Evidence map›Paper›PMID 20080630›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Estrogen receptor acting in cis enhances WT and mutant p53 transactivation at canonical and noncanonical p53 target sequences.

Daniel Menendez, Alberto Inga, Michael A Resnick

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 47 citations in OpenAlex.

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  12. SRC IncreasesMolecular and cellular biology · 2018
    Article
  13. Diverse p53/DNA binding modes expand the repertoire of p53 response elements.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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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

3 authors at 1 institution in 1 country.

Daniel MenendezLaboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Alberto Inga
Michael A Resnick
National Institutes of Health · US

Funding

Human Genes Affecting Chromosome Metabolism and Stress ResponseZIAES065079 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MENENDEZ RENDON, DANIEL · 2009 to 2021
$12.5M
ISOLATION &CHARACTERIZATION OF GENES AFFECTING YEAST CHROMOSOME METABOLISMZ01ES065079 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RESNICK, MICHAEL A · 1994 to 2008
$1.8M
Intramural NIH HHS Z01 ES065079
6 · The paper itself

Abstract

p53 is a master regulatory, sequence-specific transcription factor that directly controls expression of over 100 genes in response to various stress signals. Transactivation is generally considered to occur through p53 binding to a consensus response element (RE) composed of two 5'-RRRCWWGYYY-3' decamers. Recently, studying the human angiogenesis-related gene FLT1 we discovered that p53 can mediate limited transactivation at a noncanonical 1/2 site and could synergize with the estrogen receptor (ER) acting in cis at a nearby ER 1/2 site. To address the generality of concerted transactivation by p53 and ER, the 1/2 site in the FLT1 promoter was replaced with a variety of 1/2 sites, as well as canonical weak and strong p53 REs of human target genes. The p53 transactivation of all tested sequences was greatly enhanced by ligand-activated ER acting in cis. Furthermore, enhanced transactivation extends to several cancer-associated p53 mutants with altered function, suggesting ER-dependent mutant p53 activity for at least some REs. The enhanced transactivation was also found with p63 and p73. We propose a general synergistic relationship between p53 family and ER master regulators in transactivation of p53 target canonical and noncanonical REs, which might be poorly responsive to p53 on their own. This relationship greatly expands the transcriptional master network regulated by p53 in terms of genes affected and levels of expression and has implications for the appearance and possible treatments of cancer.

Indexed as

MutationTranscriptional ActivationBase SequenceCell Line, TumorEstrogen Receptor alphaEstrogen Receptor betaGene Expression Regulation, NeoplasticHumansNeoplasmsProtein BindingResponse ElementsTumor Suppressor Protein p53Vascular Endothelial Growth Factor Receptor-1ESR1 protein, humanEstrogen Receptor alphaEstrogen Receptor betaFLT1 protein, humanTP53 protein, humanTumor Suppressor Protein p53Vascular Endothelial Growth Factor Receptor-1

Identifiers

PMID20080630
PMCPMC2824383
OpenAlexW2035435589

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.