Evidence map›Paper›PMID 20716666›Full record

ArticleGenome research2010

p53 binds preferentially to genomic regions with high DNA-encoded nucleosome occupancy.

Efrat Lidor Nili, Yair Field, Yaniv Lubling, Jonathan Widom, Moshe Oren, Eran Segal

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
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  4. Review
  5. p53motifDB: integration of genomic information and tumour suppressor p53 binding motifs.Database : the journal of biological databases and curation · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Profiling Accessible Chromatin and Nucleosomes in the Mammalian Genome.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Pioneer factors and their in vitro identification methods.Molecular genetics and genomics : MGG · 2020
    Review
  20. Article

6 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

6 authors at 2 institutions in 2 countries.

Efrat Lidor NiliDepartment of Molecular Cell Biology, The Weizmann Institute, Rehovot 76100, Israel.
Yair Field
Yaniv Lubling
Jonathan Widom
Moshe Oren
Eran Segal
Weizmann Institute of Science · ILNorthwestern University · US

Funding

TRANS-NETWORK PROJECTSU54CA143869 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WIDOM, JONATHAN · 2009 to 2013
$12.8M
Genome-wide analysis of regulated chromosomal domains: From mechanisms to cancerR01CA119176 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI REGEV, AVIV, SEGAL, ERAN · 2006 to 2015
$3.7M
Functional analysis of the p53 tumor suppressorR37CA040099 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI OREN, MOSHE · 2003 to 2012
$2.2M
NCI NIH HHS 5R01CA119176-03NCI NIH HHS R01 CA119176NCI NIH HHS R37 CA040099NCI NIH HHS R37 CA40099NCI NIH HHS U54 CA143869NCI NIH HHS U54 CA143869-01
6 · The paper itself

Abstract

The human transcription factor TP53 is a pivotal roadblock against cancer. A key unresolved question is how the p53 protein selects its genomic binding sites in vivo out of a large pool of potential consensus sites. We hypothesized that chromatin may play a significant role in this site-selection process. To test this, we used a custom DNA microarray to measure p53 binding at approximately 2000 sites predicted to possess high-sequence specificity, and identified both strongly bound and weakly bound sites. When placed within a plasmid, weakly bound sites become p53 responsive and regain p53 binding when stably integrated into random genomic locations. Notably, strongly bound sites reside preferentially within genomic regions whose DNA sequence is predicted to encode relatively high intrinsic nucleosome occupancy. Using in vivo nucleosome occupancy measurements under conditions where p53 is inactive, we experimentally confirmed this prediction. Furthermore, upon p53 activation, nucleosomes are partially displaced from a relatively broad region surrounding the bound p53 sites, and this displacement is rapidly reversed upon inactivation of p53. Thus, in contrast to the general assumption that transcription-factor binding is preferred in sites that have low nucleosome occupancy prior to factor activation, we find that p53 binding occurs preferentially within a chromatin context of high intrinsic nucleosome occupancy.

Indexed as

AnimalsBinding SitesCell LineChromatin ImmunoprecipitationGenes, p53Genome, HumanHumansMiceMolecular Sequence DataNucleosomesOligonucleotide Array Sequence AnalysisProtein BindingTumor Suppressor Protein p53NucleosomesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID20716666
PMCPMC2945185
OpenAlexW2123868608

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.