Evidence map›Paper›PMID 26372730›Full record

ArticleOncotarget2015

Genome-wide analysis of p53 transcriptional programs in B cells upon exposure to genotoxic stress in vivo.

Claudia Tonelli, Marco J Morelli, Salvatore Bianchi, Luca Rotta, Thelma Capra, Arianna Sabò, Stefano Campaner, Bruno Amati

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability.Journal of experimental & clinical cancer research : CR · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Co-Operativity between MYC and BCL-2 Pro-Survival Proteins in Cancer.International journal of molecular sciences · 2021
    Review
  11. iDEP Web Application for RNA-Seq Data Analysis.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Molecular biology of the cell · 2019
    Article
  16. The multiple mechanisms that regulate p53 activity and cell fate.Nature reviews. Molecular cell biology · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 3 institutions in 1 country.

Claudia TonelliDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan, Italy.
Marco J MorelliCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
Salvatore BianchiCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
Luca RottaDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan, Italy.
Thelma CapraDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan, Italy.
Arianna SabòCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
Stefano CampanerCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT), Milan, Italy.
Bruno AmatiDepartment of Experimental Oncology, European Institute of Oncology (IEO), Milan, Italy.
European Institute of Oncology · ITItalian Institute of Technology · ITCenter for Genomic Science · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor p53 is a transcription factor that coordinates the cellular response to DNA damage. Here we provide an integrated analysis of p53 genomic occupancy and p53-dependent gene regulation in the splenic B and non-B cell compartments of mice exposed to whole-body ionizing radiation, providing insight into general principles of p53 activity in vivo. In unstressed conditions, p53 bound few genomic targets; induction of p53 by ionizing radiation increased the number of p53 bound sites, leading to highly overlapping profiles in the different cell types. Comparison of these profiles with chromatin features in unstressed B cells revealed that, upon activation, p53 localized at active promoters, distal enhancers, and a smaller set of unmarked distal regions. At promoters, recognition of the canonical p53 motif as well as binding strength were associated with p53-dependent transcriptional activation, but not repression, indicating that the latter was most likely indirect. p53-activated targets constituted the core of a cell type-independent response, superimposed onto a cell type-specific program. Core response genes included most of the known p53-regulated genes, as well as many new ones. Our data represent a unique characterization of the p53-regulated response to ionizing radiation in vivo.

Indexed as

DNA DamageWhole-Body IrradiationAnimalsBinding SitesB-LymphocytesCells, CulturedGene Expression ProfilingGene Expression RegulationGenome-Wide Association StudyGenotypeMice, Inbred C57BLMice, KnockoutPhenotypePromoter Regions, GeneticProtein BindingRNA, MessengerRNA, MessengerTumor Suppressor Protein p53B cellschromatinDNA damagep53transcription

Identifiers

PMID26372730
PMCPMC4694782
OpenAlexW1787076101

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.