Evidence map›Paper›PMID 28484266›Full record

ArticleLeukemia2017

RNA editing signature during myeloid leukemia cell differentiation.

C Rossetti, E Picardi, M Ye, G Camilli, A M D'Erchia, L Cucina, F Locatelli, L Fianchi, L Teofili, G Pesole and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025
    Review
  6. Loss of growth differentiation factor 15 exacerbates lung injury in neonatal mice.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  7. Article
  8. Article
  9. RNA binding proteins in MLL-rearranged leukemia.Experimental hematology & oncology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

12 authors at 4 institutions in 1 country.

C RossettiDepartment of Biology and Biotechnology 'Charles Darwin', University La Sapienza, Rome, Italy.
E PicardiDepartment of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, Bari, Italy.
M YeDepartment of Biology and Biotechnology 'Charles Darwin', University La Sapienza, Rome, Italy.
G CamilliDepartment of Biology and Biotechnology 'Charles Darwin', University La Sapienza, Rome, Italy.
A M D'ErchiaDepartment of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, Bari, Italy.
L CucinaDepartment of Pediatric Oncohaematology, Bambino Gesù Children's Hospital IRCCS, Rome, Italy.
F LocatelliDepartment of Pediatric Oncohaematology, Bambino Gesù Children's Hospital IRCCS, Rome, Italy.
L FianchiInstitute of Hematology, Catholic University, Rome, Italy.
L TeofiliInstitute of Hematology, Catholic University, Rome, Italy.
G PesoleDepartment of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, Bari, Italy.ORCID 0000-0003-3663-0859
A GalloDepartment of Pediatric Oncohaematology, Bambino Gesù Children's Hospital IRCCS, Rome, Italy.
R SorrentinoDepartment of Biology and Biotechnology 'Charles Darwin', University La Sapienza, Rome, Italy.
Sapienza University of Rome · ITInstitute of Biomembranes, Bioenergetics and Molecular Biotechnologies · ITBambino Gesù Children's Hospital · ITUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenosine deaminases acting on RNA (ADARs) are key proteins for hematopoietic stem cell self-renewal and for survival of differentiating progenitor cells. However, their specific role in myeloid cell maturation has been poorly investigated. Here we show that ADAR1 is present at basal level in the primary myeloid leukemia cells obtained from patients at diagnosis as well as in myeloid U-937 and THP1 cell lines and its expression correlates with the editing levels. Upon phorbol-myristate acetate or Vitamin D3/granulocyte macrophage colony-stimulating factor (GM-CSF)-driven differentiation, both ADAR1 and ADAR2 enzymes are upregulated, with a concomitant global increase of A-to-I RNA editing. ADAR1 silencing caused an editing decrease at specific ADAR1 target genes, without, however, interfering with cell differentiation or with ADAR2 activity. Remarkably, ADAR2 is absent in the undifferentiated cell stage, due to its elimination through the ubiquitin-proteasome pathway, being strongly upregulated at the end of the differentiation process. Of note, peripheral blood monocytes display editing events at the selected targets similar to those found in differentiated cell lines. Taken together, the data indicate that ADAR enzymes play important and distinct roles in myeloid cells.

Indexed as

RNA EditingTranscriptomeAdenosine DeaminaseCell DifferentiationCell Line, TumorCholecalciferolCluster AnalysisComputational BiologyGene Expression ProfilingGene Expression Regulation, LeukemicGene OntologyGene SilencingGranulocyte-Macrophage Colony-Stimulating FactorHigh-Throughput Nucleotide SequencingHumansLeukemia, MyeloidADAR protein, humanAdenosine DeaminaseCholecalciferolGranulocyte-Macrophage Colony-Stimulating FactorRNA-Binding Proteins

Identifiers

PMID28484266
PMCPMC5729351
OpenAlexW2612851203

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.