Evidence map›Paper›PMID 16636674›Full record

ArticleOncogene2006

AP-2alpha and AP-2gamma are transcriptional targets of p53 in human breast carcinoma cells.

H Li, G S Watts, M M Oshiro, B W Futscher, F E Domann

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

H LiDepartment of Radiation Oncology, Free Radical and Radiation Biology Program, University of Iowa, Iowa City, IA 52242, USA.
G S Watts
M M Oshiro
B W Futscher
F E Domann
University of Arizona · USUniversity of Iowa · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI George S Watts · 1994 to 2026
$36.7M
THERAPIES BASED ON ANTIOXIDANT ENZYME MODULATIONP01CA066081 · NCI · UNIVERSITY OF IOWA · PI OBERLEY, LARRY · 1996 to 2005
$7.7M
Genomic Methylation--Mechanism to Alter Tumor PhenotypesR01CA065662 · NCI · UNIVERSITY OF ARIZONA · PI FUTSCHER, BERNARD W · 2001 to 2009
$2.3M
Epigenetic factors governing SOD2 gene expressionR01CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2003 to 2007
$1.3M
DNA METHYLATION AND SOD2/MNSOD GENE EXPRESSIONR29CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 1998 to 2002
$321k
Chromatin Remodeling and SOD2 Expression in CancerR56CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2009 to 2009
$266k
GENOMIC METHYLATION--A MECHANISM TO ALTER PHENOTYPESR29CA065662 · NCI · UNIVERSITY OF ARIZONA · PI FUTSCHER, BERNARD W · 1996 to 2000
$106k
NCI NIH HHS CA65662NCI NIH HHS CA66081NCI NIH HHS CA73612NCI NIH HHS P30 CA023074NIEHS NIH HHS P30 ES006694
6 · The paper itself

Abstract

Activating enhancer-binding protein 2alpha (AP-2alpha) and activating enhancer-binding protein 2gamma (AP-2gamma) are transcription factors that bind GC-rich consensus sequences and regulate the expression of many downstream genes. AP-2alpha and AP-2gamma interact with p53 both physically and functionally. Expression microarray results in human breast carcinoma cells with forced p53 expression revealed AP-2gamma as a putative transcriptional target of p53. To confirm and extend these findings we measured the effects of forced p53 expression in human breast carcinoma cells by real-time reverse transcription-PCR, Western blotting, electrophoretic gel mobility shift assays, promoter reporter, chromatin immunoprecipitation and chromatin accessibility assays. Wild-type p53 expression rapidly induced not only AP-2gamma but also AP-2alpha mRNA. The subsequent increase in these proteins led to increased AP-2 DNA-binding and transactivating activity. Candidate p53-binding sites were identified in the AP-2alpha and AP-2gamma promoters. p53 binding to these cis-elements in vivo was also observed, together with a relaxation of chromatin structure in these regions. Finally, expression of either AP-2alpha or gamma inhibited growth of human breast carcinoma cells in vitro. Taken together, our findings indicate that these AP-2 genes are targets for transcriptional activation by p53 and suggest that AP-2 proteins may mediate some of the downstream effects of p53 expression such as inhibition of proliferation.

Indexed as

Genes, p53AdenocarcinomaBreast NeoplasmsCell DivisionCell Line, TumorDNA PrimersFemaleGenes, ReporterHumansOligonucleotide Array Sequence AnalysisPlasmidsReverse Transcriptase Polymerase Chain ReactionTranscription Factor AP-2Transcription, GeneticTransfectionDNA PrimersTranscription Factor AP-2

Identifiers

PMID16636674
OpenAlexW1972646045

What Socratic 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 Socratic graph.