Evidence map›Paper›PMID 29262328›Full record

ArticleCell reports2017

Association with Aurora-A Controls N-MYC-Dependent Promoter Escape and Pause Release of RNA Polymerase II during the Cell Cycle.

Gabriele Büchel, Anne Carstensen, Ka-Yan Mak, Isabelle Roeschert, Eoin Leen, Olga Sumara, Julia Hofstetter, Steffi Herold, Jacqueline Kalb, Apoorva Baluapuri and 9 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

64 citing papers in PubMed, 107 citations in OpenAlex.

  1. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. MYC: The Guardian of Its Own Chaos.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

4 more citing papers are in PubMed but not listed here.

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 at 6 institutions in 4 countries.

Gabriele BüchelTheodor Boveri Institute and Comprehensive Cancer Center Mainfranken, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Anne CarstensenTheodor Boveri Institute and Comprehensive Cancer Center Mainfranken, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Ka-Yan MakTheodor Boveri Institute and Comprehensive Cancer Center Mainfranken, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Isabelle RoeschertTheodor Boveri Institute and Comprehensive Cancer Center Mainfranken, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Eoin LeenFaculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK; University of Leicester, Leicester LE1 9HN, UK.
Olga SumaraTheodor Boveri Institute and Comprehensive Cancer Center Mainfranken, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Julia HofstetterCancer Systems Biology Group, Biochemistry and Molecular Biology, University of Würzburg, 97074 Würzburg, Germany.
Steffi HeroldTheodor Boveri Institute and Comprehensive Cancer Center Mainfranken, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Jacqueline KalbTheodor Boveri Institute and Comprehensive Cancer Center Mainfranken, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Apoorva BaluapuriCancer Systems Biology Group, Biochemistry and Molecular Biology, University of Würzburg, 97074 Würzburg, Germany.
Evon PoonDivision of Clinical Studies and Cancer Therapeutics, The Institute of Cancer Research, The Royal Marsden NHS Trust, 15 Cotswold Rd., Belmont, Sutton, Surrey SM2 5NG, UK.
Colin KwokDivision of Clinical Studies and Cancer Therapeutics, The Institute of Cancer Research, The Royal Marsden NHS Trust, 15 Cotswold Rd., Belmont, Sutton, Surrey SM2 5NG, UK.
Louis CheslerDivision of Clinical Studies and Cancer Therapeutics, The Institute of Cancer Research, The Royal Marsden NHS Trust, 15 Cotswold Rd., Belmont, Sutton, Surrey SM2 5NG, UK.
Hans Michael MaricDepartment of Drug Design and Pharmacology, Center for Biopharmaceuticals, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark.
David S RickmanWeill Cornell Medicine, Sandra and Edward Meyer Cancer Center, 413 E. 69(th) Street, New York, NY 10021, USA.
Elmar WolfCancer Systems Biology Group, Biochemistry and Molecular Biology, University of Würzburg, 97074 Würzburg, Germany.
Richard BaylissFaculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK; University of Leicester, Leicester LE1 9HN, UK.
Susanne WalzComprehensive Cancer Center Mainfranken, Core Unit Bioinformatics, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.
Martin EilersTheodor Boveri Institute and Comprehensive Cancer Center Mainfranken, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany. Electronic address: martin.eilers@biozentrum.uni-wuerzburg.de.
Comprehensive Cancer Center Mainfranken · DEUniversity of Würzburg · DEInstitute of Cancer Research · GBUniversity of Leeds · GBUniversity of Copenhagen · DKWeill Cornell Medicine · US

Funding

Cancer Research UK 18339Cancer Research UK 23302
6 · The paper itself

Abstract

MYC proteins bind globally to active promoters and promote transcriptional elongation by RNA polymerase II (Pol II). To identify effector proteins that mediate this function, we performed mass spectrometry on N-MYC complexes in neuroblastoma cells. The analysis shows that N-MYC forms complexes with TFIIIC, TOP2A, and RAD21, a subunit of cohesin. N-MYC and TFIIIC bind to overlapping sites in thousands of Pol II promoters and intergenic regions. TFIIIC promotes association of RAD21 with N-MYC target sites and is required for N-MYC-dependent promoter escape and pause release of Pol II. Aurora-A competes with binding of TFIIIC and RAD21 to N-MYC in vitro and antagonizes association of TOP2A, TFIIIC, and RAD21 with N-MYC during S phase, blocking N-MYC-dependent release of Pol II from the promoter. Inhibition of Aurora-A in S phase restores RAD21 and TFIIIC binding to chromatin and partially restores N-MYC-dependent transcriptional elongation. We propose that complex formation with Aurora-A controls N-MYC function during the cell cycle.

Indexed as

S PhaseAurora Kinase ACell Cycle ProteinsCell Line, TumorDNA-Binding ProteinsDNA, IntergenicDNA Topoisomerases, Type IIHumansN-Myc Proto-Oncogene ProteinNuclear ProteinsPhosphoproteinsPromoter Regions, GeneticProtein BindingRNA Polymerase IITranscription Elongation, GeneticTranscription Factors, TFIIIAurora Kinase ACell Cycle ProteinsDNA-Binding ProteinsDNA, IntergenicDNA Topoisomerases, Type IIN-Myc Proto-Oncogene ProteinNuclear ProteinsPhosphoproteinsRAD21 protein, humanRNA Polymerase IITranscription Factors, TFIIITranscription Factor TFIIICAurora-AMYCneuroblastomaN-MYCpause releaseRAD21TFIIIC

Identifiers

PMID29262328
PMCPMC5746598
OpenAlexW2776442772

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.