Evidence map›Paper›PMID 36709354›Full record

ArticleLeukemia2023

The histone demethylase JMJD2C constitutes a novel NFE2 target gene that is required for the survival of JAK2

Anne Marie Staehle, Jan Caspar Peeken, Georg Vladimirov, Mirjam Elisabeth Hoeness, Sarolta Bojtine Kovacs, Nikolaos Karantzelis, Albert Gruender, Christoph Koellerer, Jonas Samuel Jutzi, Heike Luise Pahl and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  6. KDM4 Demethylases: Structure, Function, and Inhibitors.Advances in experimental medicine and biology · 2023
    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

11 authors at 2 institutions in 2 countries.

Anne Marie StaehleDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
Jan Caspar PeekenDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
Georg VladimirovDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.ORCID http://orcid.org/0000-0003-0056-8803
Mirjam Elisabeth HoenessDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
Sarolta Bojtine KovacsDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
Nikolaos KarantzelisDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
Albert GruenderDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
Christoph KoellererDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
Jonas Samuel JutziDivision of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.ORCID http://orcid.org/0000-0002-1977-153X
Heike Luise Pahl *Division of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany. heike.pahl@klinikum.uni-freiburg.de.ORCID http://orcid.org/0000-0003-2857-2396
Hans Felix Staehle *Division of Molecular Hematology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg im Breisgau, Germany.
University of Freiburg · DEBrigham and Women's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor NFE2 is overexpressed in most patients with myeloproliferative neoplasms (MPN). Moreover, mutations in NFE2, found in a subset of MPN patients, strongly predispose for transformation to acute leukemia. Transgenic mice overexpressing NFE2 as well as mice harboring NFE2 mutations display an MPN phenotype and spontaneously develop leukemia. However, the molecular mechanisms effecting NFE2-driven leukemic transformation remain incompletely understood. Here we show that the pro-leukemic histone demethylase JMJD2C constitutes a novel NFE2 target gene. JMJD2C expression is elevated in MPN patients as well as in NFE2 transgenic mice. Moreover, we show that loss of JMJD2C selectively impairs proliferation of JAK2

Indexed as

Leukemia, Myeloid, AcuteMyeloproliferative DisordersAnimalsGene Expression RegulationHistone DemethylasesHumansJanus Kinase 2Jumonji Domain-Containing Histone DemethylasesMiceMice, TransgenicMutationNF-E2 Transcription Factor, p45 SubunitHistone DemethylasesJanus Kinase 2Jmjd2c protein, mouseJumonji Domain-Containing Histone DemethylasesKDM4C protein, humanNfe2 protein, mouseNF-E2 Transcription Factor, p45 Subunit

Identifiers

PMID36709354
PMCPMC10079541
OpenAlexW4318339173

What OpenQuestion holds

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LicenceCC BY
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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.