Evidence map›Paper›PMID 22513088›Full record

ArticleMolecular biology of the cell2012

Regulation of Wnt signaling by the tumor suppressor adenomatous polyposis coli does not require the ability to enter the nucleus or a particular cytoplasmic localization.

David M Roberts, Mira I Pronobis, John S Poulton, Eric G Kane, Mark Peifer

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 30 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.

David M RobertsDepartment of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280, USA.
Mira I Pronobis
John S Poulton
Eric G Kane
Mark Peifer
University of North Carolina at Chapel Hill · USFranklin & Marshall College · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Integrated Training in Cancer Model SystemsT32CA009156 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1985 to 2020
$19.7M
A model system to study the tumor suppressor APCR01GM067236 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PEIFER, MARK A. · 2002 to 2015
$2.8M
Mechanisms of Armadillo/Beta-catenin degradationF32GM076898 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERTS, DAVID M · 2006 to 2008
$145k
Drosophila APC as a Model for Cytoskeletal Regulation and Cancer BiologyF32GM095127 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI POULTON, JOHN SHAW · 2010 to 2011
$99k
NCI NIH HHS P30 CA016086NCI NIH HHS T32 CA 009156NCI NIH HHS T32 CA009156NIGMS NIH HHS F32 GM-076898NIGMS NIH HHS F32 GM076898NIGMS NIH HHS F32 GM-095127NIGMS NIH HHS F32 GM095127NIGMS NIH HHS R01 GM067236NIGMS NIH HHS R01 GM67236
6 · The paper itself

Abstract

Wnt signaling plays key roles in development and disease. The tumor suppressor adenomatous polyposis coli (APC) is an essential negative regulator of Wnt signaling. Its best-characterized role is as part of the destruction complex, targeting the Wnt effector β-catenin (βcat) for phosphorylation and ultimate destruction, but several studies suggested APC also may act in the nucleus at promoters of Wnt-responsive genes or to shuttle βcat out for destruction. Even in its role in the destruction complex, APC's mechanism of action remains mysterious. We have suggested APC positions the destruction complex at the appropriate subcellular location, facilitating βcat destruction. In this study, we directly tested APC's proposed roles in the nucleus or in precisely localizing the destruction complex by generating a series of APC2 variants to which we added tags relocalizing otherwise wild-type APC to different cytoplasmic locations. We tested these for function in human colon cancer cells and Drosophila embryos. Strikingly, all rescue Wnt regulation and down-regulate Wnt target genes in colon cancer cells, and most restore Wnt regulation in Drosophila embryos null for both fly APCs. These data suggest that APC2 does not have to shuttle into the nucleus or localize to a particular subcellular location to regulate Wnt signaling.

Indexed as

Wnt Signaling PathwayActive Transport, Cell NucleusAnimalsArmadillo Domain Proteinsbeta CateninCell LineageCell Line, TumorCell MembraneCell NucleusColorectal NeoplasmsCytoskeletal ProteinsDown-RegulationDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianFatty Acids, Unsaturatedadenomatous polyposis coli protein 2Armadillo Domain ProteinsARM protein, Drosophilabeta CateninCytoskeletal ProteinsDrosophila ProteinsFatty Acids, Unsaturatedleptomycin BMutant ProteinsNuclear Localization SignalsTCF Transcription FactorsTranscription Factors

Identifiers

PMID22513088
PMCPMC3364170
OpenAlexW2093069227

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.