ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Mtap2 is a constituent of the protein network that regulates twik-related K+ channel expression and trafficking.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 62 citations in OpenAlex.
- The research progress into cellular mechanosensitive ion channels mediating cancer pain.Channels (Austin, Tex.) · 2025Review
- The potassium channel KNature communications · 2025Article
- Thermosensitivity of TREK K2P channels is controlled by a PKA switch and depends on the microtubular network.Pflugers Archiv : European journal of physiology · 2025Article
- Review
- Sortilin-Mediated Inhibition of TREK1/2 Channels in Primary Sensory Neurons Promotes Prediabetic Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Epigenetics Involvement in Oxaliplatin-Induced Potassium Channel Transcriptional Downregulation and Hypersensitivity.Molecular neurobiology · 2021Article
- Pressure-dependent modulation of inward-rectifying KAmerican journal of physiology. Cell physiology · 2019Article
- Role of TREK-1 in Health and Disease, Focus on the Central Nervous System.Frontiers in pharmacology · 2019Review
- Antagonistic Effect of a Cytoplasmic Domain on the Basal Activity of Polymodal Potassium Channels.Frontiers in molecular neuroscience · 2018Article
- Involvement of intracellular transport in TREK-1c current run-up in 293T cells.Channels (Austin, Tex.) · 2017Article
- Two-pore Domain Potassium Channels in Astrocytes.Experimental neurobiology · 2016Review
- Heterodimerization within the TREK channel subfamily produces a diverse family of highly regulated potassium channels.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The Popeye domain containing protein family--A novel class of cAMP effectors with important functions in multiple tissues.Progress in biophysics and molecular biology · 2016Review
- Genetic Deletion of TREK-1 or TWIK-1/TREK-1 Potassium Channels does not Alter the Basic Electrophysiological Properties of Mature Hippocampal Astrocytes In Situ.Frontiers in cellular neuroscience · 2016Article
- Alternatively Spliced Human TREK-1 Variants Alter TREK-1 Channel Function and Localization.Biology of reproduction · 2015Article
- The family of K2P channels: salient structural and functional properties.The Journal of physiology · 2015Review
- Much more than a leak: structure and function of K₂p-channels.Pflugers Archiv : European journal of physiology · 2015Review
- Endocytosis as a mode to regulate functional expression of two-pore domain potassium (K₂p) channels.Pflugers Archiv : European journal of physiology · 2015Review
- Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept.British journal of pharmacology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Twik-related K+ (TREK) channels produce background currents that regulate cell excitability. In vivo, TREK-1 is involved in neuronal processes including neuroprotection against ischemia, general anesthesia, pain perception, and mood. Recently, we demonstrated that A-kinase anchoring protein AKAP150 binds to a major regulatory domain of TREK-1, promoting drastic changes in channel regulation by polyunsaturated fatty acids, pH, and stretch, and by G-protein-coupled receptors to neurotransmitters and hormones. Here, we show that the microtubule-associated protein Mtap2 is another constituent of native TREK channels in the brain. Mtap2 binding to TREK-1 and TREK-2 does not affect directly channel properties but enhances channel surface expression and current density. This effect relies on Mtap2 binding to microtubules. Mtap2 and AKAP150 interacting sites in TREK-1 are distinct and both proteins can dock simultaneously. Their effects on TREK-1 surface expression and activation are cumulative. In neurons, the three proteins are simultaneously detected in postsynaptic dense bodies. AKAP150 and Mtap2 put TREK channels at the center of a complex protein network that finely tunes channel trafficking, addressing, and regulation.
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.