Evidence map›Paper›PMID 32071436›Full record

ReviewNature reviews. Molecular cell biology2020

Target gene-independent functions of MYC oncoproteins.

Apoorva Baluapuri, Elmar Wolf, Martin Eilers

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers.

0numbers the graph read from it
0cells of the map it votes in
208citing papers in PubMed
14.9field-weighted citation impact, top 1% 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

208 citing papers in PubMed, 303 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Targeting CDKs in the RNAPII transcription cycle.Nature reviews. Drug discovery · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Journal of the American Heart Association · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Dynamic Supercoiling Sponsors Transcription Amplification by MYC.bioRxiv : the preprint server for biology · 2026
    Article
  18. Article
  19. Article
  20. Review

148 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

3 authors at 1 institution in 1 country.

Apoorva BaluapuriTheodor Boveri Institute, Department of Biochemistry and Molecular Biology, Biocenter, University of Würzburg, Am Hubland, Würzburg, Germany.ORCID http://orcid.org/0000-0002-3723-7891
Elmar WolfTheodor Boveri Institute, Department of Biochemistry and Molecular Biology, Biocenter, University of Würzburg, Am Hubland, Würzburg, Germany.ORCID http://orcid.org/0000-0002-5299-6335
Martin EilersTheodor Boveri Institute, Department of Biochemistry and Molecular Biology, Biocenter, University of Würzburg, Am Hubland, Würzburg, Germany. martin.eilers@biozentrum.uni-wuerzburg.de.ORCID http://orcid.org/0000-0002-0376-6533
University of Würzburg · DE

Funding

European Research Council 669771European Research Council 759139
6 · The paper itself

Abstract

Oncoproteins of the MYC family are major drivers of human tumorigenesis. Since a large body of evidence indicates that MYC proteins are transcription factors, studying their function has focused on the biology of their target genes. Detailed studies of MYC-dependent changes in RNA levels have provided contrasting models of the oncogenic activity of MYC proteins through either enhancing or repressing the expression of specific target genes, or as global amplifiers of transcription. In this Review, we first summarize the biochemistry of MYC proteins and what is known (or is unclear) about the MYC target genes. We then discuss recent progress in defining the interactomes of MYC and MYCN and how this information affects central concepts of MYC biology, focusing on mechanisms by which MYC proteins modulate transcription. MYC proteins promote transcription termination upon stalling of RNA polymerase II, and we propose that this mechanism enhances the stress resilience of basal transcription. Furthermore, MYC proteins coordinate transcription elongation with DNA replication and cell cycle progression. Finally, we argue that the mechanism by which MYC proteins regulate the transcription machinery is likely to promote tumorigenesis independently of global or relative changes in the expression of their target genes.

Indexed as

Transcription, GeneticCarcinogenesisCell CycleCell ProliferationDNA ReplicationHumansNeoplasmsN-Myc Proto-Oncogene ProteinOncogene ProteinsProto-Oncogene Proteins c-mycTranscription FactorsMYCN protein, humanMYC protein, humanN-Myc Proto-Oncogene ProteinOncogene ProteinsProto-Oncogene Proteins c-mycTranscription Factors

Identifiers

PMID32071436
PMCPMC7611238
OpenAlexW3007097494

What OpenQuestion holds

Textmetadata
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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.