Evidence map›Paper›PMID 29844320›Full record

ArticleNature communications2018

Tumour-associated missense mutations in the dMi-2 ATPase alters nucleosome remodelling properties in a mutation-specific manner.

Kristina Kovač, Anja Sauer, Igor Mačinković, Stephan Awe, Florian Finkernagel, Helen Hoffmeister, Andreas Fuchs, Rolf Müller, Christina Rathke, Gernot Längst and 1 more

Open access · goldAbstract 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Human mutation · 2026
    Review
  4. NuRD chromatin remodeling is required to repair exogenous DSBs in thebioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. How does CHD4 slide nucleosomes?Biochemical Society transactions · 2024
    Review
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  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
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  19. Article
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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

11 authors at 2 institutions in 1 country.

Kristina KovačInstitute for Molecular Biology and Tumour Research, University of Marburg, 35043, Marburg, Germany.ORCID http://orcid.org/0000-0002-6962-8790
Anja SauerInstitute for Molecular Biology and Tumour Research, University of Marburg, 35043, Marburg, Germany.
Igor MačinkovićInstitute for Molecular Biology and Tumour Research, University of Marburg, 35043, Marburg, Germany.
Stephan AweInstitute for Molecular Biology and Tumour Research, University of Marburg, 35043, Marburg, Germany.
Florian FinkernagelInstitute for Molecular Biology and Tumour Research, University of Marburg, 35043, Marburg, Germany.ORCID http://orcid.org/0000-0002-1141-7499
Helen HoffmeisterInstitute of Biochemistry, Genetics and Microbiology, University of Regensburg, 93053, Regensburg, Germany.
Andreas FuchsInstitute of Biochemistry, Genetics and Microbiology, University of Regensburg, 93053, Regensburg, Germany.ORCID http://orcid.org/0000-0002-7230-4121
Rolf MüllerInstitute for Molecular Biology and Tumour Research, University of Marburg, 35043, Marburg, Germany.
Christina RathkeDepartment of Biology, Philipps-University Marburg, Karl-von-Frisch-Straße 8, 35043, Marburg, Germany.
Gernot LängstInstitute of Biochemistry, Genetics and Microbiology, University of Regensburg, 93053, Regensburg, Germany.
Alexander BrehmInstitute for Molecular Biology and Tumour Research, University of Marburg, 35043, Marburg, Germany. brehm@imt.uni-marburg.de.
Philipps University of Marburg · DEUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATP-dependent chromatin remodellers are mutated in more than 20% of human cancers. The consequences of these mutations on enzyme function are poorly understood. Here, we characterise the effects of CHD4 mutations identified in endometrial carcinoma on the remodelling properties of dMi-2, the highly conserved Drosophila homologue of CHD4. Mutations from different patients have surprisingly diverse defects on nucleosome binding, ATPase activity and nucleosome remodelling. Unexpectedly, we identify both mutations that decrease and increase the enzyme activity. Our results define the chromodomains and a novel regulatory region as essential for nucleosome remodelling. Genetic experiments in Drosophila demonstrate that expression of cancer-derived dMi-2 mutants misregulates differentiation of epithelial wing structures and produces phenotypes that correlate with their nucleosome remodelling properties. Our results help to define the defects of CHD4 in cancer at the mechanistic level and provide the basis for the development of molecular approaches aimed at restoring their activity.

Indexed as

Adenosine TriphosphatasesAdenosine TriphosphateAnimalsAutoantigensCell LineDisease Models, AnimalDNA-Binding ProteinsDrosophilaDrosophila ProteinsEndometrial NeoplasmsFemaleHumansMi-2 Nucleosome Remodeling and Deacetylase ComplexMutation, MissenseNucleosomesProtein BindingAdenosine TriphosphatasesAdenosine TriphosphateAutoantigensCHD4 protein, humanDNA-Binding ProteinsDrosophila ProteinsMi-2 Nucleosome Remodeling and Deacetylase ComplexMi-2 protein, DrosophilaNucleosomes

Identifiers

PMID29844320
PMCPMC5974244
OpenAlexW2806339888

What OpenQuestion holds

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Registered trials

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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.