Evidence map›Paper›PMID 24516781›Full record

ArticlePeerJ2014

Ligand determinants of fatty acid activation of the pronociceptive ion channel TRPA1.

William John Redmond, Liuqiong Gu, Maxime Camo, Peter McIntyre, Mark Connor

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

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  8. Phospho-Mimetic Mutation at Ser602 Inactivates Human TRPA1 Channel.International journal of molecular sciences · 2020
    Article
  9. Article
  10. Terpenoids Commonly Found inCannabis and cannabinoid research · 2020
    Article
  11. Cannabinoid Ligands Targeting TRP Channels.Frontiers in molecular neuroscience · 2018
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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

5 authors at 2 institutions in 1 country.

William John RedmondAustralian School of Advanced Medicine, Macquarie University , NSW , Australia.
Liuqiong GuDepartment of Pharmacology, University of Melbourne , Parkville , Victoria , Australia.
Maxime CamoAustralian School of Advanced Medicine, Macquarie University , NSW , Australia.
Peter McIntyreDepartment of Pharmacology, University of Melbourne , Parkville , Victoria , Australia ; Health Innovations Research Institute and School of Medical Sciences, RMIT University , Melbourne , Victoria , Australia.
Mark ConnorAustralian School of Advanced Medicine, Macquarie University , NSW , Australia.
Macquarie University · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and purpose. Arachidonic acid (AA) and its derivatives are important modulators of cellular signalling. The transient receptor potential cation channel subfamily A, member 1 (TRPA1) is a cation channel with important functions in mediating cellular responses to noxious stimuli and inflammation. There is limited information about the interactions between AA itself and TRPA1, so we investigated the effects of AA and key ethanolamide and amino acid/neurotransmitter derivatives of AA on hTRPA1. Experimental approach. HEK 293 cells expressing hTRPA1 were studied by measuring changes in intracellular calcium ([Ca] i ) with a fluorescent dye and by standard whole cell patch clamp recordings. Key results. AA (30 μM) increased fluorescence in hTRPA1 expressing cells by 370% (notional EC 50 13 μM). The covalent TRPA1 agonist cinnamaldehyde (300 μM) increased fluorescence by 430% (EC 50, 11 μM). Anandamide (230%) and N-arachidonoyl tyrosine (170%) substantially activated hTRPA1 at 30 μM, however, N-arachidonoyl conjugates of glycine and taurine were less effective while N-acyl conjugates of 5-HT did not affect hTRPA1. Changing the acyl chain length or the number and position of double bonds reduced fatty acid efficacy at hTRPA1. Mutant hTRPA1 (Cys621, Cys641 and Cys665 changed to Ser) could be activated by AA (100 μM, 40% of wild type) but not by cinnamaldehyde (300 μM). Conclusions and implications. AA is a more potent activator of TRPA1 than its ethanolamide or amino acid/neurotransmitter derivatives and acts via a mechanism distinct from that of cinnamaldehyde, further underscoring the likelyhood of multiple pharmacologically exploitable sites on hTRPA1.

Indexed as

Arachidonic acidArachidonoyl amino acid/neurotransmitter conjugateInflammationPainTRP channel

Identifiers

PMID24516781
PMCPMC3913255
OpenAlexW2065390732

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.