Evidence map›Paper›PMID 11689703›Full record

ArticleMolecular and cellular biology2001

Cell density and phosphorylation control the subcellular localization of adenomatous polyposis coli protein.

F Zhang, R L White, K L Neufeld

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. 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
2.5field-weighted citation impact, top 10% 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, 70 citations in OpenAlex.

  1. Review
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  11. Aryl hydrocarbon receptor suppresses intestinal carcinogenesis in ApcMin/+ mice with natural ligands.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  12. Article
  13. A flow cytometric assay for the study of E3 ubiquitin ligase activity.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2009
    Article
  14. Article
  15. Article
  16. Nuclear APC.Advances in experimental medicine and biology · 2009
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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.

F ZhangDepartment of Oncological Sciences, University of Utah, Salt Lake City, Utah 84112, USA.
R L White
K L Neufeld
University of Utah · US

Funding

TCF/LEF function during intestinal maintenance and colon tumorigenesisP01CA073992 · NCI · UNIVERSITY OF UTAH · PI NEKLASON, DEBORAH WOOD · 1998 to 2014
$29.7M
NCI NIH HHS 5PO1 CA73992-02NCI NIH HHS P01 CA073992
6 · The paper itself

Abstract

Loss of functional adenomatous polyposis coli protein (APC) leads to uncontrolled proliferation of colonic epithelial cells, as evidenced by polyp formation, a prelude to carcinogenesis. As a tumor suppressor, APC targets the oncogene beta-catenin for proteasome-mediated cytoplasmic degradation. Recently, it was demonstrated that APC also interacts with nuclear beta-catenin, thereby reducing beta-catenin's activity as a transcription cofactor and enhancing its nuclear export. The first objective of this study was to analyze how cellular context affected APC distribution. We determined that cell density but not cell cycle influenced APC's subcellular distribution, with predominantly nuclear APC found in subconfluent MDCK and intestinal epithelial cells but both cytoplasmic and nuclear APC in superconfluent cells. Redistribution of APC protein did not depend on continual nuclear export. Focusing on the two defined nuclear localization signals in the C-terminal third of APC (NLS1(APC) and NLS2(APC)), we found that phosphorylation at the CK2 site increased and phosphorylation at the PKA site decreased NLS2(APC)-mediated nuclear translocation. Cell density-mediated redistribution of beta-galactosidase was achieved by fusion to NLS2(APC) but not to NLS1(APC). Both the CK2 and PKA sites were important for this density-mediated redistribution, and pharmacological agents that target CK2 and PKA instigated relocalization of endogenous APC. Our data provide evidence that physiological signals such as cell density regulate APC's nuclear distribution, with phosphorylation sites near NLS2(APC) being critical for this regulation.

Indexed as

Receptors, Cytoplasmic and NuclearActive Transport, Cell NucleusAdenomatous Polyposis Coli ProteinAnimalsCell CountCell CycleCell LineDogsEnzyme InhibitorsEpithelial CellsExportin 1 ProteinFibroblastsGenes, ReporterIntestinal MucosaIntracellular FluidKaryopherinsAdenomatous Polyposis Coli ProteinEnzyme InhibitorsExportin 1 ProteinKaryopherinsNuclear Localization SignalsReceptors, Cytoplasmic and NuclearRecombinant Fusion Proteins

Identifiers

PMID11689703
PMCPMC99979
OpenAlexW2143844562

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.