Evidence map›Paper›PMID 24597762›Full record

ArticleThe Biochemical journal2014

GDF15 regulates Kv2.1-mediated outward K+ current through the Akt/mTOR signalling pathway in rat cerebellar granule cells.

Chang-Ying Wang, An-Qi Huang, Meng-Hua Zhou, Yan-Ai Mei

Open access · hybridAbstract read
In one paragraph

Article in The Biochemical journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. GDF-15 in Pulmonary and Critical Care Medicine.American journal of respiratory cell and molecular biology · 2019
    Article
  11. GDF15 and Growth Control.Frontiers in physiology · 2018
    Review
  12. Article
  13. Chronic CaThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. 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 2 institutions in 1 country.

Chang-Ying Wang*State Key Laboratory of Medical Neurobiology, School of Life Sciences and Institutes of Brain Science, Fudan University, Shanghai 200433, China.
An-Qi Huang*State Key Laboratory of Medical Neurobiology, School of Life Sciences and Institutes of Brain Science, Fudan University, Shanghai 200433, China.
Meng-Hua Zhou*State Key Laboratory of Medical Neurobiology, School of Life Sciences and Institutes of Brain Science, Fudan University, Shanghai 200433, China.
Yan-Ai Mei*State Key Laboratory of Medical Neurobiology, School of Life Sciences and Institutes of Brain Science, Fudan University, Shanghai 200433, China.
Fudan University · CNState Key Laboratory of Medical Neurobiology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GDF15 (growth/differentiation factor 15), a novel member of the TGFβ (transforming growth factor β) superfamily, plays critical roles in the central and peripheral nervous systems, but the signal transduction pathways and receptor subtypes involved are not well understood. In the present paper, we report that GDF15 specifically increases the IK (delayed-rectifier outward K+ current) in rat CGNs (cerebellar granule neurons) in time- and concentration-dependent manners. The GDF15-induced amplification of the IK is mediated by the increased expression and reduced lysosome-dependent degradation of the Kv2.1 protein, the main α-subunit of the IK channel. Exposure of CGNs to GDF15 markedly induced the phosphorylation of ERK (extracellular-signal-regulated kinase), Akt and mTOR (mammalian target of rapamycin), but the GDF15-induced IK densities and increased expression of Kv2.1 were attenuated only by Akt and mTOR, and not ERK, inhibitors. Pharmacological inhibition of the Src-mediated phosphorylation of TGFβR2 (TGFβ receptor 2), not TGFβR1, abrogated the effect of GDF15 on IK amplification and Kv2.1 induction. Immunoprecipitation assays showed that GDF15 increased the tyrosine phosphorylation of TGFβRII in the CGN lysate. The results of the present study reveal a novel regulation of Kv2.1 by GDF15 mediated through the TGFβRII-activated Akt/mTOR pathway, which is a previously uncharacterized Smad-independent mechanism of GDF15 signalling.

Indexed as

Signal TransductionAnimalsAnimals, NewbornCells, CulturedCerebellumGrowth Differentiation Factor 15HumansOncogene Protein v-aktProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIShab Potassium ChannelsTOR Serine-Threonine KinasesGDF15 protein, humanGrowth Differentiation Factor 15KCNB1 protein, humanMTOR protein, humanOncogene Protein v-aktProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIShab Potassium ChannelsTOR Serine-Threonine Kinases

Identifiers

PMID24597762
PMCPMC4000135
OpenAlexW2038181834

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.