Evidence map›Paper›PMID 22346748›Full record

ArticlePLoS pathogens2012

Degradation of cellular mir-27 by a novel, highly abundant viral transcript is important for efficient virus replication in vivo.

Lisa Marcinowski, Mélanie Tanguy, Astrid Krmpotic, Bernd Rädle, Vanda J Lisnić, Lee Tuddenham, Béatrice Chane-Woon-Ming, Zsolt Ruzsics, Florian Erhard, Corinna Benkartek and 7 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

136 citing papers in PubMed, 208 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Target-Directed miRNA Degradation: Mechanisms and Significance.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

76 more citing papers are in PubMed but not listed here.

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

17 authors at 7 institutions in 5 countries.

Lisa MarcinowskiMax von Pettenkofer-Institute, Ludwig-Maximilians-University Munich, Munich, Germany.
Mélanie Tanguy
Astrid Krmpotic
Bernd Rädle
Vanda J Lisnić
Lee Tuddenham
Béatrice Chane-Woon-Ming
Zsolt Ruzsics
Florian Erhard
Corinna Benkartek
Marina Babic
Ralf Zimmer
Joanne Trgovcich
Ulrich H Koszinowski
Stipan Jonjic
Sébastien Pfeffer
Lars Dölken
Ludwig-Maximilians-Universität München · DEUniversity of Rijeka · HRArchitecture et Réactivité de l'arN · FRUniversité de Strasbourg · FRMedizinische Hochschule Hannover · DEThe Ohio State University · USUniversity of Cambridge · GB

Funding

Viral evasion of NK cellsR01AI083201 · NIAID · UNIVERSITY OF RIJEKA--MEDICAL FACULTY · PI JONJIC, STIPAN · 2009 to 2012
$331k
European Research Council 260767Medical Research Council G1002523Medical Research Council RG65594NIAID NIH HHS 1R01AI083201-01NIAID NIH HHS R01 AI083201Wellcome Trust 092096
6 · The paper itself

Abstract

Cytomegaloviruses express large amounts of viral miRNAs during lytic infection, yet, they only modestly alter the cellular miRNA profile. The most prominent alteration upon lytic murine cytomegalovirus (MCMV) infection is the rapid degradation of the cellular miR-27a and miR-27b. Here, we report that this regulation is mediated by the ∼1.7 kb spliced and highly abundant MCMV m169 transcript. Specificity to miR-27a/b is mediated by a single, apparently optimized, miRNA binding site located in its 3'-UTR. This site is easily and efficiently retargeted to other cellular and viral miRNAs by target site replacement. Expression of the 3'-UTR of m169 by an adenoviral vector was sufficient to mediate its function, indicating that no other viral factors are essential in this process. Degradation of miR-27a/b was found to be accompanied by 3'-tailing and -trimming. Despite its dramatic effect on miRNA stability, we found this interaction to be mutual, indicating potential regulation of m169 by miR-27a/b. Most interestingly, three mutant viruses no longer able to target miR-27a/b, either due to miRNA target site disruption or target site replacement, showed significant attenuation in multiple organs as early as 4 days post infection, indicating that degradation of miR-27a/b is important for efficient MCMV replication in vivo.

Indexed as

3' Untranslated RegionsAnimalsArgonaute ProteinsBinding SitesCell LineCytomegalovirus InfectionsDown-RegulationGene Expression RegulationHigh-Throughput Nucleotide SequencingHumansMiceMice, Inbred BALB CMice, SCIDMicroRNAsMuromegalovirusMutation3' Untranslated RegionsAgo2 protein, mouseArgonaute ProteinsMicroRNAsMirn27 microRNA, mouseRNA, Viral

Identifiers

PMID22346748
PMCPMC3276556
OpenAlexW1998318447

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.