Evidence map›Paper›PMID 30915712›Full record

ArticleMolecular neurobiology2019

Dopamine D1 Receptor (D1R) Expression Is Controlled by a Transcriptional Repressor Complex Containing DISC1.

Yeongjun Suh, Su-Jin Noh, Saebom Lee, Bo Kyoung Suh, Su Been Lee, Jinhyuk Choi, Jaehoon Jeong, Sangjune Kim, Sang Ki Park

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. 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

9 authors at 3 institutions in 2 countries.

Yeongjun SuhDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.
Su-Jin NohDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.
Saebom LeeThe Russell H. Morgan Department of Radiology and Radiological Sciences, The Johns Hopkins University of School of Medicine, Baltimore, MD, USA.
Bo Kyoung SuhDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.
Su Been LeeDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.
Jinhyuk ChoiDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.
Jaehoon JeongNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Sangjune KimNeurodegeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University of School of Medicine, Baltimore, MD, USA.
Sang Ki ParkDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea. skpark@postech.ac.kr.ORCID http://orcid.org/0000-0003-1023-7864
Pohang University of Science and Technology · KRJohns Hopkins University · USNational Institutes of Health · US

Funding

National Research Foundation of Korea 2015M3C7A1030964National Research Foundation of Korea 2017M3C7A1047875National Research Foundation of Korea 2017R1A2B2009031National Research Foundation of Korea 2017R1A5A1015366
6 · The paper itself

Abstract

Disrupted-in-Schizophrenia 1 (DISC1) is a scaffold protein implicated in various psychiatric diseases. Dysregulation of the dopamine system has been associated with DISC1 deficiency, while the molecular mechanism is unclear. In this study, we propose a novel molecular mechanism underlying the transcriptional regulation of the dopamine D1 receptor (D1R) in the striatum via DISC1. We verified the increase in D1R at the transcriptional level in the striatum of DISC1-deficient mouse models and altered histone acetylation status at the D1r locus. We identified a functional interaction between DISC1 and Krüppel-like factor 16 (KLF16). KLF16 translocates DISC1 into the nucleus and forms a regulatory complex by recruiting SIN3A corepressor complexes to the D1r locus. Moreover, DISC1-deficient mice have altered D1R-mediated signaling in the striatum and exhibit hyperlocomotion in response to cocaine; the blockade of D1R suppresses these effects. Taken together, our results suggest that nuclear DISC1 plays a critical role in the transcriptional regulation of D1R in the striatal neuron, providing a mechanistic link between DISC1 and dopamine-related psychiatric symptoms.

Indexed as

Transcription, GeneticAnimalsBehavior, AnimalCell NucleusCo-Repressor ProteinsCorpus StriatumGenetic LociKruppel-Like Transcription FactorsMice, Inbred C57BLNerve Tissue ProteinsProtein BindingProtein TransportReceptors, Dopamine D1Repressor ProteinsSignal TransductionSin3 Histone Deacetylase and Corepressor ComplexCo-Repressor ProteinsDisc1 protein, mouseKlf16 protein, mouseKruppel-Like Transcription FactorsNerve Tissue ProteinsReceptors, Dopamine D1Repressor ProteinsSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexDISC1Dopamine D1 receptorKLF16SIN3ATranscriptional repression

Identifiers

PMID30915712
PMCPMC6728282
OpenAlexW2923187353

What OpenQuestion holds

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LicenceCC BY
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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.