Evidence map›Paper›PMID 27996211›Full record

ArticleCNS neuroscience & therapeutics2017

GSK-3β Interacts with Dopamine D1 Receptor to Regulate Receptor Function: Implication for Prefrontal Cortical D1 Receptor Dysfunction in Schizophrenia.

Jing-Ru Wang, Pei-Hua Sun, Zhao-Xiang Ren, Herbert Y Meltzer, Xue-Chu Zhen

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Dopamine DJournal of biomedical science · 2020
    Article
  11. Review
  12. Article
  13. Molecular neuropsychiatry · 2018
    Review
  14. 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

5 authors at 2 institutions in 2 countries.

Jing-Ru WangJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, Jiangsu, China.
Pei-Hua SunJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, Jiangsu, China.
Zhao-Xiang RenJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, Jiangsu, China.
Herbert Y MeltzerDepartment of Psychiatry and Behavioral Sciences, Northwestern Feinberg School of Medicine, Chicago, IL, USA.
Xue-Chu ZhenJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, Jiangsu, China.
Soochow University · CNNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionImpaired dopamine D1 receptor (D1R) function in prefrontal cortex (PFC) is believed to contribute to the PFC hypofunction that has been hypothesized to be associated with negative symptoms and cognitive deficits in schizophrenia. It is therefore critical to understand the mechanisms for modulation of D1R function.

aimsTo investigate the physical interaction and functional modulation between D1R and GSK-3β.

resultsD1R and GSK-3β physically interact in cultured cells and native brain tissues. This direct interaction was found to occur at the S(417)PALS(421) motif in the C-terminus of D1R. Inhibition of GSK-3β impaired D1R activation along with a decrease in D1R-GSK-3β interaction. GSK-3β inhibition reduced agonist-stimulated D1R desensitization and endocytosis, the latter associated with the reduction of membrane translocation of β-arrestin-2. Similarly, inhibition of GSK-3β in rat PFC also resulted in impaired D1R activation and association with GSK-3β. Moreover, in a NMDA antagonist animal model of schizophrenia, we detected a decrease in prefrontal GSK-3β activity and D1R-GSK-3β association and decreased D1R activation in the PFC.

conclusionsThe present work identified GSK-3β as a new interacting protein for D1R functional regulation and revealed a novel mechanism for GSK-3β-regulated D1R function which may underlie D1R dysfunction in schizophrenia.

Indexed as

Adjuvants, ImmunologicAnimalsbeta-ArrestinsCyclic AMPDisease Models, AnimalDopamine AgonistsEndocytosisEnzyme InhibitorsFenoldopamGlycogen Synthase Kinase 3 betaGuanosine 5'-O-(3-Thiotriphosphate)HEK293 CellsHumansIndolesLithium ChlorideMaleimidesAdjuvants, Immunologicbeta-ArrestinsCyclic AMPDopamine AgonistsEnzyme InhibitorsFenoldopamGlycogen Synthase Kinase 3 betaGuanosine 5'-O-(3-Thiotriphosphate)IndolesLithium ChlorideMaleimidesReceptors, Dopamine D1SB 216763DesensitizationDopamine D1 receptorGSK-3βInternalizationSchizophreniaβ-arrestin

Identifiers

PMID27996211
PMCPMC6492711
OpenAlexW2563594192

What OpenQuestion holds

Textmetadata
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Registered trials

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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.