ArticleBiophysical journal2016
The Voltage Activation of Cortical KCNQ Channels Depends on Global PIP2 Levels.
Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Intellectual Disability and Potassium Channelopathies: A Systematic Review.Frontiers in genetics · 2020Pooled it
- Therapeutic potential of small molecules that block receptor-induced Kv7/M-current suppression in neuroprotection, seizures, and pain.British journal of pharmacology · 2026Article
- Mislocalization of KCNQ2 Channels as a Pathogenic Mechanism in KCNQ2 Developmental and Epileptic Encephalopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Role of Glycerophospholipid Metabolism in Epilepsy.Current neuropharmacology · 2026Review
- Endoplasmic Reticulum and Mitochondrial Calcium Handling Dynamically Shape Slow Afterhyperpolarizations in Vasopressin Magnocellular Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Dehydroepiandrosterone Sulfate (DHEAS) Is an Endogenous Kv7 Channel Modulator That Reduces Kv7/M-Current Suppression and Inflammatory Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- KCNQ2/3 Gain-of-Function Variants and Cell Excitability: Differential Effects in CA1 versus L2/3 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Gain of function due to increased opening probability by twoProceedings of the National Academy of Sciences of the United States of America · 2022Article
- KCNQ2 and KCNQ5 form heteromeric channels independent of KCNQ3.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Dishevelled coordinates phosphoinositide kinases PI4KIIIα and PIP5KIγ for efficient PtdInsP2 synthesis.Journal of cell science · 2022Article
- PIPCommunications biology · 2021Article
- Er81 Transcription Factor Fine-Tunes Striatal Cholinergic Interneuron Activity and Drives Habit Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Chemical modulation of Kv7 potassium channels.RSC medicinal chemistry · 2021Review
- KCNQ3 is the principal target of retigabine in CA1 and subicular excitatory neurons.Journal of neurophysiology · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- PIPProceedings of the National Academy of Sciences of the United States of America · 2020Review
- Epileptic channelopathies caused by neuronal Kv7 (KCNQ) channel dysfunction.Pflugers Archiv : European journal of physiology · 2020Review
- Identifying mutation hotspots reveals pathogenetic mechanisms of KCNQ2 epileptic encephalopathy.Scientific reports · 2020Article
- TwoFrontiers in physiology · 2020Article
- A Novel Kv7.3 Variant in the Voltage-Sensing SFrontiers in physiology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The slow afterhyperpolarization (sAHP) is a calcium-activated potassium conductance with critical roles in multiple physiological processes. Pharmacological and genetic data suggest that KCNQ channels partly mediate the sAHP. However, these channels are not typically open within the observed voltage range of the sAHP. Recent work has shown that the sAHP is gated by increased PIP2 levels, which are generated downstream of calcium binding by neuronal calcium sensors such as hippocalcin. Here, we examined whether changes in PIP2 levels could shift the voltage-activation range of KCNQ channels. In HEK293T cells, expression of the PIP5 kinase PIPKIγ90, which increases global PIP2 levels, shifted the KCNQ voltage activation to within the operating range of the sAHP. Further, the sensitivity of this effect on KCNQ3 channels appeared to be higher than that on KCNQ2. Therefore, we predict that KCNQ3 plays an essential role in maintaining the sAHP under low PIP2 conditions. In support of this notion, we find that sAHP inhibition by muscarinic receptors that increase phosphoinositide turnover in neurons is enhanced in Kcnq3-knockout mice. Likewise, the presence of KCNQ3 is essential for maintaining the sAHP when hippocalcin is ablated, a condition that likely impairs PIP2 generation. Together, our results establish the relationship between PIP2 and the voltage dependence of cortical KCNQ channels (KCNQ2/3, KCNQ3/5, and KCNQ5), and suggest a possible mechanism for the involvement of KCNQ channels in the sAHP.
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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.