Evidence map›Paper›PMID 15388797›Full record

ArticleNucleic acids research2004

In silico identification of transcriptional regulators associated with c-Myc.

Ran Elkon, Karen I Zeller, Chaim Linhart, Chi V Dang, Ron Shamir, Yosef Shiloh

Open access · bronzeAbstract readEvaluation Study
In one paragraph

Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. MYC cofactors: molecular switches controlling diverse biological outcomes.Cold Spring Harbor perspectives in medicine · 2014
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Deregulation of common genes by c-Myc and its direct target, MT-MC1.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  15. Article
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

6 authors at 1 institution in 1 country.

Ran ElkonThe David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Israel.
Karen I Zeller
Chaim Linhart
Chi V Dang
Ron Shamir
Yosef Shiloh
Tel Aviv University · IL

Funding

C-MYC TARGETS IN THE PATHOGENESIS OF HUMAN CANCERSR01CA057341 · NCI · WISTAR INSTITUTE · PI DANG, CHI V. · 1992 to 2021
$8.3M
TRAINING PROGRAM IN HEMATOLOGYT32HL007525 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ROBERT A BRODSKY · 1985 to 2026
$6.2M
NCI NIH HHS R01 CA057341NCI NIH HHS R01CA057341NHLBI NIH HHS T32 HL007525NHLBI NIH HHS T32HL07525
6 · The paper itself

Abstract

The development of powerful experimental strategies for functional genomics and accompanying computational tools has brought major advances in the delineation of transcriptional networks in organisms ranging from yeast to human. Regulation of transcription of eukaryotic genes is to a large extent combinatorial. Here, we used an in silico approach to identify transcription factors (TFs) that form recurring regulatory modules with c-Myc, a protein encoded by an oncogene that is frequently disregulated in human malignancies. A recent study identified, on a genomic scale, human genes whose promoters are bound by c-Myc and its heterodimer partner Max in Burkitt's lymphoma cells. Using computational methods, we identified nine TFs whose binding-site signatures are highly overrepresented in this promoter set of c-Myc targets, pointing to possible functional links between these TFs and c-Myc. Binding sites of most of these TFs are also enriched on the set of mouse homolog promoters, suggesting functional conservation. Among the enriched TFs, there are several regulators known to control cell cycle progression. Another TF in this set, EGR-1, is rapidly activated by numerous stress challenges and plays a central role in angiogenesis. Experimental investigation confirmed that c-Myc and EGR-1 bind together on several target promoters. The approach applied here is general and demonstrates how computational analysis of functional genomics experiments can identify novel modules in complex networks of transcriptional regulation.

Indexed as

Computational BiologyGenomicsAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBasic-Leucine Zipper Transcription FactorsBinding SitesConserved SequenceDNA-Binding ProteinsEarly Growth Response Protein 1HumansImmediate-Early ProteinsMicePromoter Regions, GeneticProto-Oncogene Proteins c-mycTranscription FactorsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBasic-Leucine Zipper Transcription FactorsDNA-Binding ProteinsEarly Growth Response Protein 1EGR1 protein, humanEgr1 protein, mouseImmediate-Early ProteinsMAX protein, humanMax protein, mouseMyc associated factor XProto-Oncogene Proteins c-mycTranscription Factors

Identifiers

PMID15388797
PMCPMC521640
OpenAlexW1996493047

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.