ReviewPflugers Archiv : European journal of physiology2015
Properties, regulation, pharmacology, and functions of the K₂p channel, TRESK.
Review in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 41 citations in OpenAlex.
- The cornea-trigeminal axis: potassium channels as master regulators of ocular surface homeostasis and sensory transduction.Frontiers in cell and developmental biology · 2026Review
- Migraine is a dysfunction of neuronal potassium ion channels.Frontiers in neurology · 2025Review
- A cellular atlas of calcineurin signaling.Biochimica et biophysica acta. Molecular cell research · 2023Review
- Two-Pore-Domain Potassium (KCells · 2021Review
- Contribution of K2P Potassium Channels to Cardiac Physiology and Pathophysiology.International journal of molecular sciences · 2021Review
- Article
- The Polysite Pharmacology of TREK KAdvances in experimental medicine and biology · 2021Article
- The Pharmacology of Two-Pore Domain Potassium Channels.Handbook of experimental pharmacology · 2021Article
- Ion Channel Dysfunction and Neuroinflammation in Migraine and Depression.Frontiers in pharmacology · 2021Review
- The Background KInternational journal of molecular sciences · 2020Review
- Altered functional properties of a missense variant in the TRESK KPflugers Archiv : European journal of physiology · 2020Article
- Advances in genetics of migraine.The journal of headache and pain · 2019Review
- Glial CaeLife · 2019Article
- Spilanthol Enhances Sensitivity to Sodium in Mouse Taste Bud Cells.Chemical senses · 2019Article
- Regulatory Effect of General Anesthetics on Activity of Potassium Channels.Neuroscience bulletin · 2018Review
- Ion channelopathies and migraine pathogenesis.Molecular genetics and genomics : MGG · 2017Review
- Selective and state-dependent activation of TRESK (KBritish journal of pharmacology · 2017Article
- Phosphatidylinositol (4,5)-bisphosphate dynamically regulates the KScientific reports · 2017Article
- Isoflurane Preconditioning Induces Neuroprotection by Up-Regulation of TREK1 in a Rat Model of Spinal Cord Ischemic Injury.Biomolecules & therapeutics · 2016Article
- Effects of analgesics and antidepressants on TREK-2 and TRESK currents.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TWIK-related spinal cord K(+) channel (TRESK) is the gene product of KCNK18, the last discovered leak potassium K2P channel gene. Under resting conditions, TRESK is constitutively phosphorylated at two regulatory regions. Protein kinase A (PKA) and microtubule affinity-regulating (MARK) kinases can be applied in experiments to phosphorylate these sites of TRESK expressed in Xenopus oocytes, respectively. Upon generation of a calcium signal, TRESK is dephosphorylated and thereby activated by calcineurin. In this process, the binding of calcineurin to the channel by non-catalytic interacting sites is essential. The phosphorylation/dephosphorylation regulatory process is modified by 14-3-3 proteins. Human, but not murine TRESK is also activated by protein kinase C. TRESK is expressed most abundantly in sensory neurons of the dorsal root ganglia (DRG) and trigeminal ganglia, and the channel modifies certain forms of nociceptive afferentation. In a large pedigree, a dominant negative mutant TRESK allele was found to co-segregate perfectly with migraine phenotype. While this genetic defect may be responsible only for a very small fraction of migraine cases, specific TRESK activation is expected to exert beneficial effect in common forms of the disease.
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.