Evidence map›Paper›PMID 41659653›Full record

ArticlebioRxiv : the preprint server for biology2026

Dynamic Supercoiling Sponsors Transcription Amplification by MYC.

Rajiv Kumar Jha, Fedor Kouzine, Bo Wang, James D Phelan, Subhendu K Das, Brian A Lewis, David Levens

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Rajiv Kumar JhaGene Regulation Section, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD 20892-1500, USA.ORCID 0000-0001-7439-1321
Fedor KouzineGene Regulation Section, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD 20892-1500, USA.
Bo WangGene Regulation Section, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD 20892-1500, USA.
James D PhelanLymphoid Malignancies Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1500, USA.
Subhendu K DasGene Regulation Section, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD 20892-1500, USA.
Brian A LewisGene Regulation Section, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD 20892-1500, USA.
David LevensGene Regulation Section, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute (NCI), Bethesda, MD 20892-1500, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MYC dysregulation occurs in most cancers provoking, profound changes in gene expression. Although sometimes considered to be an E-box-dependent transcription factor, an alternate model posits MYC to be a universal amplifier of active genes. Although MYC is associated with accelerated pause release, the full extent of its participation in the transcription cycle remains poorly illuminated. MYC also stimulates topoisomerases to resolve topological issues that complicate DNA transactions; whether and how this stimulation is coordinated with or independent of its transcriptional role has not been examined. We have developed a genetic tool that discriminates between MYC's ability to activate versus amplify reporter gene expression in any cell. This system enables the interrogation of genes, cofactors, and compounds that execute or modulate MYC activity. Using a combination of biochemical and cellular assays, we reveal the dynamic interplay between MYC-driven transcription amplification and DNA supercoiling. The early stages of transcription are highly sensitive to the level of DNA supercoiling. Reducing the activity of TOP1 either through genetic knockdown or low-dose inhibition potentiates transcription amplification by MYC. This enhancement is associated with pre-initiation complex (PIC) stabilization by DNA supercoiling. MYC helps to mobilize these stabilized PICs.

Indexed as

DNA supercoilingMYCTopoisomeraseTranscription-Amplifier

Identifiers

PMID41659653
PMCPMC12879662

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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.