Evidence map›Paper›PMID 18278067›Full record

ArticleOncogene2008

Mechanisms of regulatory diversity within the p53 transcriptional network.

J M Espinosa

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2008. 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
7.3field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
  2. A molecular mechanism for the "digital" response of p53 to stress.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Article
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  5. International journal of molecular sciences · 2021
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  17. Role of the nucleus in apoptosis: signaling and execution.Cellular and molecular life sciences : CMLS · 2015
    Review
  18. Article
  19. Article
  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

1 author at 1 institution in 1 country.

J M EspinosaDepartment of Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder, Boulder, CO 80309, USA. joaquin.espinosa@colorado.edu
University of Colorado Boulder · US

Funding

Stress- and Promoter-Specific Mechanisms of Transcritpional Activation by p53R01CA117907 · NCI · UNIVERSITY OF COLORADO DENVER · PI ESPINOSA, JOAQUIN M. · 2006 to 2022
$4.4M
NCI NIH HHS R01 CA117907NCI NIH HHS R01-CA117907
6 · The paper itself

Abstract

p53 is arguably the most intensively studied protein to date, yet there is much that we ignore about its function as a transcription factor. The p53-dependent transcriptional program is remarkably flexible, as it varies with the nature of p53-activating stimuli, the cell type and the duration of the activation signal. This flexibility may allow cells to mount alternative responses to p53 activation, such as cell cycle arrest or apoptosis. Here, I organize the available data into two alternative models to explain how this regulatory diversity is achieved.

Indexed as

Models, BiologicalAnimalsApoptosisCell CycleHumansTranscription, GeneticTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID18278067
PMCPMC2914794
OpenAlexW1976010548

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.