Evidence map›Paper›PMID 25706283›Full record

ArticlePloS one2015

Inverse agonistic action of 3-iodothyronamine at the human trace amine-associated receptor 5.

Juliane Dinter, Jessica Mühlhaus, Carolin Leonie Wienchol, Chun-Xia Yi, Daniela Nürnberg, Silke Morin, Annette Grüters, Josef Köhrle, Torsten Schöneberg, Matthias Tschöp and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 82 citations in OpenAlex.

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  20. 3-Iodothyronamine and Derivatives: New Allies Against Metabolic Syndrome?International journal of molecular sciences · 2020
    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

13 authors at 3 institutions in 1 country.

Juliane DinterInstitut für Experimentelle Pädiatrische Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Jessica MühlhausInstitut für Experimentelle Pädiatrische Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Carolin Leonie WiencholInstitut für Experimentelle Pädiatrische Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Chun-Xia YiInstitute for Diabetes and Obesity, Helmholtz-Zentrum München, German Research Center for Environmental Health, München, Germany.
Daniela NürnbergInstitut für Experimentelle Pädiatrische Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Silke MorinInstitute for Diabetes and Obesity, Helmholtz-Zentrum München, German Research Center for Environmental Health, München, Germany.
Annette GrütersInstitut für Experimentelle Pädiatrische Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Josef KöhrleInstitut für Experimentelle Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Torsten SchönebergInstitut für Biochemie, Molekulare Biochemie, Medizinische Fakultät, University of Leipzig, Leipzig, Germany.
Matthias TschöpInstitut für Experimentelle Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Heiko KrudeInstitut für Experimentelle Pädiatrische Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Gunnar KleinauInstitut für Experimentelle Pädiatrische Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Heike BiebermannInstitut für Experimentelle Pädiatrische Endokrinologie, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEHelmholtz Zentrum München · DELeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveApplication of 3-iodothyronamine (3-T1AM) results in decreased body temperature and body weight in rodents. The trace amine-associated receptor (TAAR) 1, a family A G protein-coupled receptor, is a target of 3-T1AM. However, 3-T1AM effects still persist in mTaar1 knockout mice, which suggest so far unknown further receptor targets that are of physiological relevance. TAAR5 is a highly conserved TAAR subtype among mammals and we here tested TAAR5 as a potential 3-T1AM target. First, we investigated mouse Taar5 (mTaar5) expression in several brain regions of the mouse in comparison to mTaar1. Secondly, to unravel the full spectrum of signaling capacities, we examined the distinct Gs-, Gi/o-, G12/13-, Gq/11- and MAP kinase-mediated signaling pathways of mouse and human TAAR5 under ligand-independent conditions and after application of 3-T1AM. We found overlapping localization of mTaar1 and mTaar5 in the amygdala and ventromedial hypothalamus of the mouse brain. Second, the murine and human TAAR5 (hTAAR5) display significant basal activity in the Gq/11 pathway but show differences in the basal activity in Gs and MAP kinase signaling. In contrast to mTaar5, 3-T1AM application at hTAAR5 resulted in significant reduction in basal IP3 formation and MAP kinase signaling. In conclusion, our data suggest that the human TAAR5 is a target for 3-T1AM, exhibiting inhibitory effects on IP3 formation and MAP kinase signaling pathways, but does not mediate Gs signaling effects as observed for TAAR1. This study also indicates differences between TAAR5 orthologs with respect to their signaling profile. In consequence, 3-T1AM-mediated effects may differ between rodents and humans.

Indexed as

AnimalsCell LineChlorocebus aethiopsCOS CellsHEK293 CellsHumansLigandsMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, KnockoutReceptors, G-Protein-CoupledSignal TransductionThyroninesTrace Amine-Associated Receptors3-iodothyronamineLigandsReceptors, G-Protein-CoupledTAAR5 protein, humanTAAR5 protein, mouseThyroninesTrace Amine-Associated Receptors

Identifiers

PMID25706283
PMCPMC4382497
OpenAlexW2089647302

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.