Evidence map›Paper›PMID 30273347›Full record

ArticlePloS one2018

The DEAD-box RNA-binding protein DDX6 regulates parental RNA decay for cellular reprogramming to pluripotency.

Daisuke Kami, Tomoya Kitani, Akihiro Nakamura, Naoki Wakui, Rena Mizutani, Masahito Ohue, Fuyuki Kametani, Nobuyoshi Akimitsu, Satoshi Gojo

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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. YTHDF2 destabilizes mRNA (New York, N.Y.) · 2020
    Article
  9. Article
  10. Article
  11. Small changes, big implications: The impact of mBiochimica et biophysica acta. Gene regulatory mechanisms · 2019
    Review
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 4 institutions in 1 country.

Daisuke KamiDepartment of Regenerative Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tomoya KitaniDepartment of Cardiovascular Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Akihiro NakamuraDepartment of Pediatric Cardiology and Nephrology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Naoki WakuiDepartment of Computer Science, School of Computing, Tokyo Institute of Technology, Tokyo, Japan.
Rena MizutaniRadioisotope Center, The University of Tokyo, Tokyo, Japan.
Masahito OhueDepartment of Computer Science, School of Computing, Tokyo Institute of Technology, Tokyo, Japan.ORCID 0000-0002-0120-1643
Fuyuki KametaniDepartment of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Nobuyoshi AkimitsuRadioisotope Center, The University of Tokyo, Tokyo, Japan.
Satoshi GojoDepartment of Regenerative Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.ORCID 0000-0001-8115-7816
Kyoto Prefectural University of Medicine · JPJapan Radioisotope Association · JPTokyo Institute of Technology · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular transitions and differentiation processes require mRNAs supporting the new phenotype but also the clearance of existing mRNAs for the parental phenotype. Cellular reprogramming from fibroblasts to induced pluripotent stem cells (iPSCs) occurs at the early stage of mesenchymal epithelial transition (MET) and involves drastic morphological changes. We examined the molecular mechanism for MET, focusing on RNA metabolism. DDX6, an RNA helicase, was indispensable for iPSC formation, in addition to RO60 and RNY1, a non-coding RNA, which form complexes involved in intracellular nucleotide sensing. RO60/RNY1/DDX6 complexes formed prior to processing body formation, which is central to RNA metabolism. The abrogation of DDX6 expression inhibited iPSC generation, which was mediated by RNA decay targeting parental mRNAs supporting mesenchymal phenotypes, along with microRNAs, such as miR-302b-3p. These results show that parental mRNA clearance is a prerequisite for cellular reprogramming and that DDX6 plays a central role in this process.

Indexed as

Cellular ReprogrammingDEAD-box RNA HelicasesEpithelial-Mesenchymal TransitionFibroblastsGene ExpressionGene Expression Regulation, DevelopmentalHumansImmunoprecipitationInduced Pluripotent Stem CellsMicroRNAsProto-Oncogene ProteinsRibonucleoproteinsRNA, Small InterferingRNA StabilityRNA, UntranslatedSS-A AntigenDDX6 protein, humanDEAD-box RNA HelicasesMicroRNAsMIRN302A microRNA, humanProto-Oncogene ProteinsRibonucleoproteinsRNA, Small InterferingRNA, UntranslatedSS-A Antigen

Identifiers

PMID30273347
PMCPMC6166933
OpenAlexW2895514652

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.