Evidence map›Paper›PMID 29019003›Full record

ArticleJournal of molecular neuroscience : MN2017

Role of Dynein Axonemal Heavy Chain 6 Gene Expression as a Possible Biomarker for Huntington's Disease: a Translational Study.

Lorena B Areal, Lorraine P Pereira, Fabiola M Ribeiro, Isabella G Olmo, Marcelo R Muniz, Maria do Carmo Rodrigues, Patrik F Costa, Cristina Martins-Silva, Stephen S G Ferguson, Daniela A M Guimarães and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2017. 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
0.1field-weighted citation impact, top 55% 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, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. DYNLT1 gene expression is downregulated in whole blood of patients at different Huntington's disease stages.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    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

11 authors at 4 institutions in 2 countries.

Lorena B ArealLaboratory of Molecular and Behavioral Neurobiology, Health Sciences Center, Federal University of Espirito Santo, Vitória, ES, Brazil.
Lorraine P PereiraGraduate Program in Biochemistry and Pharmacology, Health Sciences Center, Federal University of Espírito Santo, Vitória, ES, Brazil.
Fabiola M RibeiroGraduate Program in Neuroscience, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
Isabella G OlmoGraduate Program in Neuroscience, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
Marcelo R MunizDepartment of Clinical Medicine, Health Science Center, Federal University of Espírito Santo, Vitória, Brazil.
Maria do Carmo RodriguesDepartment of Clinical Medicine, Health Science Center, Federal University of Espírito Santo, Vitória, Brazil.
Patrik F CostaDepartment of Physiotherapy, School of Sciences, Santa Casa de Misericordia de Vitoria, Vitória, ES, Brazil.
Cristina Martins-SilvaLaboratory of Molecular and Behavioral Neurobiology, Health Sciences Center, Federal University of Espirito Santo, Vitória, ES, Brazil.
Stephen S G FergusonDepartment of Cellular and Molecular Medicine, Brain and Mind Research Institute and Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.
Daniela A M GuimarãesGraduate Program in Biochemistry and Pharmacology, Health Sciences Center, Federal University of Espírito Santo, Vitória, ES, Brazil.
Rita G W PiresLaboratory of Molecular and Behavioral Neurobiology, Health Sciences Center, Federal University of Espirito Santo, Vitória, ES, Brazil. rita.pires@ufes.br.
Universidade Federal do Espírito Santo · BRUniversidade Federal de Minas Gerais · BREscola Superior de Ciências da Santa Casa de Misericórdia de Vitória · BRUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by motor dysfunction, cognitive deficits, and psychiatric symptoms. The primary genetic cause is an expansion of cytosine adenine guanine (CAG) nucleotides of the huntingtin gene, which codes an important protein involved with neuronal signaling. The severity of HD correlates with the number of CAG repeats and individuals with longer expansions have an earlier onset and more severe symptoms. A microarray study conducted by our research group showed alteration in DNAH6 gene (encoding dynein axonemal heavy chain 6). DNAH6 belongs to dynein family, whose members are constituents of the microtubule-associated motor proteins and is downregulated in the striatum of a HD mouse model (knockin Hdh

Indexed as

AnimalsBiomarkersCase-Control StudiesDown-RegulationDyneinsHumansHuntingtin ProteinHuntington DiseaseMiceNerve Tissue ProteinsNuclear ProteinsTranslational Research, BiomedicalBiomarkersDyneinsHtt protein, mouseHuntingtin ProteinNerve Tissue ProteinsNuclear ProteinsDynein heavy chain 6Gene expressionHuntington’s diseaseMicroarray

Identifiers

PMID29019003
OpenAlexW2763762406

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.