Evidence map›Paper›PMID 26580832›Full record

ArticleJournal of cellular physiology2016

The Role of Kv1.2 Channel in Electrotaxis Cell Migration.

Gaofeng Zhang, Mathew Edmundson, Vsevolod Telezhkin, Yu Gu, Xiaoqing Wei, Paul J Kemp, Bing Song

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Electric Pulses Can Influence Galvanotaxis ofBioMed research international · 2018
    Article
  7. 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

7 authors at 3 institutions in 2 countries.

Gaofeng ZhangDepartment of Dermatology, No. 1 Hospital of China Medical University, Shenyang, China.
Mathew EdmundsonSchool of Dentistry, College of Biomedical and Life Sciences, Cardiff University, Cardiff, United Kingdom.
Vsevolod TelezhkinSchool of Biosciences, College of Biomedical and Life Sciences, Cardiff University, Cardiff, United Kingdom.
Yu GuSchool of Dentistry, College of Biomedical and Life Sciences, Cardiff University, Cardiff, United Kingdom.
Xiaoqing WeiSchool of Dentistry, College of Biomedical and Life Sciences, Cardiff University, Cardiff, United Kingdom.
Paul J KempSchool of Biosciences, College of Biomedical and Life Sciences, Cardiff University, Cardiff, United Kingdom.
Bing SongDepartment of Dermatology, No. 1 Hospital of China Medical University, Shenyang, China.
Cardiff University · GBUniversity of Wales · GBChina Medical University · CN

Funding

European Research Council 243261Wellcome Trust 082887
6 · The paper itself

Abstract

Voltage-gated potassium Kv1.2 channels play pivotal role in maintaining of resting membrane potential and, consequently, regulation of cellular excitability of neurons. Endogenously generated electric field (EF) have been proven as an important regulator for cell migration and tissue repair. The mechanisms of ion channel involvement in EF-induced cell responses are extensively studied but largely are poorly understood. In this study we generated three COS-7 clones with different expression levels of Kv1.2 channel, and confirmed their functional variations with patch clamp analysis. Time-lapse imaging analysis showed that EF-induced cell migration response was Kv1.2 channel expression level depended. Inhibition of Kv1.2 channels with charybdotoxin (ChTX) constrained the sensitivity of COS-7 cells to EF stimulation more than their motility. Immunocytochemistry and pull-down analyses demonstrated association of Kv1.2 channels with actin-binding protein cortactin and its re-localization to the cathode-facing membrane at EF stimulation, which confirms the mechanism of EF-induced directional migration. This study displays that Kv1.2 channels represent an important physiological link in EF-induced cell migration. The described mechanism suggests a potential application of EF which may improve therapeutic performance in curing injuries of neuronal and/or cardiac tissue repair, post operational therapy, and various degenerative syndromes.

Indexed as

Cell MovementAnimalsChlorocebus aethiopsCortactinCOS CellsDose-Response Relationship, DrugElectric StimulationImmunoprecipitationKv1.1 Potassium ChannelMembrane PotentialsPatch-Clamp TechniquesPotassium Channel BlockersProtein BindingSignal TransductionTime FactorsTime-Lapse ImagingCortactinKcna1 protein, mouseKv1.1 Potassium ChannelPotassium Channel Blockers

Identifiers

PMID26580832
PMCPMC4832312
OpenAlexW2180808288

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.