Evidence map›Paper›PMID 29263133›Full record

ArticleRNA (New York, N.Y.)2018

miR-222 isoforms are differentially regulated by type-I interferon.

Charlotte Nejad, Katherine A Pillman, Katherine J Siddle, Geneviève Pépin, Minna-Liisa Änkö, Claire E McCoy, Traude H Beilharz, Lluís Quintana-Murci, Gregory J Goodall, Cameron P Bracken and 1 more

Abstract read
In one paragraph

Article in RNA (New York, N.Y.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. IsomiR stoichiometry changes as disease biomarkers.Molecular therapy. Nucleic acids · 2025
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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

11 authors.

Charlotte NejadCentre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, Monash University, Clayton, Victoria 3168, Australia.
Katherine A PillmanCentre for Cancer Biology, SA Pathology and University of South Australia, Adelaide, South Australia 5000, Australia.
Katherine J SiddleDepartment of Organismic and Evolutionary Biology, FAS Center for Systems Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
Geneviève PépinCentre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, Monash University, Clayton, Victoria 3168, Australia.ORCID 0000-0001-8625-050X
Minna-Liisa ÄnköDepartment of Anatomy and Developmental Biology, Monash University, Victoria 3800, Australia.
Claire E McCoyDepartment of Molecular and Translational Science, Monash University, Clayton, Victoria 3168, Australia.
Traude H BeilharzDevelopment and Stem Cells Program, Biomedicine Discovery Institute, Monash University, Victoria 3800, Australia.
Lluís Quintana-MurciInstitut Pasteur, Unit of Human Evolutionary Genetics, CNRS URA3012, Paris 75015, France.
Gregory J GoodallCentre for Cancer Biology, SA Pathology and University of South Australia, Adelaide, South Australia 5000, Australia.
Cameron P BrackenCentre for Cancer Biology, SA Pathology and University of South Australia, Adelaide, South Australia 5000, Australia.
Michael P GantierCentre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, Monash University, Clayton, Victoria 3168, Australia.ORCID 0000-0003-3740-698X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endogenous microRNAs (miRNAs) often exist as multiple isoforms (known as "isomiRs") with predominant variation around their 3'-end. Increasing evidence suggests that different isomiRs of the same family can have diverse functional roles, as recently demonstrated with the example of miR-222-3p 3'-end variants. While isomiR levels from a same miRNA family can vary between tissues and cell types, change of templated isomiR stoichiometry to stimulation has not been reported to date. Relying on small RNA-sequencing analyses, we demonstrate here that miR-222-3p 3'-end variants >23 nt are specifically decreased upon interferon (IFN) β stimulation of human fibroblasts, while shorter isoforms are spared. This length-dependent dynamic regulation of long miR-222-3p 3'-isoforms and >40 other miRNA families was confirmed in human monocyte-derived dendritic cells following infection with

Indexed as

Computational BiologyDendritic CellsFibroblastsGene Expression ProfilingHumansInterferon Type IMicroRNAsRNA 3' End ProcessingRNA InterferenceRNA IsoformsSalmonella InfectionsSalmonella typhimuriumSequence Analysis, RNAInterferon Type IMicroRNAsMIR222, humanRNA IsoformsinterferonisomiRmicroRNA isoformstem–loop RT-qPCRTaqman miRNA assays

Identifiers

PMID29263133
PMCPMC5824353

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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.