Evidence map›Paper›PMID 18604232›Full record

ArticleBritish journal of pharmacology2008

Production of a specific extracellular inhibitor of TRPM3 channels.

J Naylor, C J Milligan, F Zeng, C Jones, D J Beech

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

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  5. TRPM3-Induced Gene Transcription Is under Epigenetic Control.Pharmaceuticals (Basel, Switzerland) · 2022
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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.

J NaylorInstitute of Membrane and Systems Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
C J Milligan
F Zeng
C Jones
D J Beech
University of Leeds · GBLoughborough University · GB

Funding

Biotechnology and Biological Sciences Research CouncilBritish Heart FoundationWellcome Trust
6 · The paper itself

Abstract

background and purposeIsoform-specific ion channel blockers are useful for target validation in drug discovery and can provide the basis for new therapeutic agents and aid in determination of physiological functions of ion channels. The aim of this study was to generate a specific blocker of human TRPM3 channels as a tool to help investigations of this member of the TRP cationic channel family. EXPERIMENTAL APPROACH: A polyclonal antibody (TM3E3) was made to a conserved peptide of the third extracellular (E3) loop of TRPM3 and tested for binding and functional effect. Studies of channel activity were made by whole-cell planar patch-clamp and fura-2 intracellular Ca(2+) measurement. KEY

resultsIonic current mediated by TRPM3 was inhibited partially by TM3E3 over a period of 5-10 min. Ca(2+) entry in TRPM3-expressing cells was also partially inhibited by TM3E3 in a peptide-specific manner and independently of the type of agonist used to activate TRPM3. TM3E3 had no effect on TRPC5, TRPV4, TRPM2 or an endogenous ATP response. CONCLUSIONS AND IMPLICATIONS: The data show the successful development of a specific TRPM3 inhibitor and give further confidence in E3 targeting as an approach to producing isoform-specific ion channel blockers.

Indexed as

AntibodiesCalciumCell LineFluorescent DyesFura-2HumansKidneyPatch-Clamp TechniquesProtein BindingTRPM Cation ChannelsAntibodiesCalciumFluorescent DyesFura-2TRPM3 protein, humanTRPM Cation Channels

Identifiers

PMID18604232
PMCPMC2579657
OpenAlexW2169520037

What OpenQuestion holds

Textmetadata
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.