Evidence map›Paper›PMID 21623162›Full record

ArticleCell cycle (Georgetown, Tex.)2011

Kinetic profiling of the c-Myc transcriptome and bioinformatic analysis of repressed gene promoters.

Chui-Sun Yap, Abigail L Peterson, Gastone Castellani, John M Sedivy, Nicola Neretti

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Gene Transactivation and Transrepression in MYC-Driven Cancers.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Review
  12. Policing Cancer: Vitamin D Arrests the Cell Cycle.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. Review
  16. Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis.Journal of experimental & clinical cancer research : CR · 2018
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

Chui-Sun YapDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA.
Abigail L Peterson
Gastone Castellani
John M Sedivy
Nicola Neretti
Brown University · US

Funding

WNT SIGNALING IN HEPATOCELLULAR CARCINOMAP20RR015578 · NCRR · BROWN UNIVERSITY · PI KIM, MIRAN · 2000 to 2009
$22.8M
Effectors of cellular senescence statesR37AG016694 · NIA · BROWN UNIVERSITY · PI SEDIVY, JOHN M · 2009 to 2018
$3.2M
Computational Biology of Transcriptional Networks in AgingK25AG028753 · NIA · BROWN UNIVERSITY · PI NERETTI, NICOLA · 2007 to 2011
$693k
NCRR NIH HHS P20 RR015578NIA NIH HHS K25 AG028753NIA NIH HHS R37 AG016694NIGMS NIH HHS R01 GM040960
6 · The paper itself

Abstract

Mammalian c-Myc is a member of a small family of three related proto-oncogenic transcription factors. c-Myc has an unusually broad array of regulatory functions, which include roles in cell cycle and apoptosis, a variety of metabolic functions, cell differentiation, senescence, and stem cell maintenance. c-Myc modulates the expression of a very large number of genes, but the magnitude of the majority of the regulatory effects is only 2-fold or less. c-Myc can both activate and repress the promoters of its target genes. Identification of genes directly regulated by c-Myc has been an enduring question in the field. We report here microarray expression profiling of a high resolution time course of c-Myc induction, using fibroblast cells in which c-Myc activity can be modulated from null to physiological. The c-Myc transcriptome dataset presented is the largest reported to date with 4,186 differentially regulated genes (1,826 upregulated, 2,360 downregulated, 1% FDR). The gene expression patterns fit well with the known biological functions of c-Myc. We describe several novel findings and present tools for further data mining. Although the mechanisms of transcriptional activation by c-Myc are well understood, how c-Myc represses an even greater number of genes remains incompletely described. One mechanism involves the binding of c-Myc to other, positively acting transcription factors, and interfering with their activities. We identified rapid-response genes likely to be direct c-Myc targets, and analyzed the promoters of the repressed genes to identify transcription factors that could be targets of c-Myc repression.

Indexed as

Gene Expression RegulationPromoter Regions, GeneticTranscriptomeAnimalsAntineoplastic Agents, HormonalCell LineCitric Acid CycleComputational BiologyFibroblastsGene ExpressionGene Expression ProfilingMicroarray AnalysisMultigene FamilyProto-Oncogene Proteins c-mycRatsSignal TransductionAntineoplastic Agents, HormonalProto-Oncogene Proteins c-mycTamoxifen

Identifiers

PMID21623162
PMCPMC3154366
OpenAlexW2039181243

What OpenQuestion holds

Textmetadata
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.