Evidence map›Paper›PMID 28628091›Full record

ArticleNature immunology2017

The BTG2-PRMT1 module limits pre-B cell expansion by regulating the CDK4-Cyclin-D3 complex.

Elmar Dolezal, Simona Infantino, Friedel Drepper, Theresa Börsig, Aparajita Singh, Thomas Wossning, Gina J Fiala, Susana Minguet, Bettina Warscheid, David M Tarlinton and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

43 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  18. Review
  19. Review
  20. Physiological genomics · 2022
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Elmar DolezalDepartment for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
Simona InfantinoWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Friedel DrepperBIOSS Centre of Biological Signalling Studies, Albert-Ludwigs University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0002-2043-5795
Theresa BörsigDepartment for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
Aparajita SinghDepartment for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
Thomas WossningMax Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Gina J FialaDepartment for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
Susana MinguetDepartment for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
Bettina WarscheidBIOSS Centre of Biological Signalling Studies, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
David M TarlintonWalter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
Hassan JumaaDepartment for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
David MedgyesiDepartment for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.ORCID http://orcid.org/0000-0002-0973-4495
Michael RethDepartment for Molecular Immunology, Faculty of Biology, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
University of Freiburg · DEThe University of Melbourne · AUMax Planck Institute of Immunobiology and Epigenetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Developing pre-B cells in the bone marrow alternate between proliferation and differentiation phases. We found that protein arginine methyl transferase 1 (PRMT1) and B cell translocation gene 2 (BTG2) are critical components of the pre-B cell differentiation program. The BTG2-PRMT1 module induced a cell-cycle arrest of pre-B cells that was accompanied by re-expression of Rag1 and Rag2 and the onset of immunoglobulin light chain gene rearrangements. We found that PRMT1 methylated cyclin-dependent kinase 4 (CDK4), thereby preventing the formation of a CDK4-Cyclin-D3 complex and cell cycle progression. Moreover, BTG2 in concert with PRMT1 efficiently blocked the proliferation of BCR-ABL1-transformed pre-B cells in vitro and in vivo. Our results identify a key molecular mechanism by which the BTG2-PRMT1 module regulates pre-B cell differentiation and inhibits pre-B cell leukemogenesis.

Indexed as

AnimalsCell Cycle CheckpointsCell DifferentiationCell ProliferationCyclin D3Cyclin-Dependent Kinase 4DNA-Binding ProteinsFlow CytometryGene Knockdown TechniquesGene Rearrangement, B-LymphocyteGenes, ablHomeodomain ProteinsImmediate-Early ProteinsImmunoglobulin Light ChainsLymphopoiesisMass SpectrometryBtg2 protein, mouseCcnd3 protein, mouseCdk4 protein, mouseCyclin D3Cyclin-Dependent Kinase 4DNA-Binding ProteinsHomeodomain ProteinsImmediate-Early ProteinsImmunoglobulin Light ChainsPrmt1 protein, mouseProtein-Arginine N-MethyltransferasesRAG-1 proteinRag2 protein, mouseRNA, Small InterferingTumor Suppressor Proteins

Identifiers

PMID28628091
OpenAlexW2643538966

What OpenQuestion holds

Textmetadata
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.