Evidence map›Paper›PMID 27129257›Full record

ArticleThe Journal of biological chemistry2016

A Significant Role of the Truncated Ghrelin Receptor GHS-R1b in Ghrelin-induced Signaling in Neurons.

Gemma Navarro, David Aguinaga, Edgar Angelats, Mireia Medrano, Estefanía Moreno, Josefa Mallol, Antonio Cortés, Enric I Canela, Vicent Casadó, Peter J McCormick and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. 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
2.8field-weighted citation impact, top 10% 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, 51 citations in OpenAlex.

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  12. Complexes of Ghrelin GHS-R1a, GHS-R1b, and Dopamine DThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  13. The Role of Ghrelin/GHS-R1A Signaling in Nonalcohol Drug Addictions.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Role of GPR39 in Neurovascular Homeostasis and Disease.International journal of molecular sciences · 2021
    Review
  16. Review
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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

12 authors at 4 institutions in 3 countries.

Gemma NavarroFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain, dimartts@hotmail.com.
David AguinagaFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Edgar AngelatsFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Mireia MedranoFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Estefanía MorenoFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Josefa MallolFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Antonio CortésFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Enric I CanelaFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Vicent CasadóFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Peter J McCormickthe School of Pharmacy, University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, United Kingdom, and.
Carme LluísFrom the Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, 08028 Barcelona, Spain.
Sergi Ferréthe Integrative Neurobiology Section, National Institute on Drug Abuse, Intramural Research Program, Baltimore, Maryland 21224 sferre@intra.nida.nih.gov.
Centro de Investigación Biomédica en Red · ESUniversitat de Barcelona · ESNational Institute on Drug Abuse · USNorwich Research Park · GB

Funding

Neurotransmitter Receptor Heteromers in the Striatal Spine ModuleZIADA000493 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI FERRE, SERGI · 2009 to 2025
$35.6M
6 · The paper itself

Abstract

The truncated non-signaling ghrelin receptor growth hormone secretagogue R1b (GHS-R1b) has been suggested to simply exert a dominant negative role in the trafficking and signaling of the full and functional ghrelin receptor GHS-R1a. Here we reveal a more complex modulatory role of GHS-R1b. Differential co-expression of GHS-R1a and GHS-R1b, both in HEK-293T cells and in striatal and hippocampal neurons in culture, demonstrates that GHS-R1b acts as a dual modulator of GHS-R1a function: low relative GHS-R1b expression potentiates and high relative GHS-R1b expression inhibits GHS-R1a function by facilitating GHS-R1a trafficking to the plasma membrane and by exerting a negative allosteric effect on GHS-R1a signaling, respectively. We found a preferential Gi/o coupling of the GHS-R1a-GHS-R1b complex in HEK-293T cells and, unexpectedly, a preferential Gs/olf coupling in both striatal and hippocampal neurons in culture. A dopamine D1 receptor (D1R) antagonist blocked ghrelin-induced cAMP accumulation in striatal but not hippocampal neurons, indicating the involvement of D1R in the striatal GHS-R1a-Gs/olf coupling. Experiments in HEK-293T cells demonstrated that D1R co-expression promotes a switch in GHS-R1a-G protein coupling from Gi/o to Gs/olf, but only upon co-expression of GHS-R1b. Furthermore, resonance energy transfer experiments showed that D1R interacts with GHS-R1a, but only in the presence of GHS-R1b. Therefore, GHS-R1b not only determines the efficacy of ghrelin-induced GHS-R1a-mediated signaling but also determines the ability of GHS-R1a to form oligomeric complexes with other receptors, promoting profound qualitative changes in ghrelin-induced signaling.

Indexed as

Signal TransductionAdenylyl CyclasesAnimalsCell MembraneGhrelinHEK293 CellsHippocampusHumansNeuronsProtein MultimerizationProtein SubunitsProtein TransportRats, Sprague-DawleyReceptors, Dopamine D1Receptors, GhrelinAdenylyl CyclasesGhrelinProtein SubunitsReceptors, Dopamine D1Receptors, GhrelincAMPdopamine receptorghrelinghrelin receptorHEK-293T cellsneuronoligomerizationtrafficking

Identifiers

PMID27129257
PMCPMC4933222
OpenAlexW2343538044

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.