Evidence map›Paper›PMID 30524445›Full record

ArticleFrontiers in immunology2018

The c-Myc/miR17-92/PTEN Axis Tunes PI3K Activity to Control Expression of Recombination Activating Genes in Early B Cell Development.

David Benhamou, Verena Labi, Andrew Getahun, Eli Benchetrit, Reem Dowery, Klaus Rajewsky, John C Cambier, Doron Melamed

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Overview of the Different Classes of Small RNAs During B-Cell Development.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
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  3. Determination ofFrontiers in toxicology · 2024
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  19. The Role of PTEN in Innate and Adaptive Immunity.Cold Spring Harbor perspectives in medicine · 2019
    Review
  20. Article
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

8 authors at 4 institutions in 4 countries.

David BenhamouDepartment of Immunology, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Verena LabiMax Delbrück Center for Molecular Medicine, Berlin, Germany.
Andrew GetahunDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, United States.
Eli BenchetritDepartment of Immunology, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Reem DoweryDepartment of Immunology, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Klaus RajewskyMax Delbrück Center for Molecular Medicine, Berlin, Germany.
John C CambierDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, United States.
Doron MelamedDepartment of Immunology, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Technion – Israel Institute of Technology · ILUniversity of Colorado Denver · USMax Delbrück Center · DEUniversität Innsbruck · AT

Funding

Autoimmunity risk alleles compromising B cell anergyR01AI124487 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2016 to 2020
$2.5M
NIAID NIH HHS R01 AI124487
6 · The paper itself

Abstract

Appropriate PI3K signals generated by the antigen receptor are essential to promote B cell development. Regulation of recombination activating gene (RAG)-1 and RAG-2 expression is one key process that is mediated by PI3K to ensure developmental progression and selection. When PI3K signals are too high or too low, expression of RAGs does not turn off and B cell development is impaired or blocked. Yet, the mechanism which tunes PI3K activity to control RAG expression during B cell development in the bone marrow is unknown. Recently we showed that a c-Myc/miR17-92/PTEN axis regulates PI3K activity for positive and negative selection of immature B cells. Here, we show that the c-Myc/miR17-92/PTEN axis tunes PI3K activity to control the expression of RAGs in proB cells. Using different genetically engineered mouse models we show that impaired function of the c-Myc/miR17-92/PTEN axis alters the PI3K/Akt/Foxo1 pathway to result in dis-regulated expression of RAG and a block in B cell development. Studies using 38c-13 B lymphoma cells, where RAGs are constitutively expressed, suggest that this regulatory effect is mediated post-translationally through Foxo1.

Indexed as

Gene Rearrangement, B-LymphocyteAnimalsGene Expression RegulationMiceMice, TransgenicMicroRNAsPhosphatidylinositol 3-KinasesPrecursor Cells, B-LymphoidProto-Oncogene Proteins c-mycPTEN PhosphohydrolaseRecombination, GeneticMicroRNAsMIRN17-92 microRNA, mouseMyc protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-mycPTEN PhosphohydrolasePten protein, mouseB cell developmentmicroRNAPI3K–AKT pathwayPTEN (phosphatase and tensin homolog)recombination activating gene (RAG)

Identifiers

PMID30524445
PMCPMC6262168
OpenAlexW2901357179

What OpenQuestion holds

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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.