Evidence map›Paper›PMID 37446028›Full record

ArticleInternational journal of molecular sciences2023

Transcriptional and Histone Acetylation Changes Associated with CRE Elements Expose Key Factors Governing the Regulatory Circuit in the Early Stage of Huntington's Disease Models.

Sandra Arancibia-Opazo, J Sebastián Contreras-Riquelme, Mario Sánchez, Marisol Cisternas-Olmedo, René L Vidal, Alberto J M Martin, Mauricio A Sáez

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Transcription-based comparison ofMicrobiology spectrum · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Article
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 3 institutions in 1 country.

Sandra Arancibia-OpazoChromatin, Epigenetic, and Neuroscience Laboratory, Centro de Genómica y Bioinformática, Facultad de Ciencias, Ingeniería y Tecnología, Universidad Mayor, Santiago 8580745, Chile.ORCID 0000-0003-0837-9230
J Sebastián Contreras-RiquelmePlant Genome Regulation Lab, Centro de Biotecnología Vegetal, Facultad de Ciencias de la Vida, Universidad Andrés Bello, Santiago 8370186, Chile.
Mario SánchezChromatin, Epigenetic, and Neuroscience Laboratory, Centro de Genómica y Bioinformática, Facultad de Ciencias, Ingeniería y Tecnología, Universidad Mayor, Santiago 8580745, Chile.ORCID 0000-0002-5991-9930
Marisol Cisternas-OlmedoCentro de Biología Integrativa, Facultad de Ciencias, Universidad Mayor, Santiago 8580745, Chile.
René L VidalCentro de Biología Integrativa, Facultad de Ciencias, Universidad Mayor, Santiago 8580745, Chile.ORCID 0000-0002-4305-7387
Alberto J M MartinLaboratorio de Redes Biológicas, Centro Científico y Tecnológico de Excelencia Ciencia & Vida, Fundación Ciencia & Vida, Universidad San Sebastián, Santiago 8580704, Chile.ORCID 0000-0002-6147-3325
Mauricio A SáezChromatin, Epigenetic, and Neuroscience Laboratory, Centro de Genómica y Bioinformática, Facultad de Ciencias, Ingeniería y Tecnología, Universidad Mayor, Santiago 8580745, Chile.ORCID 0000-0002-3355-7628
Universidad Mayor · CLSan Sebastián University · CLUniversidad Andrés Bello · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is a disorder caused by an abnormal expansion of trinucleotide CAG repeats within the huntingtin (Htt) gene. Under normal conditions, the CREB Binding Protein interacts with CREB elements and acetylates Lysine 27 of Histone 3 to direct the expression of several genes. However, mutant Htt causes depletion of CBP, which in turn induces altered histone acetylation patterns and transcriptional deregulation. Here, we have studied a differential expression analysis and H3K27ac variation in 4- and 6-week-old R6/2 mice as a model of juvenile HD. The analysis of differential gene expression and acetylation levels were integrated into Gene Regulatory Networks revealing key regulators involved in the altered transcription cascade. Our results show changes in acetylation and gene expression levels that are related to impaired neuronal development, and key regulators clearly defined in 6-week-old mice are proposed to drive the downstream regulatory cascade in HD. Here, we describe the first approach to determine the relationship among epigenetic changes in the early stages of HD. We determined the existence of changes in pre-symptomatic stages of HD as a starting point for early onset indicators of the progression of this disease.

Indexed as

Huntington DiseaseAcetylationAnimalsDisease Models, AnimalEpigenesis, GeneticHistonesHuntingtin ProteinMiceHistonesHuntingtin ProteincAMP response element-binding proteingene regulatory networkshistone acetylationHuntington’s diseasepolyQ diseases

Identifiers

PMID37446028
PMCPMC10341483
OpenAlexW4382777572

What OpenQuestion holds

Textmetadata
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.