Evidence map›Paper›PMID 33830014›Full record

ArticleeLife2021

A calcineurin-mediated scaling mechanism that controls a K

Chao Yi, Tim Wgm Spitters, Ezz Al-Din Ahmed Al-Far, Sen Wang, TianLong Xiong, Simian Cai, Xin Yan, Kaomei Guan, Michael Wagner, Ali El-Armouche and 1 more

Abstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Signal control during tissue regeneration in adult animals.Nature reviews. Molecular cell biology · 2026
    Review
  2. Article
  3. Article
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  5. Hallmarks of regeneration.Cell stem cell · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. International journal of molecular sciences · 2021
    Article
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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

11 authors at 4 institutions in 2 countries.

Chao Yi *School of Life Sciences and Technology, ShanghaiTech University, Shanghai, China.
Tim Wgm Spitters *School of Life Sciences and Technology, ShanghaiTech University, Shanghai, China.
Ezz Al-Din Ahmed Al-Far *Institut für Pharmakologie und Toxikologie, Technische Universität Dresden, Dresden, Germany.
Sen WangSchool of Life Sciences and Technology, ShanghaiTech University, Shanghai, China.
TianLong XiongSchool of Life Sciences and Technology, ShanghaiTech University, Shanghai, China.
Simian CaiSchool of Life Sciences and Technology, ShanghaiTech University, Shanghai, China.
Xin YanSchool of Life Sciences and Technology, ShanghaiTech University, Shanghai, China.
Kaomei GuanInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Dresden, Germany.
Michael WagnerInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Dresden, Germany.
Ali El-ArmoucheInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Dresden, Germany.
Christopher L AntosSchool of Life Sciences and Technology, ShanghaiTech University, Shanghai, China.ORCID 0000-0001-8881-8568
ShanghaiTech University · CNTU Dresden · DECenter for Excellence in Molecular Cell Science · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increase in activity of the two-pore potassium-leak channel Kcnk5b maintains allometric juvenile growth of adult zebrafish appendages. However, it remains unknown how this channel maintains allometric growth and how its bioelectric activity is regulated to scale these anatomical structures. We show the activation of Kcnk5b is sufficient to activate several genes that are part of important development programs. We provide in vivo transplantation evidence that the activation of gene transcription is cell autonomous. We also show that Kcnk5b will induce the expression of different subsets of the tested developmental genes in different cultured mammalian cell lines, which may explain how one electrophysiological stimulus can coordinately regulate the allometric growth of diverse populations of cells in the fin that use different developmental signals. We also provide evidence that the post-translational modification of serine 345 in Kcnk5b by calcineurin regulates channel activity to scale the fin. Thus, we show how an endogenous bioelectric mechanism can be regulated to promote coordinated developmental signaling to generate and scale a vertebrate appendage.

Indexed as

Transcription, GeneticAnimal FinsAnimalsAnimals, Genetically ModifiedCalcineurinFemaleHedgehog ProteinsHEK293 CellsHeLa CellsHumansIntercellular Signaling Peptides and ProteinsIon Channel GatingMaleMembrane PotentialsMorphogenesisPhosphorylationCalcineurinHedgehog ProteinsIntercellular Signaling Peptides and ProteinsLEF1 protein, zebrafishPotassiumPotassium Channels, Tandem Pore DomainShha protein, zebrafishTranscription FactorsZebrafish Proteinscalcineurindevelopmental biologyelectrophysiologypotassium channelproportional growthtissue scalingtranscriptionzebrafish

Identifiers

PMID33830014
PMCPMC8110307
OpenAlexW3142009387

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.