ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Transcriptional control of KCNQ channel genes and the regulation of neuronal excitability.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 93 citations in OpenAlex.
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- Voltage-Gated Ion Channels in Neuropathic Pain Signaling.Life (Basel, Switzerland) · 2025Review
- Hydrogen Peroxide-Induced Re-Expression of Repressor Element 1-Silencing Transcription Factor Contributes to Cardiac Vagal Dysfunction in Type 2 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2025Article
- Functional diversities within neurons and astrocytes in the adult rat auditory cortex revealed by single-nucleus RNA sequencing.Scientific reports · 2024Article
- Cellular and Molecular Mechanisms Underlying Altered Excitability of Cardiac Efferent Neurons in Cirrhotic Rats.Biomedicines · 2024Article
- TET1 Participates in Complete Freund's Adjuvant-induced Trigeminal Inflammatory Pain by Regulating Kv7.2 in a Mouse Model.Neuroscience bulletin · 2024Article
- Selective KCNQ2/3 Potassium Channel Opener ICA-069673 Inhibits Excitability in Mouse Vagal Sensory Neurons.The Journal of pharmacology and experimental therapeutics · 2024Article
- The Epigenetics of Neuropathic Pain: A Systematic Update.International journal of molecular sciences · 2023Review
- Corticotropin-releasing hormone neurons in the central nucleus of amygdala are required for chronic stress-induced hypertension.Cardiovascular research · 2023Article
- Repressor element 1-silencing transcription factor deficiency yields profound hearing loss through KeLife · 2022Article
- Modelling the Human Blood-Brain Barrier in Huntington Disease.International journal of molecular sciences · 2022Article
- Hyperexcitable arousal circuits drive sleep instability during aging.Science (New York, N.Y.) · 2022Article
- The functions of repressor element 1-silencing transcription factor in models of epileptogenesis and post-ischemia.Metabolic brain disease · 2021Review
- Epigenetics Involvement in Oxaliplatin-Induced Potassium Channel Transcriptional Downregulation and Hypersensitivity.Molecular neurobiology · 2021Article
- Peripheral Voltage-Gated Cation Channels in Neuropathic Pain and Their Potential as Therapeutic Targets.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021Article
- Prevention of brain damage after traumatic brain injury by pharmacological enhancement of KCNQ (Kv7, "M-type") KJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Functional responses of the hippocampus to hyperexcitability depend on directed, neuron-specific KCNQ2 KHippocampus · 2020Article
- Inhibition of M/KFrontiers in molecular neuroscience · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Regulation of the resting membrane potential and the repolarization of neurons are important in regulating neuronal excitability. The potassium channel subunits Kv7.2 and Kv7.3 play a key role in stabilizing neuronal activity. Mutations in KCNQ2 and KCNQ3, the genes encoding Kv7.2 and Kv7.3, cause a neonatal form of epilepsy, and activators of these channels have been identified as novel antiepileptics and analgesics. Despite the observations that regulation of these subunits has profound effects on neuronal function, almost nothing is known about the mechanisms responsible for controlling appropriate expression levels. Here we identify two mechanisms responsible for regulating KCNQ2 and KCNQ3 mRNA levels. We show that the transcription factor Sp1 activates expression of both KCNQ2 and KCNQ3, whereas the transcriptional repressor REST (repressor element 1-silencing transcription factor) represses expression of both of these genes. Furthermore, we show that transcriptional regulation of KCNQ genes is mirrored by the correlated changes in M-current density and excitability of native sensory neurons. We propose that these mechanisms are important in the control of excitability of neurons and may have implications in seizure activity and pain.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.