Evidence map›Paper›PMID 21084835›Full record

ArticleCell cycle (Georgetown, Tex.)2010

Dual association by TFAP2A during activation of the p21cip/CDKN1A promoter.

Angelo G Scibetta, Ping-Pui Wong, KaYi V Chan, Monica Canosa, Helen C Hurst

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

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  13. Genetics of aplasia cutis reveal novel regulators of skin morphogenesis.The Journal of investigative dermatology · 2015
    Review
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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 1 institution in 1 country.

Angelo G ScibettaCentre for Tumour iology, Institute of Cancer, London, UK.
Ping-Pui Wong
KaYi V Chan
Monica Canosa
Helen C Hurst
Queen Mary University of London · GB

Funding

Cancer Research UK C6775/A6250
6 · The paper itself

Abstract

The cyclin-dependent kinase inhibitor p21cip/CDKN1A is induced to promote growth arrest in response to a variety of stimuli in normal cells and loss of correct regulation of this gene is frequently observed in cancer. In particular, the upregulation of CDKN1A by p53 is considered to be a central mechanism of tumour suppression. Other transcription factors with tumour suppressor activity can also regulate CDKN1A, including the developmentally regulated factor, TFAP2A. Here we identify a novel AP-2 binding site within the proximal promoter of the CDKN1A gene and show this is required for optimal, p53-independent expression of p21cip/CDKN1A. We further describe a non-tumourgenic breast epithelial cell line model to study the role of endogenous TFAP2A and p53 in the control of drug-induced p21cip expression using ChIP. Maximal expression of CDKN1A requires TFAP2A which binds to two regions of the promoter: the proximal region where the AP-2 site lies and upstream near the major p53 binding site. The pattern of binding alters with time post-induction, with the proximal, p53-independent site becoming more important at later stages of p21cip induction. This pattern of promoter interaction by TFAP2A is distinct from that seen for the TFAP2C family member which represses CDKN1A expression.

Indexed as

Promoter Regions, GeneticBase SequenceBinding SitesCell Line, TumorChromatin ImmunoprecipitationCyclin-Dependent Kinase Inhibitor p21HumansProtein BindingTranscription Factor AP-2Tumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p21TFAP2A protein, humanTranscription Factor AP-2Tumor Suppressor Protein p53

Identifiers

PMID21084835
PMCPMC3048049
OpenAlexW1963744470

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.