Evidence map›Paper›PMID 18690048›Full record

ArticleChannels (Austin, Tex.)

Channel regulation by extracellular redox protein.

David J Beech, Piruthivi Sukumar

Open access · goldAbstract read
In one paragraph

Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Thiol-Disulfide Exchange Reactions in the Mammalian Extracellular Environment.Annual review of chemical and biomolecular engineering · 2016
    Review
  3. Article
  4. Article
  5. Review
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.

David J BeechInstitute of Membrane and Systems Biology, Faculty of Biological Sciences, University of Leeds, Leeds, England, UK. d.j.beech@leeds.ac.uk
Piruthivi Sukumar
University of Leeds · GB

Funding

Wellcome Trust 083857
6 · The paper itself

Abstract

The most widely studied stimuli for ion channel activation are changes in membrane voltage and binding of a chemical ligand in a pocket of the channel protein. While modulation by redox potential has also been appreciated our study shows previously unrecognised channel activation via electron donation from the extracellular redox protein thioredoxin (TRX).(1) The ion channel type involved is a member of the Transient Receptor Potential (TRP) family. Activation by TRX led us to consider the relevance of TRP channels to the inflammatory condition of rheumatoid arthritis, where functions of ion channels are relatively unknown and TRX concentrations are high. TRP channel activation was found to be inhibitory for secretion of matrix metalloproteinases, suggesting activation by TRX may have a protective role against disease. Here we expand on our original article and discuss the potential wider implications of the findings in terms of concepts for channel activation and relevance to other ion channel types and systems.

Indexed as

Gene Expression RegulationOxidation-ReductionAnimalsArthritis, RheumatoidCalciumCationsCells, CulturedDisulfidesHumansInflammationIon ChannelsLigandsModels, BiologicalSignal TransductionThioredoxinsCalciumCationsDisulfidesIon ChannelsLigandsThioredoxins

Identifiers

PMID18690048
PMCPMC2645063
OpenAlexW1982594737

What OpenQuestion holds

Textmetadata
LicenceTDM
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.