Evidence map›Paper›PMID 24587241›Full record

ArticlePloS one2014

Anatomical transcriptome of G protein-coupled receptors leads to the identification of a novel therapeutic candidate GPR52 for psychiatric disorders.

Hidetoshi Komatsu, Minoru Maruyama, Shuuhei Yao, Tokuyuki Shinohara, Kensuke Sakuma, Sachiko Imaichi, Tomoko Chikatsu, Kanako Kuniyeda, Foo Kok Siu, Lam Sock Peng and 10 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 72 citations in OpenAlex.

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  4. Research Progress of G Protein-coupled Receptor 52 on Central Nervous System Diseases.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2026
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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

20 authors at 2 institutions in 2 countries.

Hidetoshi KomatsuCentral Nervous System Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Minoru MaruyamaCardiovascular and Metabolic Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Shuuhei YaoBiomolecular Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Tokuyuki ShinoharaAdvanced Science Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Kensuke SakumaCardiovascular and Metabolic Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Sachiko ImaichiAdvanced Science Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Tomoko ChikatsuCardiovascular and Metabolic Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Kanako KuniyedaExtra Value Generation and General Medicine Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Foo Kok SiuTSP CNS Phenotyping, Takeda Pharmaceutical Company Limited, Singapore.
Lam Sock PengTSP CNS Phenotyping, Takeda Pharmaceutical Company Limited, Singapore.
Katherine ZhuoTSP Transgenic pipeline, Takeda Pharmaceutical Company Limited, Singapore.
Lay Sock MunTSP Transgenic pipeline, Takeda Pharmaceutical Company Limited, Singapore.
Tan Min HanTSP Transgenic pipeline, Takeda Pharmaceutical Company Limited, Singapore.
Yoshio MatsumotoBiomolecular Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Tadatoshi HashimotoResearch Administration Department, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Nobuyuki MiyajimaBiomolecular Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Yasuaki ItohPharmaceutical Marketing Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Kazuhiro OgiAdvanced Science Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Yugo HabataCardiovascular and Metabolic Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Masaaki MoriCardiovascular and Metabolic Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Kanagawa, Japan.
Takeda (Japan) · JPTakeda (Singapore) · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many drugs of abuse and most neuropharmacological agents regulate G protein-coupled receptors (GPCRs) in the central nervous system (CNS)_ENREF_1. The striatum, in which dopamine D1 and D2 receptors are enriched, is strongly innervated by the ventral tegmental area (VTA), which is the origin of dopaminergic cell bodies of the mesocorticolimbic dopamine system_ENREF_3 and plays a central role in the development of psychiatric disorders_ENREF_4. Here we report the comprehensive and anatomical transcript profiling of 322 non-odorant GPCRs in mouse tissue by quantitative real-time PCR (qPCR), leading to the identification of neurotherapeutic receptors exclusively expressed in the CNS, especially in the striatum. Among them, GPR6, GPR52, and GPR88, known as orphan GPCRs, were shown to co-localize either with a D2 receptor alone or with both D1 and D2 receptors in neurons of the basal ganglia. Intriguingly, we found that GPR52 was well conserved among vertebrates, is Gs-coupled and responsive to the antipsychotic drug, reserpine. We used three types of transgenic (Tg) mice employing a Cre-lox system under the control of the GPR52 promoter, namely, GPR52-LacZ Tg, human GPR52 (hGPR52) Tg, and hGPR52-GFP Tg mice. Detailed histological investigation suggests that GPR52 may modulate dopaminergic and glutamatergic transmission in neuronal circuits responsible for cognitive function and emotion. In support of our prediction, GPR52 knockout and transgenic mice exhibited psychosis-related and antipsychotic-like behaviors, respectively. Therefore, we propose that GPR52 has the potential of being a therapeutic psychiatric receptor. This approach may help identify potential therapeutic targets for CNS diseases.

Indexed as

TranscriptomeAmino Acid SequenceAnimalsAntipsychotic AgentsBehavior, AnimalCognitionConserved SequenceCorpus StriatumDopaminergic NeuronsEmotionsGene Expression ProfilingGene Expression RegulationHumansMiceMice, TransgenicMolecular Sequence DataAntipsychotic AgentsGPR52 protein, humanGpr52 protein, mouseGPR6 protein, mouseGpr88 protein, mouseReceptors, Dopamine D1Receptors, Dopamine D2Receptors, G-Protein-CoupledReserpine

Identifiers

PMID24587241
PMCPMC3938596
OpenAlexW1983435506

What OpenQuestion holds

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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.