Evidence map›Paper›PMID 25799583›Full record

ArticlePloS one2015

Alternative polyadenylation allows differential negative feedback of human miRNA miR-579 on its host gene ZFR.

Ludwig Christian Hinske, Pedro A F Galante, Elisabeth Limbeck, Patrick Möhnle, Raphael B Parmigiani, Lucila Ohno-Machado, Anamaria A Camargo, Simone Kreth

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

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  19. FAMLF is a target of miR-181b in Burkitt lymphoma.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
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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

8 authors at 3 institutions in 2 countries.

Ludwig Christian HinskeResearch Group Molecular Medicine, Department of Anaesthesiology, Clinic of the University of Munich, Munich, Germany.
Pedro A F GalanteMolecular Oncology Center, Sírio Libanês Hospital, São Paulo, Brazil.
Elisabeth LimbeckMolecular Oncology Center, Sírio Libanês Hospital, São Paulo, Brazil.
Patrick MöhnleResearch Group Molecular Medicine, Department of Anaesthesiology, Clinic of the University of Munich, Munich, Germany.
Raphael B ParmigianiMolecular Oncology Center, Sírio Libanês Hospital, São Paulo, Brazil.
Lucila Ohno-MachadoDivision of Biomedical Informatics, University of California San Diego, La Jolla, California, United States of America.
Anamaria A CamargoMolecular Oncology Center, Sírio Libanês Hospital, São Paulo, Brazil.
Simone KrethResearch Group Molecular Medicine, Department of Anaesthesiology, Clinic of the University of Munich, Munich, Germany.
Hospital São Paulo · BRHospital Sírio-Libanês · BRUniversity of California, San Diego · US

Funding

iDASH: Integrating Data for Analysis, Anonymization, and SharingU54HL108460 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OHNO-MACHADO, LUCILA · 2010 to 2015
$19.1M
Global Health Informatics for Cancer ResearchD43TW007015 · FIC · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OHNO-MACHADO, LUCILA · 2004 to 2013
$2.2M
FIC NIH HHS D43 TW007015FIC NIH HHS D43TW007015NHLBI NIH HHS U54 HL108460NHLBI NIH HHS U54HL108460
6 · The paper itself

Abstract

About half of the known miRNA genes are located within protein-coding host genes, and are thus subject to co-transcription. Accumulating data indicate that this coupling may be an intrinsic mechanism to directly regulate the host gene's expression, constituting a negative feedback loop. Inevitably, the cell requires a yet largely unknown repertoire of methods to regulate this control mechanism. We propose APA as one possible mechanism by which negative feedback of intronic miRNA on their host genes might be regulated. Using in-silico analyses, we found that host genes that contain seed matching sites for their intronic miRNAs yield longer 32UTRs with more polyadenylation sites. Additionally, the distribution of polyadenylation signals differed significantly between these host genes and host genes of miRNAs that do not contain potential miRNA binding sites. We then transferred these in-silico results to a biological example and investigated the relationship between ZFR and its intronic miRNA miR-579 in a U87 cell line model. We found that ZFR is targeted by its intronic miRNA miR-579 and that alternative polyadenylation allows differential targeting. We additionally used bioinformatics analyses and RNA-Seq to evaluate a potential cross-talk between intronic miRNAs and alternative polyadenylation. CPSF2, a gene previously associated with alternative polyadenylation signal recognition, might be linked to intronic miRNA negative feedback by altering polyadenylation signal utilization.

Indexed as

Feedback, PhysiologicalPolyadenylationCell Line, TumorCleavage And Polyadenylation Specificity FactorComputational BiologyGene Expression RegulationHumansIntronsMicroRNAsRNA-Binding ProteinsCleavage And Polyadenylation Specificity FactorMicroRNAsMIRN579 microRNA, humanRNA-Binding ProteinsZFR protein, human

Identifiers

PMID25799583
PMCPMC4370670
OpenAlexW2044076622

What OpenQuestion holds

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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.