Genomes and Genes
Gene Symbol: KCNQ3
Description: potassium voltage-gated channel subfamily Q member 3
Alias: BFNC2, EBN2, KV7.3, potassium voltage-gated channel subfamily KQT member 3, potassium channel subunit alpha KvLQT3, potassium channel, voltage gated KQT-like subfamily Q, member 3, potassium channel, voltage-gated, subfamily Q, member 3, potassium voltage-gated channel, KQT-like subfamily, member 3, voltage-gated potassium channel subunit Kv7.3
Publications190 found, 100 shown here
- Affinity for phosphatidylinositol 4,5-bisphosphate determines muscarinic agonist sensitivity of Kv7 K+ channelsCiria C Hernandez
Department of Physiology, University of Texas Health Science Center, San Antonio, TX 78229, USA
J Gen Physiol 134:437-48. 2009..We were able to fully reproduce our data and extract a consistent set of PIP(2) affinities...
- A pore mutation in a novel KQT-like potassium channel gene in an idiopathic epilepsy familyC Charlier
Department of Human Genetics, University of Utah, Salt Lake City 84112, USA
Nat Genet 18:53-5. 1998..Here we describe an additional member, KCNQ3. We mapped this new gene to chromosome 8, between markers D8S256 and D8S284 on a radiation hybrid map...
- KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channelH S Wang
Institute of Molecular Cardiology, Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, NY 11794, USA
Science 282:1890-3. 1998..The biophysical properties, sensitivity to pharmacological blockade, and expression pattern of the KCNQ2 and KCNQ3 potassium channels were determined. It is concluded that both these subunits contribute to the native M-current.
- KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafnessC Kubisch
Zentrum fur Molekulare Neurobiologie Hamburg, Universitat Hamburg, Germany
Cell 96:437-46. 1999..Whereas mutations in KCNQ1 cause deafness by affecting endolymph secretion, the mechanism leading to KCNQ4-related hearing loss is intrinsic to outer hair cells...
- Surface expression and single channel properties of KCNQ2/KCNQ3, M-type K+ channels involved in epilepsyM Schwake
Zentrum für Molekulare Neurobiologie Hamburg ZMNH, Universitat Hamburg, Martinistrasse 85, D 20246 Hamburg, Germany
J Biol Chem 275:13343-8. 2000Mutations in either KCNQ2 or KCNQ3 underlie benign familial neonatal convulsions (BFNC), an inherited epilepsy. The corresponding proteins are co-expressed in broad regions of the brain and associate to heteromeric K(+) channels...
- The identification and characterization of a noncontinuous calmodulin-binding site in noninactivating voltage-dependent KCNQ potassium channelsEva Yus-Najera
Instituto Cajal, Consejo Superior de Investigaciones, Avenida, Dr Arce 37, 28002 Madrid, Spain
J Biol Chem 277:28545-53. 2002..CaM co-immunoprecipitates with KCNQ2, KCNQ3, or KCNQ5 subunits better in the absence than in the presence of Ca2+...
- Calmodulin is an auxiliary subunit of KCNQ2/3 potassium channelsHua Wen
Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Neurosci 22:7991-8001. 2002Calmodulin (CaM) was identified as a KCNQ2 and KCNQ3 potassium channel-binding protein, using a yeast two-hybrid screen...
- A carboxy-terminal domain determines the subunit specificity of KCNQ K+ channel assemblyMichael Schwake
Centre for Molecular Neurobiology Hamburg, ZMNH, Falkenried 94, Germany
EMBO Rep 4:76-81. 2003..KCNQ1 assembles with KCNE beta-subunits but not with other KCNQ alpha-subunits. By contrast, KCNQ3 interacts with KCNQ2, KCNQ4 and KCNQ5...
- Polarized axonal surface expression of neuronal KCNQ channels is mediated by multiple signals in the KCNQ2 and KCNQ3 C-terminal domainsHee Jung Chung
Departments of Physiology and Biochemistry, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143
Proc Natl Acad Sci U S A 103:8870-5. 2006..Mutations in KCNQ2 and KCNQ3 cause benign familial neonatal convulsions (BFNC), dominantly inherited epilepsy and myokymia...
- Altered KCNQ3 potassium channel function caused by the W309R pore-helix mutation found in human epilepsyAkira Uehara
Department of Physiology, School of Medicine, Fukuoka University, 45 1, 7 chome Nanakuma, Jonan ku, Fukuoka 814 0180, Japan
J Membr Biol 222:55-63. 2008..A missense mutation causing the replacement of the corresponding residues with an arginine (W309R) occurs in KCNQ3 subunits forming part of M-channels...
- KCNQ2 and KCNQ3 mutations contribute to different idiopathic epilepsy syndromesB A Neubauer
Department of Pediatric Neurology, University of Giessen Marburg, Feulgenstrasse 12, D 35385 Giessen, Germany
Neurology 71:177-83. 2008..To explore the involvement of M-type potassium channels KCNQ2, Q3, and Q5 in the pathogenesis of common idiopathic epilepsies...
- Determinants within the turret and pore-loop domains of KCNQ3 K+ channels governing functional activityOleg Zaika
Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, USA
Biophys J 95:5121-37. 2008..KCNQ1 and KCNQ4 homomers and KCNQ2/3 heteromers yield large currents, whereas KCNQ2 and KCNQ3 homomers yield small currents...
- A pore residue of the KCNQ3 potassium M-channel subunit controls surface expressionJuan Camilo Gómez-Posada
Unidad de Biofisica, Centro Mixto Consejo Superior de Investigaciones Científicas Universidad del País Vasco Euskal Herriko Unibertsitatea UPV EHU, Leioa, Spain
J Neurosci 30:9316-23. 2010KCNQ2 (Kv7.2) and KCNQ3 (Kv7.3) are the principal subunits underlying the potassium M-current, which exerts a strong control on neuronal excitability...
- Regulation of neuronal M-channel gating in an isoform-specific manner: functional interplay between calmodulin and syntaxin 1AAdi Etzioni
Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel
J Neurosci 31:14158-71. 2011Whereas neuronal M-type K(+) channels composed of KCNQ2 and KCNQ3 subunits regulate firing properties of neurons, presynaptic KCNQ2 subunits were demonstrated to regulate neurotransmitter release by directly influencing presynaptic ..
- Kv7 channels can function without constitutive calmodulin tetheringJuan Camilo Gómez-Posada
Unidad de Biofisica, Consejo Superior de Investigaciones Científicas Universidad del País Vasco Euskal Herriko Unibersitatea, Leioa, Spain
PLoS ONE 6:e25508. 2011..However, we have identified a presumably phosphomimetic mutation S511D that permits calmodulin-independent function. Thus, our data reveal that constitutive tethering of calmodulin is not required for Kv7 channel function...
- Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsyB C Schroeder
Zentrum fur Molekulare Neurobiologie Hamburg, Universitat Hamburg, Germany
Nature 396:687-90. 1998..neonatal convulsions (BFNC), an autosomal dominant epilepsy of infancy, is caused by mutations in the KCNQ2 or the KCNQ3 potassium channel genes...
- Three mechanisms underlie KCNQ2/3 heteromeric potassium M-channel potentiationAinhoa Etxeberria
Instituto Cajal Consejo Superior de Investigaciones Científicas CSIC, 28002 Madrid, Spain
J Neurosci 24:9146-52. 2004..Notably, in terms of excitation, mutations in either KCNQ2 or KCNQ3 lead to benign neonatal familial convulsions...
- Impact of our understanding of the genetic aetiology of epilepsyR M Gardiner
Department of Paediatrics, Royal Free and University College Medical School, UCL, Rayne Institute, London, UK
J Neurol 247:327-34. 2000..lobe epilepsy is caused by mutations in CHRNA4, benign familial neonatal convulsions by mutations in KCNQ2 and KCNQ3, and generalised epilepsy with febrile seizures plus by mutations in SCN1B...
- Involvement of KCNQ2 subunits in [3H]dopamine release triggered by depolarization and pre-synaptic muscarinic receptor activation from rat striatal synaptosomesMaria Martire
Institute of Pharmacology, School of Medicine, Catholic University of S Heart, Rome, Italy
J Neurochem 102:179-93. 2007KCNQ2 and KCNQ3 subunits encode for the muscarinic-regulated current (I(KM)), a sub-threshold voltage-dependent K+ current regulating neuronal excitability...
- Participation of KCNQ (Kv7) potassium channels in myogenic control of cerebral arterial diameterXi Zoë Zhong
Ion Channels and Cell Signaling Centre, Division of Basic Medical Sciences, St George s University of London, London SW17 0RE, UK
J Physiol 588:3277-93. 2010..KCNQ4 message was more abundant than KCNQ5 = KCNQ1, but KCNQ2 and KCNQ3 message levels were negligible. Kv7.1, Kv7.4 and Kv7...
- Nervous system KV7 disorders: breakdown of a subthreshold brakeSnezana Maljevic
Neurologische Klinik und Institut für Angewandte Physiologie, Universitat Ulm, Zentrum Klinische Forschung, Helmholtzstr 8 1, D 89081 Ulm, Germany
J Physiol 586:1791-801. 2008..cardiac arrhythmia (long QT syndrome) with or without congenital deafness (KCNQ1), a neonatal epilepsy (KCNQ2 and KCNQ3) and progressive deafness alone (KCNQ4)...
- Expression of a calmodulin-binding KCNQ2 potassium channel fragment modulates neuronal M-current and membrane excitabilityMohammad Shahidullah
Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Proc Natl Acad Sci U S A 102:16454-9. 2005KCNQ2 and KCNQ3 ion channel pore-forming subunits coassemble to form a heteromeric voltage-gated potassium channel that underlies the neuronal M-current...
- Regulation of the voltage-gated K(+) channels KCNQ2/3 and KCNQ3/5 by serum- and glucocorticoid-regulated kinase-1Friderike Schuetz
School of Biomedical Sciences and Queensland Brain Institute, University of Queensland, Brisbane, Queensland, Australia
Am J Physiol Cell Physiol 295:C73-80. 2008The voltage-gated KCNQ2/3 and KCNQ3/5 K(+) channels regulate neuronal excitability. We recently showed that KCNQ2/3 and KCNQ3/5 channels are regulated by the ubiquitin ligase Nedd4-2...
- M channel KCNQ2 subunits are localized to key sites for control of neuronal network oscillations and synchronization in mouse brainE C Cooper
Department of Neurology, University of California, San Francisco, San Francisco, California 94143 0725, USA
J Neurosci 21:9529-40. 2001..1 sec) at subthreshold membrane potentials. KCNQ2 associates with KCNQ3, a homolog, to form heteromeric channels responsible for the M current (I(M)) in superior cervical ganglion (SCG) ..
- A spontaneous mutation involving Kcnq2 (Kv7.2) reduces M-current density and spike frequency adaptation in mouse CA1 neuronsJames F Otto
Anticonvulsant Drug Development Program, Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah 84112, USA
J Neurosci 26:2053-9. 2006..Mutations in two subunits (KCNQ2 and KCNQ3; Kv7.2 and Kv7...
- Ion channels and epilepsyH Lerche
Department of Applied Physiology, Univeristy of Ulm, Germany
Am J Med Genet 106:146-59. 2001..benign familial neonatal convulsions by mutations in potassium channels constituting the M-current (KCNQ2, KCNQ3), generalized epilepsy with febrile seizures plus by mutations in subunits of the voltage-gated sodium channel or ..
- Channelopathies can cause epilepsy in manOrtrud K Steinlein
Institute of Human Genetics, Friedrich Wilhelms University of Bonn, Wilhelmstrasse 31, D 53111 Bonn, Germany
Eur J Pain 6:27-34. 2002..lead to familial nocturnal frontal lobe epilepsy, while defects in the voltage-gated potassium channels KCNQ2 and KCNQ3 have recently been found to cause benign familial neonatal convulsions...
- [Genetic background of epilepsies]Anna Kelemen
Orszagos Pszichiatriai es Neurologiai Intezet, Budapest
Ideggyogy Sz 57:141-51. 2004..in familial nocturnal frontal lobe epilepsy, while defects in the voltage gated potassium channels (KCNQ2 and KCNQ3) have been identified in benign familial neonatal convulsions...
- Atypical gating of M-type potassium channels conferred by mutations in uncharged residues in the S4 region of KCNQ2 causing benign familial neonatal convulsionsMaria Virginia Soldovieri
Section of Pharmacology, Department of Neuroscience, University of Naples Federico II, 80131 Naples, Italy
J Neurosci 27:4919-28. 2007Heteromeric assembly of KCNQ2 and KCNQ3 subunits underlie the M-current (I(KM)), a slowly activating and noninactivating neuronal K(+) current...
- Decreased subunit stability as a novel mechanism for potassium current impairment by a KCNQ2 C terminus mutation causing benign familial neonatal convulsionsMaria Virginia Soldovieri
Division of Pharmacology, Department of Neuroscience, University of Naples Federico II, 80131 Naples
J Biol Chem 281:418-28. 2006KCNQ2 and KCNQ3 K+ channel subunits underlie the muscarinic-regulated K+ current (I(KM)), a widespread regulator of neuronal excitability...
- Impaired M-current and neuronal excitabilityMotohiro Okada
Department of Neuropsychiatry, Hirosaki University, Hirosaki, Japan
Epilepsia 43:36-8. 2002..Several mutations of either KCNQ2 or KCNQ3, members of the KCNQ-related K+-channel (KCNQ-channel) family, were identified as a cause of BFNC...
- Neonatal epilepsy syndromes and GEFS+: mechanistic considerationsDaniel L Burgess
Baylor College of Medicine, Houston, TX, USA
Epilepsia 46:51-8. 2005..genes encode voltage-gated Na+ channel subunits (SCN1A, SCN2A, SCN1B), voltage-gated K+ channel subunits (KCNQ2, KCNQ3), and a ligand-gated neurotransmitter receptor subunit (GABRG2)...
- [Benign familial neonatal convulsions: molecular pathology and diagnosis]O K Steinlein
Institut fur Humangenetik, Rheinische Friedrich Wilhelms Universitat Bonn
Nervenarzt 71:611-5. 2000..Linkage studies located genes to chromosome 20q13.3 and 8q24, and the voltage-gated potassium channels KCNQ2 and KCNQ3 were recently identified...
- The voltage-gated potassium channel KCNQ2 in Taiwanese children with febrile convulsionsI Ching Chou
Department of Pediatrics, China Medical College Hospital, Taichung, Taiwan
Neuroreport 13:1971-3. 2002Mutations in the voltage-gated potassium channel genes KCNQ2 and KCNQ3 have been found to cause benign familial neonatal convulsions...
- A novel missense mutation (N258S) in the KCNQ2 gene in a Turkish family afflicted with benign familial neonatal convulsions (BFNC)Ozlem Yalcin
Department of Molecular Biology and Genetics, Bogazici University, Istanbul, Turkey
Turk J Pediatr 49:385-9. 2007..The disease is caused by mutations in the two homologous genes KCNQ2 and KCNQ3 that encode the subunits of the voltage-gated potassium channel...
- De novo KCNQ2 mutations in patients with benign neonatal seizuresL R F Claes
Department of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology VIB, University of Antwerp, Antwerpen, Belgium
Neurology 63:2155-8. 2004..Mutations have been identified in the voltage-gated potassium ion channels KCNQ2 and KCNQ3. The authors performed a mutation analysis of KCNQ2 and KCNQ3 in six patients of whom four had no family history ..
- Zinc pyrithione-mediated activation of voltage-gated KCNQ potassium channels rescues epileptogenic mutantsQiaojie Xiong
Department of Neuroscience, High Throughput Biology Center, School of Medicine, Johns Hopkins University, 733 North Broadway, Baltimore, Maryland 21205, USA
Nat Chem Biol 3:287-96. 2007..Human mutations of KCNQ2 and KCNQ3 potassium channel genes result in reduction or loss of channel activity and cause benign familial neonatal ..
- Electroconvulsive seizure thresholds and kindling acquisition rates are altered in mouse models of human KCNQ2 and KCNQ3 mutations for benign familial neonatal convulsionsJames F Otto
Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, USA
Epilepsia 50:1752-9. 2009Benign familial neonatal convulsions (BFNC) is caused by mutations in the KCNQ2 and KCNQ3 genes, which encode subunits of the M-type potassium channel...
- Electrophysiological properties of human adipose tissue-derived stem cellsXiaowen Bai
Department of Molecular Pathology, University of Texas, MD Anderson Cancer Center, Houston, Texas 77054, USA
Am J Physiol Cell Physiol 293:C1539-50. 2007..TTX) are present in undifferentiated hASCs and their potential physiological function in these cells as a basic understanding for future in vitro experiments and in vivo clinical investigations...
- [Potassium channelopathies and Morvan's syndromes]Georges Serratrice
Membre de l Académie nationale de médecine
Bull Acad Natl Med 194:391-406; discussion 406-7. 2010..Kv7 channel mutations (in KNQ2 and KCNQ3) are responsible for benign familial neonatal seizures...
- Idiopathic epilepsies with a monogenic mode of inheritanceO K Steinlein
Institute of Human Genetics, University of Bonn, Germany
Epilepsia 40:9-11. 1999..Two highly homologous voltage-gated potassium channels, KCNQ2 and KCNQ3, were found to be mutated in benign familial neonatal convulsions.
- Germ-line mutation of KCNQ2, p.R213W, in a Japanese family with benign familial neonatal convulsionAhmad H Sadewa
Department of Public Health, Kobe University Graduate School of Medicine, Kobe, Japan
Pediatr Int 50:167-71. 2008Benign familial neonatal convulsion (BFNC) is an autosomal-dominantly inherited epilepsy of neonates. The KCNQ2 and KCNQ3 genes have been cloned as the responsible genes for BFNC...
- Estrogen regulation of genes important for K+ channel signaling in the arcuate nucleusTroy A Roepke
Department of Physiology and Pharmacology, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239, USA
Endocrinology 148:4937-51. 2007..We found that EB significantly increased the expression of KCNQ5 and Kv4.1 and decreased expression of KCNQ3 and AKAP in the rostral arcuate. In the caudal arcuate, EB increased KCNQ5, Kir2.4, Kv4...
- In situ measurement of airway surface liquid [K+] using a ratioable K+-sensitive fluorescent dyeWan Namkung
Departments of Medicine and Physiology, University of California, San Francisco, California 94143, USA
J Biol Chem 284:15916-26. 2009..Functional and expression studies indicated the involvement of [K(+)] channels KCNQ1, KCNQ3, and KCNQ5 as determinants of ASL [K(+)]...
- The specific slow afterhyperpolarization inhibitor UCL2077 is a subtype-selective blocker of the epilepsy associated KCNQ channelsHeun Soh
Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT 06269, USA
Mol Pharmacol 78:1088-95. 2010..We found that the effect of UCL2077 on KCNQ3 is bimodal: currents are enhanced at negative membrane potentials and inhibited at positive potentials...
- Disruption of the epilepsy KCNQ2 gene results in neural hyperexcitabilityH Watanabe
Pharmaceutical Frontier Research Laboratories, Japan Tobacco, Yokohama Department of Neurology, School of Medicine, Keio University, Tokyo, Japan
J Neurochem 75:28-33. 2000..Recently, two novel voltage-dependent potassium channel genes, KCNQ2 and KCNQ3, were identified by positional cloning as being responsible for BFNC...
- Alternative splicing of KCNQ2 potassium channel transcripts contributes to the functional diversity of M-currentsZ Pan
Department of Neurobiology and Behavior and Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, NY 11794, USA
J Physiol 531:347-58. 2001..These transcripts encoded channel subunits that, when co-expressed with the KCNQ3 subunit, activated and deactivated approximately 2.5 times more slowly than other isoforms...
- Genes and mutations in idiopathic epilepsyO K Steinlein
Institute of Human Genetics, University of Bonn, Germany
Am J Med Genet 106:139-45. 2001..found in familial nocturnal frontal lobe epilepsy, while defects in the voltage-gated potassium channels KCNQ2 and KCNQ3 have recently been identified in benign familial neonatal convulsions...
- A novel KCNQ2 K+ channel mutation in benign neonatal convulsions and centrotemporal spikesG Coppola
Department of Child Neuropsychiatry, 2nd University of Naples, Italy
Neurology 61:131-4. 2003..Electrophysiologic studies showed that mutant K+ channel subunits failed to give rise to functional homomeric channels or exert dominant-negative effects when expressed with KCNQ2/KCNQ3 subunits.
- M channels containing KCNQ2 subunits modulate norepinephrine, aspartate, and GABA release from hippocampal nerve terminalsMaria Martire
Institute of Pharmacology, School of Medicine, Catholic University of Sacred Heart, 00168 Rome, Italy
J Neurosci 24:592-7. 2004..an effect that was abolished by antibody preabsorption with the KCNQ2 immunizing peptide; antibodies against KCNQ3 subunits were ineffective...
- Ionic permeation and conduction properties of neuronal KCNQ2/KCNQ3 potassium channelsDavid L Prole
Department of Pharmacology and MRC Centre for Synaptic Plasticity, University of Bristol, Bristol, United Kingdom
Biophys J 86:1454-69. 2004..subunits to the properties of heteromeric KCNQ2/3 channels was demonstrated by studying homomeric KCNQ2 and KCNQ3 channels, which displayed contrasting ionic selectivities...
- Immunohistochemical analysis of KCNQ3 potassium channels in mouse brainJulia Geiger
Department of Neurology, University of Ulm, Germany
Neurosci Lett 400:101-4. 2006..Mutations in KCNQ2/KCNQ3 channels can cause benign familial neonatal convulsions (BFNC)...
- A common ankyrin-G-based mechanism retains KCNQ and NaV channels at electrically active domains of the axonZongming Pan
Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
J Neurosci 26:2599-613. 2006..Here, antibodies against four different KCNQ2 and KCNQ3 polypeptide epitopes show these subunits concentrated at the axonal initial segment (AIS) and node of Ranvier...
- K+ M-current regulates the transition to seizures in immature and adult hippocampusCuie Qiu
Drexel University College of Medicine, 245 15th Street, Philadelphia, PA 19348, U S A
Epilepsia 48:2047-58. 2007..The nature of this window of vulnerability is unclear. We address this issue using a hippocampal slice model, to study the effects of I(M) blockade or augmentation on epileptiform activity...
- Multiple KCNQ potassium channel subtypes mediate basal anion secretion from the human airway epithelial cell line Calu-3Shasta L Moser
Department of Physiology and Biophysics, Dalhousie University, B3H 1X5, Halifax, Nova Scotia, Canada
J Membr Biol 221:153-63. 2008..that Calu-3 cells express KCNQ1, using reverse transcriptase polymerase chain reaction we determined expression of KCNQ3, KCNQ4 and KCNQ5 mRNA transcripts...
- Functional analysis of novel KCNQ2 mutations found in patients with Benign Familial Neonatal ConvulsionsLinda Volkers
Complex Genetics Section, DBG Department of Medical Genetics, University Medical Center Utrecht, The Netherlands
Neurosci Lett 462:24-9. 2009..It is linked to mutations in the potassium channel genes KCNQ2 and KCNQ3. These encode for Kv7.2 and Kv7...
- Neonatal seizures and long QT syndrome: a cardiocerebral channelopathy?Sarah E Heron
SA Pathology at Women s and Children s Hospital, North Adelaide, SA, Australia
Epilepsia 51:293-6. 2010..No mutations were found in the genes (KCNQ2, KCNQ3) associated with BFNS, and CGH was negative...
- The M-current inhibitor XE991 decreases the stimulation threshold for long-term synaptic plasticity in healthy mice and in models of cognitive diseaseAngela Fontán-Lozano
Division de Neurociencias, Universidad Pablo de Olavide de Sevilla, Carretera de Utrera Km 1, Seville, Spain
Hippocampus 21:22-32. 2011..Together, these results show that inhibition of the M-current as a general strategy may be useful to enhance cognitive capacities in healthy and aging individuals, as well as in those with neurodegenerative diseases...
- Isoform-specific prolongation of Kv7 (KCNQ) potassium channel opening mediated by new molecular determinants for drug-channel interactionsZhaobing Gao
Department of Neuroscience, High Throughput Biology Center, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21205, USA
J Biol Chem 285:28322-32. 2010Kv7 channels, especially Kv7.2 (KCNQ2) and Kv7.3 (KCNQ3), are key determinants for membrane excitability in the brain...
- KCNQ channels show conserved ethanol block and function in ethanol behaviourSonia Cavaliere
School of Physiology and Pharmacology, University of Bristol, Bristol, Avon, United Kingdom
PLoS ONE 7:e50279. 2012....
- Suppression of KCNQ/M (Kv7) potassium channels in dorsal root ganglion neurons contributes to the development of bone cancer pain in a rat modelQin Zheng
Neuroscience Research Institute and Department of Neurobiology, Peking University, Beijing, PR China
Pain 154:434-48. 2013..on intratibial injection of MRMT-1 tumour cells, we documented a prominent decrease in expression of KCNQ2 and KCNQ3 proteins and a reduction of M-current density in small-sized dorsal root ganglia (DRG) neurons, which were ..
- Bladder contractility is modulated by Kv7 channels in pig detrusorJulie Svalø
Smooth Muscle Research Center, Department of Clinical Biochemistry, Copenhagen University Hospital at Koege, Denmark
Eur J Pharmacol 715:312-20. 2013..Thus, we have shown that Kv7.4 channels are expressed and functionally active in pig detrusor, and that the use of selective Kv7.4 channel modulators in the treatment of detrusor overactivity seems promising...
- A change in configuration of the calmodulin-KCNQ channel complex underlies Ca2+-dependent modulation of KCNQ channel activityAnastasia Kosenko
Department of Pharmacology, University of California Irvine, Irvine, California, United States of America
PLoS ONE 8:e82290. 2013..In contrast, in homomeric KCNQ3 channels, calcium facilitated calmodulin binding...
- Kv7.2 regulates the function of peripheral sensory neuronsChih H King
Department of Neuroscience, The University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, 19104
J Comp Neurol 522:3262-80. 2014..Taken together, our results suggest that the loss of Kv7.2 activity increases the excitability of primary sensory neurons...
- Potassium channel genes and benign familial neonatal epilepsySnezana Maljevic
Department of Neurology and Epileptology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany Electronic address
Prog Brain Res 213:17-53. 2014..Among them, KCNQ2 and KCNQ3, coding for KV7.2 and KV7...
- Functional analysis of potassium channels in Kv7.2 G271V mutant causing early onset familial epilepsyJuanjuan Wang
Department of Neonatology, First Affiliated Hospital of Xi an Jiaotong University, No 277, Yanta West Road, Xi an, Shaanxi 710061, People s Republic of China Ion Channel Disease Laboratory, Key Laboratory of Environment and Gene Associated Diseases, Ministry of Education, Xi an Jiaotong University, No 277, Yanta West Road, Xi an, Shaanxi 710061, People s Republic of China
Brain Res 1616:112-22. 2015....
- An Ankyrin-G N-terminal Gate and Protein Kinase CK2 Dually Regulate Binding of Voltage-gated Sodium and KCNQ2/3 Potassium ChannelsMingxuan Xu
From the Molecular Neuropharmacology Laboratory, Department of Neurology
J Biol Chem 290:16619-32. 2015..Analogous "anchor" peptides within intracellular domains of vertebrate KCNQ2, KCNQ3, and Nav channel α-subunits bind Ankyrin-G (AnkG), thereby mediating concentration of those channels at AISs and ..
- Epilepsy-causing mutations in Kv7.2 C-terminus affect binding and functional modulation by calmodulinPaolo Ambrosino
Dept of Medicine and Health Sciences, University of Molise, Campobasso, Italy
Biochim Biophys Acta 1852:1856-66. 2015..2 modulation as a potential therapeutic approach for Kv7.2-related epilepsies. ..
- Novel KCNQ3 Mutation in a Large Family with Benign Familial Neonatal Epilepsy: A Rare Cause of Neonatal SeizuresSnezana Maljevic
Department of Neurology and Epileptology, Hertie Institute for Clinical Brain Research, University of Tubingen, Heidelberg, Germany The Florey Institute of Neuroscience and Mental Health, Melbourne, Vic, Australia
Mol Syndromol 7:189-196. 2016..2 and Kv7.3, encoded by KCNQ2 and KCNQ3. While most BFNS families carry alterations in KCNQ2, mutations in KCNQ3 appear to be less ..
- M-currents (Kv7.2-7.3/KCNQ2-KCNQ3) Are Responsible for Dysfunctional Autonomic Control in Hypertensive RatsTorill Berg
Division of Physiology, Department of Molecular Medicine, Institute for Basic Medical Sciences, University of Oslo Oslo, Norway
Front Physiol 7:584. 2016..Retigabine eliminated the increased bradycardia observed in reserpinized SHR. XE-991 also increased 3,4-DAP-stimulated catecholamine release, but not after hexamethonium or reserpine...
- Subthreshold changes of voltage-dependent activation of the K(V)7.2 channel in neonatal epilepsyJessica Hunter
Department of Human Genetics, Emory University, 615 Michael Street, Whitehead Building, Suite 301, Atlanta, Georgia 30322, USA
Neurobiol Dis 24:194-201. 2006..familial neonatal convulsions (BFNC) is an epileptic disorder caused by dominant mutations in the genes KCNQ2 and KCNQ3 encoding the K+ channels K(V)7.2 and K(V)7.3. We identified two novel KCNQ2 mutations in two BFNC families...
- Pharmacogenetics of new analgesicsJorn Lotsch
Pharmazentrum frankfurt ZAFES, Institute of Clinical Pharmacology, Goethe University, Frankfurt am Main, Germany
Br J Pharmacol 163:447-60. 2011..This addresses voltage-gated sodium, calcium and potassium channels, for which SCN9A, CACNA1B, KCNQ2 and KCNQ3, respectively, are primary gene candidates because they code for the subunits of the respective channels targeted ..
- [New antiepileptic drugs, and therapeutic considerations]Zoltán Szupera
Pest Megyei Flór Ferenc Kórház, Neurológiai Osztály, Kistarcsa
Ideggyogy Sz 64:329-32. 2011..However, it will take the consideration of new concepts in shaping the new therapeutic algorithm...
- Capturing distinct KCNQ2 channel resting states by metal ion bridges in the voltage-sensor domainOrit Gourgy-Hacohen
Department of Physiology and Pharmacology, Tel Aviv University, Tel Aviv 69978, Israel
J Gen Physiol 144:513-27. 2014..KCNQ2 can coassemble with the KCNQ3 subunit to mediate the IM current that regulates neuronal excitability...
- Functional and molecular evidence for Kv7 channel subtypes in human detrusor from patients with and without bladder outflow obstructionJulie Svalø
Smooth Muscle Research Center, Department of Clinical Biochemistry, Copenhagen University Hospital, Koege, Denmark Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark
PLoS ONE 10:e0117350. 2015..We found mRNA expression of KCNQ1, KCNQ3-KCNQ5 and KCNE1-5 in the human urinary bladder from patients with normal bladder function (n = 7) and in patients ..
- The Novel KV7.2/KV7.3 Channel Opener ICA-069673 Reveals Subtype-Specific Functional Roles in Guinea Pig Detrusor Smooth Muscle Excitability and ContractilityAaron Provence
Department of Drug Discovery and Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina, Columbia, South Carolina
J Pharmacol Exp Ther 354:290-301. 2015..In conclusion, using the novel KV7.2/KV7.3 channel activator ICA-069673, this study provides strong evidence for a critical role for the KV7.2- and KV7.3-containing channels in DSM function at both cellular and tissue levels. ..
- Sequence determinants of subtype-specific actions of KCNQ channel openersAlice W Wang
Department of Pharmacology, Alberta Diabetes Institute, University of Alberta, Edmonton, AB, Canada
J Physiol 595:663-676. 2017..The present study describes the marked specificity of ICA069673 for KCNQ2 vs. KCNQ3, and exploits this property to investigate determinants of KCNQ subtype specificity...
- Localization of a gene for benign adult familial myoclonic epilepsy to chromosome 8q23.3-q24.1M Mikami
Department of Neuropsychiatry, Ehime University School of Medicine, Ehime 791 0295 Japan
Am J Hum Genet 65:745-51. 1999..8q have been recognized-one on chromosome 8q13-21 (familial febrile convulsion) and two others on chromosome 8q24 (KCNQ3 and childhood absence epilepsy)-the locus assigned here is distinct from these three epilepsy-related loci...
- Molecular correlates of the M-current in cultured rat hippocampal neuronsM M Shah
Wellcome Laboratory for Molecular Pharmacology, Department of Pharmacology, University College London, Gower Street, UK
J Physiol 544:29-37. 2002..In sympathetic neurons, M-channels are thought to be composed of a heteromeric assembly of KCNQ2 and KCNQ3 K(+) channel subunits...
- Regulation of KCNQ2/KCNQ3 current by G protein cycling: the kinetics of receptor-mediated signaling by GqByung Chang Suh
Department of Physiology and Biophysics, University of Washington School of Medicine, G 424 Health Sciences Building, Box 357290, Seattle, WA 98195 7290, USA
J Gen Physiol 123:663-83. 2004..the kinetics and mechanism of M1 muscarinic receptor-mediated regulation of the cloned neuronal M channel, KCNQ2/KCNQ3 (Kv7.2/Kv7.3)...
- Recent developments on KCNQ potassium channel openersYong Jin Wua
Department of Neuroscience Chemistry, Bristol Myers Squibb Pharmaceutical Research Institute, 5 Research Parkway, Wallingford, Connecticut 06492, USA
Curr Med Chem 12:453-60. 2005..Within the KCNQ family, the combination of the KCNQ2/KCNQ3 proteins, and the KCNQ5/KCNQ3 arrangement has been identified as the molecular correlates of the different M-..
- An M-like potassium current in the guinea pig cochleaGuihua Liang
Center for Hearing and Communication Research and Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
ORL J Otorhinolaryngol Relat Spec 67:75-82. 2005..Results from RT-PCR analysis indicated that genes encoding M channel subunits KCNQ2 and KCNQ3 are expressed in the guinea pig cochlea...
- [3H]linopirdine binding to rat brain membranes is not relevant for M-channel interactionChristian Wolff
Deparment of in vitro Pharmacology, UCB SA, CNS Preclinical Research, Chemin du Foriest R4, 1420 Braine L Alleud, Belgium
Eur J Pharmacol 518:10-7. 2005..molecule and demonstrated to specifically block the potassium current generated by the brain specific KCNQ2-KCNQ3 proteins (M-channel)...
- [Advances in the studies on the molecular and genetic aspects of epilepsy]Xu Wang
Center for Human Genome Research, Huazhong University of Science and Technology, Wuhan 430074, China
Zhongguo Yi Xue Ke Xue Yuan Xue Bao 27:388-93. 2005..The majority of the genes encode ion channels, including voltage-gated potassium channels KCNQ2 and KCNQ3, sodium channels SCN1A, SCN2A, and SCN1B, chloride channels CLCN2, and ligand-gated ion channels CHRNA4, CHRNB2, ..
- Cholinergic suppression of KCNQ channel currents enhances excitability of striatal medium spiny neuronsWeixing Shen
Department of Physiology, Institute for Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
J Neurosci 25:7449-58. 2005..Single-cell reverse transcriptase-PCR confirmed the expression of KCNQ2, KCNQ3, and KCNQ5 mRNAs in medium spiny neurons...
- Neutralization of a negative charge in the S1-S2 region of the KV7.2 (KCNQ2) channel affects voltage-dependent activation in neonatal epilepsyThomas V Wuttke
Neurological Clinic, University of Ulm, Germany
J Physiol 586:545-55. 2008The voltage-gated potassium channels KV7.2 and KV7.3 (genes KCNQ2 and KCNQ3) constitute a major component of the M-current controlling the firing rate in many neurons...
- A schizophrenia-linked mutation in PIP5K2A fails to activate neuronal M channelsOlga Fedorenko
Department of Physiology, University of Tuebingen, Gmelinstr 5, 72076, Tuebingen, Germany
Psychopharmacology (Berl) 199:47-54. 2008..Activation of KCNQ accordingly attenuates the central stimulating effects of dopamine, cocaine, methylphenidate, and phenylcyclidine...
- Advances on the genetics of Mendelian idiopathic epilepsiesStephanie Baulac
CRICM UPMC Paris6 UMR S975 Inserm U975 CNRS UMR 7225, F 75013, Bâtiment Pharmacie, Hôpital de Pitié Salpêtrière, 47 Boulevard de l Hopital, 75013 Paris, France
Clin Lab Med 30:911-29. 2010..strategies in multigenerational families with autosomal dominant transmission have revealed 11 genes (KCNQ2, KCNQ3, CHRNA4, CHRNA2, CHRNB2, SCN1B, SCN1A, SCN2A, GABRG2, GABRA1, and LGI1) and numerous loci for febrile seizures and ..
- Potential role of KCNQ/M-channels in regulating neuronal differentiation in mouse hippocampal and embryonic stem cell-derived neuronal culturesXin Zhou
Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA
Exp Neurol 229:471-83. 2011..It is composed of the molecular counterparts KCNQ2 and KCNQ3 (also named Kv7.2 and Kv7.3) channels and expressed in the soma and dendrites of neurons...
- Benign neonatal sleep myoclonus: an autosomal dominant form not allelic to KCNQ2 or KCNQ3Zaid Afawi
Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel
J Child Neurol 27:1260-3. 2012..We used microsatellite markers to determine if the disorder was possibly linked to KCNQ2 or KCNQ3, the 2 genes that cause most cases of benign familial neonatal seizures, a disorder that it could be easily ..
- Distinct subunit contributions to the activation of M-type potassium channels by PI(4,5)P2Vsevolod Telezhkin
Department of Neuroscience, Physiology, and Pharmacology, University College London, London, WC1E 6BT, England, UK
J Gen Physiol 140:41-53. 2012..3 and Kv7.2 subunits, respectively, that channels can open when only the two Kv7.3 subunits have bound DiC(8)-PI(4,5)P(2), and that maximum channel opening requires binding to all four subunits...
- Oral mexiletine for lidocaine-responsive neonatal epilepsyMika Nakazawa
Department of Pediatrics, Juntendo University Faculty of Medicine, Japan Department of Pediatrics, Juntendo Nerima Hospital, Japan
Brain Dev 35:667-9. 2013..No mutation was identified in any of four genes: SCN1A, SCN1B, KCNQ2, and KCNQ3. Our patient demonstrates that oral mexiletine can be useful for long-term treatment of patients with lidocaine-..
- Expression of voltage-dependent potassium channels in first trimester human placentaeH D Mistry
Division of Women s Health, King s College London, Women s Health Academic Centre, KHP, St Thomas Hospital, Westminster Bridge Road, London SE1 7EH, UK Department of Nephrology, Hypertension, Clinical Pharmacology and of Clinical Research, University of Bern, Berne CH 3010, Switzerland Electronic address
Placenta 35:337-40. 2014..The aim was to determine KCNQ and KCNE mRNA expression and assess protein expression/localisation of the KCNQ3 and KCNE5 isoforms in first trimester placental tissue...
- KCNQ5 K(+) channels control hippocampal synaptic inhibition and fast network oscillationsPawel Fidzinski
1 Leibniz Institut für Molekulare Pharmakologie FMP, Robert Rössle Street 10, Berlin 13125, Germany 2 Max Delbrück Centrum für Molekulare Medizin MDC, Robert Rössle Street 10, Berlin 13125, Germany 3 Klinik für Neurologie, Charite Universitatsmedizin, Chariteplatz 1, Berlin 10117, Germany
Nat Commun 6:6254. 2015KCNQ2 (Kv7.2) and KCNQ3 (Kv7.3) K(+) channels dampen neuronal excitability and their functional impairment may lead to epilepsy. Less is known about KCNQ5 (Kv7.5), which also displays wide expression in the brain...
- Regulation of the neuronal KCNQ2 channel by Src--a dual rearrangement of the cytosolic termini underlies bidirectional regulation of gatingSivan Siloni
Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel
J Cell Sci 128:3489-501. 2015Neuronal M-type K(+) channels are heteromers of KCNQ2 and KCNQ3 subunits, and are found in cell bodies, dendrites and the axon initial segment, regulating the firing properties of neurons...
- Activation of m1 muscarinic acetylcholine receptor induces surface transport of KCNQ channels through a CRMP-2-mediated pathwayLing Jiang
State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, and Beijing Key Laboratory of Tumor Systems Biology, Peking University, Beijing 100191, China Department of Pharmacology, University of California, Irvine, 360 Med Surge II, Irvine, CA 92617, USA
J Cell Sci 128:4235-45. 2015..This receptor-induced surface transport was observed with KCNQ2 as well as KCNQ3 homomeric channels, but not with Kv3.1 channels...
- Noise-induced hearing loss: Neuropathic pain via Ntrk1 signalingSenthilvelan Manohar
Center for Hearing and Deafness, State University of New York at Buffalo, Buffalo, NY 14214, United States Electronic address
Mol Cell Neurosci 75:101-12. 2016..array, noise exposure upregulated mRNA expression levels of four pain/inflammatory genes, Tlr2, Oprd1, Kcnq3 and Ntrk1 and decreased mRNA expression levels of two more genes, Ccl12 and Il1β...
- Early-onset epileptic encephalopathy caused by a reduced sensitivity of Kv7.2 potassium channels to phosphatidylinositol 4,5-bisphosphateMaria Virginia Soldovieri
Department of Medicine and Health Sciences, University of Molise, Campobasso, Italy
Sci Rep 6:38167. 2016..2-EE in individuals carrying the R325G variant, further expanding the range of pathogenetic mechanisms exploitable for personalized treatment of Kv7.2-related epilepsies...
- Activation of a PTX-insensitive G protein is involved in histamine-induced recombinant M-channel modulationJuan Guo
Department of Physiology, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112, USA
J Physiol 545:767-81. 2002..The channels underlying I(M) are produced by the coassembly of KCNQ2 and KCNQ3 channel subunits and can be expressed in heterologous systems where they can be modulated by several ..
- Subunit-specific modulation of KCNQ potassium channels by Src tyrosine kinaseNikita Gamper
Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, USA
J Neurosci 23:84-95. 2003..Using whole-cell patch clamp, we found that Src modulates currents from KCNQ3, KCNQ4, and KCNQ5 homomultimers, KCNQ2/3 heteromultimers and native M current, but not currents from KCNQ1 or ..
- ANASTASIOS TZINGOUNIS; Fiscal Year: 2015..progressive hearing loss (Kcnq4) and benign familial neonatal convulsions (BFNC), a pediatric epilepsy (Kcnq2, Kcnq3)...
- Edward C Cooper; Fiscal Year: 2016DESCRIPTION (provided by applicant): Mutations in KCNQ2 or KCNQ3 cause benign familial neonatal seizures (BFNS), a dominantly-inherited, highly penetrant early-onset epilepsy syndrome...
- Developmental regulation of K+ M-current in brainMELANIE TALLENT; Fiscal Year: 2007..KCNQ subtypes of K+ channels have been shown to underlie IM; in the brain KCNQ2/KCNQ3 and KCNQ3/KCNQ5 heterotetramers appear to make up native M-channels...
- SONYA MARIE BIERBOWER; Fiscal Year: 2014..Additionally, dominant- negative KCNQ3 knock-in mice will be used in both models to confirm a specific M-channel mechanism...
- Axonal alterations in demyelinating diseasesSTEVEN SIMON SCHERER; Fiscal Year: 2011We hypothesize that in normal myelinated PNS axons, the combination of Kv1.1, Kv1.2, KCNQ2, and KCNQ3 is necessary for repolarization, and that the misexpression of Kv3...
- CARDIOVASCULAR ROLE OF SYMPATHETIC K+ CHANNEL GENESPeter Brink; Fiscal Year: 2003..These investigators have recently determined that the M-current is encoded by the KCNQ2 and KCNQ3 genes...
- SIGNALING BY VASOPRESSIN--ARTERIAL SMOOTH MUSCLE CELLSKENNETH BYRON; Fiscal Year: 2002..Finally, the effects of AVP and other hormones on [Ca2+]i and membrane currents will be examined in freshly isolated smooth muscle cells from rat mesenteric arteries. ..
- Calcium entry and vascular smooth muscle excitationKENNETH BYRON; Fiscal Year: 2006..abstract_text> ..
- ELECTRIC STUDIES OF EXCITATION, SECRETION & CONTRACTIONBertil Hille; Fiscal Year: 2007..What are the Ca 2+ buffering and flux properties of these organelles? Our work in these cells concerns processes whose failure leads to disease and whose modulation offers new therapies. ..
- Proteomic Dissection of M-channel PhosphorylationEdward Cooper; Fiscal Year: 2003....
- Molecular Biology of Calcuim Channel Gamma SubunitsDaniel Burgess; Fiscal Year: 2006....
- KCNQ channel opener efficacy for neonatal seizuresEdward Cooper; Fiscal Year: 2007..Such in vivo preclinical experiments are an essential next step toward our overall goal toward introduction of more effective treatments for neonatal seizures in humans. [unreadable] [unreadable] [unreadable]..
- Gene detection in regions linked to Alzheimer's diseaseDimitrios Avramopoulos; Fiscal Year: 2009..abstract_text> ..