Evidence map›Paper›PMID 24042502›Full record

ArticleThe Journal of physiology2013

Oxygen and mitochondrial inhibitors modulate both monomeric and heteromeric TASK-1 and TASK-3 channels in mouse carotid body type-1 cells.

Philip J Turner, Keith J Buckler

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 70 citations in OpenAlex.

  1. Acute Hypoxia Inhibits KActa physiologica (Oxford, England) · 2026
    Article
  2. Article
  3. Navigating Central Oxytocin Transport: Known Realms and Uncharted Territories.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025
    Review
  4. TASK inhibition by mild acidosis increases CaAmerican journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  5. Article
  6. Article
  7. Could respiration-driven blood oxygen changes modulate neural activity?Pflugers Archiv : European journal of physiology · 2023
    Review
  8. Neurovascular coupling: motive unknown.Trends in neurosciences · 2022
    Review
  9. Acute Oxygen-SensingFrontiers in physiology · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Expression of p11 and Heteromeric TASK Channels in Rat Carotid Body Glomus Cells and Nerve Growth Factor-differentiated PC12 Cells.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020
    Article
  17. TASK-3: New Target for Pain-Relief.Neuroscience bulletin · 2020
    Article
  18. TASK channels: channelopathies, trafficking, and receptor-mediated inhibition.Pflugers Archiv : European journal of physiology · 2020
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Philip J TurnerK. J. Buckler: Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX1 3PT, UK. keith.buckler@dpag.ox.ac.uk.
Keith J Buckler
University of Oxford · GB

Funding

British Heart Foundation PG/08/086/25849Medical Research Council G1001134Medical Research Council G101134
6 · The paper itself

Abstract

In rat arterial chemoreceptors, background potassium channels play an important role in maintaining resting membrane potential and promoting depolarization and excitation in response to hypoxia or acidosis. It has been suggested that these channels are a heterodimer of TASK-1 and TASK-3 based on their similarity to heterologously expressed TASK-1/3 fusion proteins. In this study, we sought to confirm the identity of these channels through germline ablation of Task-1 (Kcnk3) and Task-3 (Kcnk9) in mice. Background K-channels were abundant in carotid body type-1 cells from wild-type mice and comparable to those previously described in rat type-1 cells with a main conductance state of 33 pS. This channel was absent from both Task-1(-/-) and Task-3(-/-) cells. In its place we observed a larger (38 pS) K(+)-channel in Task-1(-/-) cells and a smaller (18 pS) K(+)-channel in Task-3(-/-) cells. None of these channels were observed in Task-1(-/-)/Task-3(-/-) double knock-out mice. We therefore conclude that the predominant background K-channel in wild-type mice is a TASK-1/TASK-3 heterodimer, whereas that in Task-1(-/-) mice is TASK-3 and, conversely, that in Task-3(-/-) mice is TASK-1. All three forms of TASK channel in type-1 cells were inhibited by hypoxia, cyanide and the uncoupler FCCP, but the greatest sensitivity was seen in TASK-1 and TASK-1/TASK-3 channels. In summary, the background K-channel in type-1 cells is predominantly a TASK-1/TASK-3 heterodimer. Although both TASK-1 and TASK-3 are able to couple to the oxygen and metabolism sensing pathways present in type-1 cells, channels containing TASK-1 appear to be more sensitive.

Indexed as

AnimalsCalciumCalcium SignalingCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneCarotid BodyMiceMice, KnockoutMitochondriaNerve Tissue ProteinsOxygenPotassium ChannelsPotassium Channels, Tandem Pore DomainRotenoneSodium CyanideCalciumCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneNerve Tissue ProteinsOxygenPotassium ChannelsPotassium Channels, Tandem Pore Domainpotassium channel subfamily K member 3RotenoneSodium CyanideTASK3 protein, mouse

Identifiers

PMID24042502
PMCPMC3872765
OpenAlexW1565867188

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.