Evidence map›Paper›PMID 29529098›Full record

ArticlePloS one2018

Validation of a microRNA target site polymorphism in H3F3B that is potentially associated with a broad schizophrenia phenotype.

William Manley, Michael P Moreau, Marco Azaro, Stephen K Siecinski, Gillian Davis, Steven Buyske, Veronica Vieland, Anne S Bassett, Linda Brzustowicz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. MicroRNAs in Genetic Etiology of Human Diseases.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  2. Article
  3. 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

9 authors at 3 institutions in 2 countries.

William ManleyDepartment of Genetics, Rutgers University, Piscataway, NJ, United States of America.
Michael P MoreauDepartment of Genetics, Rutgers University, Piscataway, NJ, United States of America.
Marco AzaroDepartment of Genetics, Rutgers University, Piscataway, NJ, United States of America.
Stephen K SiecinskiDepartment of Genetics, Rutgers University, Piscataway, NJ, United States of America.
Gillian DavisDepartment of Genetics, Rutgers University, Piscataway, NJ, United States of America.
Steven BuyskeDepartment of Genetics, Rutgers University, Piscataway, NJ, United States of America.
Veronica VielandBattelle Center for Mathematical Medicine, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, United States of America.
Anne S BassettClinical Genetics Research Program, Centre for Addiction and Mental Health, Toronto, ON, Canada.
Linda BrzustowiczDepartment of Genetics, Rutgers University, Piscataway, NJ, United States of America.ORCID 0000-0003-4707-9441
Rutgers, The State University of New Jersey · USCentre for Addiction and Mental Health · CANationwide Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite much progress, few genetic findings for schizophrenia have been assessed by functional validation experiments at the molecular level. We previously reported evidence for genetic linkage of broadly defined schizophrenia to chromosome 17q25 in a sample of 24 multiplex families. 2,002 SNPs under this linkage peak were analyzed for evidence of linkage disequilibrium using the posterior probability of linkage (PPL) framework. SNP rs1060120 produced the strongest evidence for association, with a PPLD|L score of 0.21. This SNP is located within the 3'UTR of the histone gene H3F3B and colocalizes with potential gene target miR-616. A custom miRNA target prediction program predicted that the binding of miR-616 to H3F3B transcripts would be altered by the allelic variants of rs1060120. We used dual luciferase assays to experimentally validate this interaction. The rs1060120 A allele significantly reduced luciferase expression, indicating a stronger interaction with miR-616 than the G allele (p = 0.000412). These results provide functional validation that this SNP could alter schizophrenia epigenetic mechanisms thereby contributing to schizophrenia-related disease risk.

Indexed as

Binding SitesPolymorphism, Single NucleotideRNA Interference3' Untranslated RegionsAllelesGene ExpressionGenes, ReporterGenetic Association StudiesGenotypeHistonesHumansLinkage DisequilibriumMicroRNAsPhenotypeRNA, MessengerSchizophrenia3' Untranslated RegionsHistonesMicroRNAsRNA, Messenger

Identifiers

PMID29529098
PMCPMC5847241
OpenAlexW2791238753

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.