ArticleCurrent neuropharmacology2010
Trafficking of neuronal two pore domain potassium channels.
Article in Current neuropharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Insights into the structure and modulation of human TWIK-2.Nature communications · 2026Article
- Thalamocortical feedback selectively controls pyramidal neuron excitability.Nature communications · 2025Article
- A 5' UTR GGN repeat controls localisation and translation of a potassium leak channel mRNA through G-quadruplex formation.Nucleic acids research · 2020Article
- Tandem pore TWIK-related potassium channels and neuroprotection.Neural regeneration research · 2019Review
- Characterization and regulation of wild-type and mutant TASK-1 two pore domain potassium channels indicated in pulmonary arterial hypertension.The Journal of physiology · 2019Article
- Bunyavirus requirement for endosomal K+ reveals new roles of cellular ion channels during infection.PLoS pathogens · 2018Article
- The C-terminal domain of Kv1.3 regulates functional interactions with the KCNE4 subunit.Journal of cell science · 2016Article
- Endocytosis as a mode to regulate functional expression of two-pore domain potassium (K₂p) channels.Pflugers Archiv : European journal of physiology · 2015Review
- K₂p channels in plants and animals.Pflugers Archiv : European journal of physiology · 2015Review
- Cell-type specific expression of p11 controls cocaine reward.Biological psychiatry · 2014Article
- Cooperative endocytosis of the endosomal SNARE protein syntaxin-8 and the potassium channel TASK-1.Molecular biology of the cell · 2014Article
- Dynamic regulation of β1 subunit trafficking controls vascular contractility.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- TREK2 expressed selectively in IB4-binding C-fiber nociceptors hyperpolarizes their membrane potentials and limits spontaneous pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Article
- Silencing of the tandem pore domain halothane-inhibited K+ channel 2 (THIK2) relies on combined intracellular retention and low intrinsic activity at the plasma membrane.The Journal of biological chemistry · 2013Article
- N-glycosylation-dependent control of functional expression of background potassium channels K2P3.1 and K2P9.1.The Journal of biological chemistry · 2013Article
- 14-3-3s are potential biomarkers for HIV-related neurodegeneration.Journal of neurovirology · 2012Review
- Leak K⁺ channel mRNAs in dorsal root ganglia: relation to inflammation and spontaneous pain behaviour.Molecular and cellular neurosciences · 2012Article
- Molecular regulations governing TREK and TRAAK channel functions.Channels (Austin, Tex.)Review
- Acid sensitive background potassium channels K2P3.1 and K2P9.1 undergo rapid dynamin-dependent endocytosis.Channels (Austin, Tex.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activity of two pore domain potassium (K2P) channels regulates neuronal excitability and cell firing. Post-translational regulation of K2P channel trafficking to the membrane controls the number of functional channels at the neuronal membrane affecting the functional properties of neurons. In this review, we describe the general features of K channel trafficking from the endoplasmic reticulum (ER) to the plasma membrane via the Golgi apparatus then focus on established regulatory mechanisms for K2P channel trafficking. We describe the regulation of trafficking of TASK channels from the ER or their retention within the ER and consider the competing hypotheses for the roles of the chaperone proteins 14-3-3, COP1 and p11 in these processes and where these proteins bind to TASK channels. We also describe the localisation of TREK channels to particular regions of the neuronal membrane and the involvement of the TREK channel binding partners AKAP150 and Mtap2 in this localisation. We describe the roles of other K2P channel binding partners including Arf6, EFA6 and SUMO for TWIK1 channels and Vpu for TASK1 channels. Finally, we consider the potential importance of K2P channel trafficking in a number of disease states such as neuropathic pain and cancer and the protection of neurons from ischemic damage. We suggest that a better understanding of the mechanisms and regulations that underpin the trafficking of K2P channels to the plasma membrane and to localised regions therein may considerably enhance the probability of future therapeutic advances in these areas.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.