Evidence map›Paper›PMID 15331612›Full record

ArticleThe Journal of biological chemistry2004

Activator protein 2alpha associates with adenomatous polyposis coli/beta-catenin and Inhibits beta-catenin/T-cell factor transcriptional activity in colorectal cancer cells.

Qingjie Li, Roderick H Dashwood

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

32 citing papers in PubMed, 54 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

2 authors at 2 institutions in 2 countries.

Qingjie LiLinus Pauling Institute and Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon 97331-6512, USA.
Roderick H Dashwood
Linus (Norway) · NOOregon University System · US

Funding

Reducing Susceptibility to Environmental Stress Throughout the Life SpanP30ES000210 · NIEHS · OREGON STATE UNIVERSITY · PI BECKMAN, JOSEPH S · 1985 to 2015
$21.4M
Transplacental Chemoprevention of Lung Tumors and LymphomasP01CA090890 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI DASHWOOD, RODERICK H · 2003 to 2014
$14.2M
Modulation of Colon Carcinogenesis by ChlorophyllinR01CA065525 · NCI · OREGON STATE UNIVERSITY · PI DASHWOOD, RODERICK H · 2004 to 2008
$1.5M
BETA CATENIN MUTATION IN PHIP AND IQ INDUCED COLON CAR01CA080176 · NCI · OREGON STATE UNIVERSITY · PI DASHWOOD, RODERICK H · 2000 to 2004
$1.3M
MODULATION OF COLON CARCINOGENESIS BY CHLOROPHYLLINR29CA065525 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI DASHWOOD, RODERICK H · 1996 to 2000
$99k
NCI NIH HHS CA65525NCI NIH HHS CA80176NCI NIH HHS CA90890NCI NIH HHS P01 CA090890NCI NIH HHS R01 CA065525NCI NIH HHS R01 CA080176NCI NIH HHS R29 CA065525NIEHS NIH HHS P30 ES000210NIEHS NIH HHS P30 ES00210
6 · The paper itself

Abstract

In most human colorectal cancers, mutations in the adenomatous polyposis coli gene (APC) or CTNNB1 constitutively activate the beta-catenin/T-cell factor (TCF)/lymphoid enhancer factor (LEF) signaling pathway. Here, we show that the transcription factor activator protein (AP)-2alpha inhibited a beta-catenin/TCF-responsive reporter in human embryonic kidney 293 cells and in two human colorectal cancer lines, despite the fact that beta-catenin and TCF-4 protein levels were unchanged in the nucleus. Co-immunoprecipitation studies revealed that AP-2alpha formed a complex with APC and beta-catenin and that AP-2alpha disrupted beta-catenin/TCF-4 interactions in the nucleus. Thus, AP-2alpha.APC.beta-catenin complex formation appears to suppress beta-catenin transactivation by shifting the pool of nuclear beta-catenin toward an inactive form, having reduced binding to TCF/LEF transcription factors. Glutathione S-transferase pull-down assays showed that AP-2alpha physically associated with APC rather than with beta-catenin, and the AP-2alpha binding site was identified in the N terminus of APC, involving both the heptad and armadillo repeat domains, whereas the APC binding site in AP-2alpha was in the basic region of the C-terminal DNA binding domain. These findings provide the first evidence for a specific interaction between the tumor suppressor protein APC and the transcription factor AP-2alpha, and they suggest a link between the Wnt signaling pathway and various other pathways of development and differentiation associated with AP-2alpha.

Indexed as

Transcription, Geneticbeta CateninCytoskeletal ProteinsDNA-Binding ProteinsGenes, APCHCT116 CellsHT29 CellsHumansSignal TransductionTCF Transcription FactorsTrans-ActivatorsTranscription Factor 7-Like 2 ProteinTranscription Factor AP-2Transcription Factorsbeta CateninCTNNB1 protein, humanCytoskeletal ProteinsDNA-Binding ProteinsTCF7L2 protein, humanTCF Transcription FactorsTFAP2A protein, humanTrans-ActivatorsTranscription Factor 7-Like 2 ProteinTranscription Factor AP-2Transcription Factors

Identifiers

PMID15331612
PMCPMC2276578
OpenAlexW2045934284

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.