Evidence map›Paper›PMID 30575719›Full record

ArticleNature communications2018

A miR-150/TET3 pathway regulates the generation of mouse and human non-classical monocyte subset.

Dorothée Selimoglu-Buet, Julie Rivière, Hussein Ghamlouch, Laura Bencheikh, Catherine Lacout, Margot Morabito, M'boyba Diop, Guillaume Meurice, Marie Breckler, Aurélie Chauveau and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

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  17. Mouse Models of CMML.International journal of molecular sciences · 2021
    Review
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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

19 authors.

Dorothée Selimoglu-BuetINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France. dorothee.selimoglubuet@gustaveroussy.fr.ORCID http://orcid.org/0000-0002-3565-2709
Julie RivièreINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Hussein GhamlouchINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Laura BencheikhINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Catherine LacoutINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Margot MorabitoINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
M'boyba DiopINSERM US23, CNRS UMS 3655, Gustave Roussy Cancer Center, 94805, Villejuif, France.ORCID http://orcid.org/0000-0002-7849-4405
Guillaume MeuriceINSERM US23, CNRS UMS 3655, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Marie BrecklerINSERM US23, CNRS UMS 3655, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Aurélie ChauveauINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Camille DebordINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Franck DebeurmeINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Raphael ItzyksonINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Nicolas ChapuisDépartement d'Immuno-Hématologie, Institut Cochin, 75014, Paris, France.
Christophe WillekensINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.ORCID http://orcid.org/0000-0001-9814-8537
Orianne Wagner-BallonDépartement d'Hématologie et d'Immunologie Biologiques, Hôpital Henri-Mondor, 94010, Créteil, France.
Olivier A BernardINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.
Nathalie DroinINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France.ORCID http://orcid.org/0000-0002-6099-5324
Eric SolaryINSERM U1170, Gustave Roussy Cancer Center, 94805, Villejuif, France. eric.solary@gustaveroussy.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-classical monocyte subsets may derive from classical monocyte differentiation and the proportion of each subset is tightly controlled. Deregulation of this repartition is observed in diverse human diseases, including chronic myelomonocytic leukemia (CMML) in which non-classical monocyte numbers are significantly decreased relative to healthy controls. Here, we identify a down-regulation of hsa-miR-150 through methylation of a lineage-specific promoter in CMML monocytes. Mir150 knock-out mice demonstrate a cell-autonomous defect in non-classical monocytes. Our pulldown experiments point to Ten-Eleven-Translocation-3 (TET3) mRNA as a hsa-miR-150 target in classical human monocytes. We show that Tet3 knockout mice generate an increased number of non-classical monocytes. Our results identify the miR-150/TET3 axis as being involved in the generation of non-classical monocytes.

Indexed as

AnimalsDioxygenasesDNA-Binding ProteinsDNA MethylationDown-RegulationFemaleGene Expression Regulation, LeukemicHumansK562 CellsLeukemia, Myelomonocytic, ChronicMaleMiceMice, KnockoutMicroRNAsMonocytesPrimary Cell CultureDioxygenasesDNA-Binding ProteinsMicroRNAsMIR150, humanMirn150 microRNA, mouseProto-Oncogene ProteinsTET3 protein, humanTet3 protein, mouse

Identifiers

PMID30575719
PMCPMC6303340

What OpenQuestion holds

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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.