | KCNQ channels | Tinnitus | Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | 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 | Index Medicus | epilepsy | tinnitus
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10. 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
temperature | benign familial neonatal convulsions | febrile seizures | ion channels | KCNQ2 | 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 | Excitability | Fluorescence | High temperature | Retention | Western blotting | Mutants | Elevation | Temperature effects | Ion channels | Potassium channels (voltage-gated) | Endoplasmic reticulum | Potassium | Fluorescence microscopy | KCNQ2 protein | Seizures | Index Medicus
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11. Full Text Conditional deletions of epilepsy-associated KCNQ2 and KCNQ3 channels from cerebral cortex cause differential effects on neuronal excitability
by Soh, Heun and Pant, Rima and LoTurco, Joseph J and Tzingounis, Anastasios V
The Journal of neuroscience, ISSN 0270-6474, 2014, Volume 34, Issue 15, pp. 5311 - 5321
M current | KCNQ3 | BFNC | Epilepsy | KCNQ2 | Neurosciences | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Pyramidal Cells - metabolism | KCNQ3 Potassium Channel - metabolism | Mice, Inbred C57BL | Epilepsy - metabolism | Epilepsy - physiopathology | KCNQ3 Potassium Channel - genetics | Nerve Tissue Proteins - genetics | Action Potentials | Nerve Tissue Proteins - metabolism | Animals | KCNQ2 Potassium Channel - metabolism | Gene Deletion | Pyramidal Cells - physiology | KCNQ2 Potassium Channel - genetics | Epilepsy - genetics | Mice | Index Medicus | epilepsy
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