Evidence map›Paper›PMID 27405468›Full record

ArticleMolecular neurobiology2017

Genome-wide Analysis of RARβ Transcriptional Targets in Mouse Striatum Links Retinoic Acid Signaling with Huntington's Disease and Other Neurodegenerative Disorders.

Anna Niewiadomska-Cimicka, Agnieszka Krzyżosiak, Tao Ye, Anna Podleśny-Drabiniok, Doulaye Dembélé, Pascal Dollé, Wojciech Krężel

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Vitamin A deficiency induces sex-specific reward processing alterations through a dysregulation of the mesolimbic dopamine transmission in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
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  10. Article
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  13. Synthetic Retinoids Beyond Cancer Therapy.Annual review of pharmacology and toxicology · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
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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

7 authors at 5 institutions in 2 countries.

Anna Niewiadomska-CimickaInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, 67404, Illkirch Cedex, France.
Agnieszka KrzyżosiakInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, 67404, Illkirch Cedex, France.
Tao YeInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, 67404, Illkirch Cedex, France.
Anna Podleśny-DrabiniokInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, 67404, Illkirch Cedex, France.
Doulaye DembéléInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, 67404, Illkirch Cedex, France.
Pascal DolléInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, 67404, Illkirch Cedex, France.
Wojciech KrężelInstitut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, 67404, Illkirch Cedex, France. krezel@igbmc.fr.
Centre National de la Recherche Scientifique · FRInstitut de génétique et de biologie moléculaire et cellulaire · FRInserm · FRMRC Laboratory of Molecular Biology · GBUniversité de Strasbourg · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid (RA) signaling through retinoic acid receptors (RARs), known for its multiple developmental functions, emerged more recently as an important regulator of adult brain physiology. How RAR-mediated regulation is achieved is poorly known, partly due to the paucity of information on critical target genes in the brain. Also, it is not clear how reduced RA signaling may contribute to pathophysiology of diverse neuropsychiatric disorders. We report the first genome-wide analysis of RAR transcriptional targets in the brain. Using chromatin immunoprecipitation followed by high-throughput sequencing and transcriptomic analysis of RARβ-null mutant mice, we identified genomic targets of RARβ in the striatum. Characterization of RARβ transcriptional targets in the mouse striatum points to mechanisms through which RAR may control brain functions and display neuroprotective activity. Namely, our data indicate with statistical significance (FDR 0.1) a strong contribution of RARβ in controlling neurotransmission, energy metabolism, and transcription, with a particular involvement of G-protein coupled receptor (p = 5.0e

Indexed as

Genome-Wide Association StudySignal TransductionTranscription, GeneticAnimalsBinding SitesDNAHuntingtin ProteinHuntington DiseaseMice, Inbred C57BLMice, KnockoutNeostriatumNeurodegenerative DiseasesProtein AggregatesProtein BindingReceptors, Retinoic AcidReproducibility of ResultsDNAHuntingtin ProteinProtein AggregatesReceptors, Retinoic Acidretinoic acid receptor betaRNA, MessengerTretinoinChIP-seqHuntington’s diseaseNucleus accumbensRARResponse elementsRetinoic acidStriatumTranscriptome

Identifiers

PMID27405468
OpenAlexW2463206793

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.