Evidence map›Paper›PMID 23377568›Full record

ArticlePflugers Archiv : European journal of physiology2013

Nerve growth factor-induced endocytosis of TWIK-related acid-sensitive K⁺ 1 channels in adrenal medullary cells and PC12 cells.

Hidetada Matsuoka, Keita Harada, Jun Nakamura, Masumi Inoue

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Dynamic regulation of TASK-1 channels under cellular stress.The journal of physiological sciences : JPS · 2026
    Article
  2. Article
  3. Insights of Endocytosis Signaling in Health and Disease.International journal of molecular sciences · 2023
    Review
  4. 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
  5. Review
  6. TASK channels: channelopathies, trafficking, and receptor-mediated inhibition.Pflugers Archiv : European journal of physiology · 2020
    Review
  7. Review
  8. Molecular mechanism for muscarinic MThe Journal of physiology · 2017
    Article
  9. Review
  10. Article
  11. 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

4 authors at 1 institution in 1 country.

Hidetada MatsuokaDepartment of Cell and Systems Physiology, University of Occupational and Environmental Health School of Medicine, Kitakyushu 807-8555, Japan.
Keita Harada
Jun Nakamura
Masumi Inoue
University of Occupational and Environmental Health Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TWIK-related acid-sensitive K(+) (TASK) channels belong to a family of two-pore domain K(+) channels which produce background K(+) currents and are involved in important physiological functions, such as acidosis detection. We have recently elucidated that TASK1-like channels function as a sensor of acidosis in rat adrenal medullary (AM) cells and thus are indispensable for the endocrine function of AM cells. Here, using pharmacological, electrophysiological and biochemical methods, we studied how the expression and localisation of TASK1 channels are regulated in rat AM cells and PC12 cells. PC12 cells were found to express not only TASK1 but also TASK3 channels, and they did not constitute a heterodimer. The exposure of AM cells and PC12 cells to nerve growth factor (NGF) induced endocytosis of TASK1, but not TASK3 channels, in a clathrin-dependent manner. Mutation analysis of the TASK1 channel revealed that the dileucine motif (LL263/264) was involved in at least part of the endocytosis. Plating GFP-TASK1-expressing PC12 cells onto a sheet of fibroblasts, which produced NGF, resulted in the endocytosis of GFP-TASK1 channels. Additionally, the expression of TASK1 channels at the protein and mRNA levels was suppressed in PC12 cells treated with NGF for 2 weeks. These results indicate that NGF suppresses the expression of TASK1 channels in the plasma membrane via not only endocytosis but also the inhibition of gene transcription. Thus, no access to NGF may play a major role for the maintenance of TASK1 channels in the cell membrane in AM cells.

Indexed as

Adrenal MedullaAmino Acid MotifsAnimalsClathrin-Coated VesiclesEndocrine CellsEndocytosisMaleMutationNerve Growth FactorNerve Tissue ProteinsNeuronsPC12 CellsPotassium Channels, Tandem Pore DomainProtein TransportRatsRats, WistarKcnk9 protein, ratNerve Growth FactorNerve Tissue ProteinsPotassium Channels, Tandem Pore Domainpotassium channel subfamily K member 3

Identifiers

PMID23377568
OpenAlexW2042809871

What OpenQuestion holds

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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.