Evidence map›Paper›PMID 18223684›Full record

ArticleOncogene2008

Nuclear GSK-3beta inhibits the canonical Wnt signalling pathway in a beta-catenin phosphorylation-independent manner.

M Caspi, A Zilberberg, H Eldar-Finkelman, R Rosin-Arbesfeld

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

48 citing papers in PubMed, 87 citations in OpenAlex.

  1. The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026
    Review
  2. Article
  3. GSK3β Regulates a Novel β-Catenin Degradation Pathway via the GID Complex in Wnt Signaling.Genes to cells : devoted to molecular & cellular mechanisms · 2025
    Article
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  7. [STE029 Overcomes EGFR-TKI Resistance in Human Lung Adenocarcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022
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  10. Review
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  15. Regulation of SIRT2 by Wnt/β-catenin signaling pathway in colorectal cancer cells.Biochimica et biophysica acta. Molecular cell research · 2021
    Article
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  20. Acquisition of a hybrid E/M state is essential for tumorigenicity of basal breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
    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

4 authors at 1 institution in 1 country.

M CaspiDepartment of Anatomy and Anthropology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
A Zilberberg
H Eldar-Finkelman
R Rosin-Arbesfeld
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beta-catenin is the central signalling molecule of the canonical Wnt pathway, where it activates target genes in a complex with lymphoid enhancer factor/T-cell factor transcription factors in the nucleus. The regulation of beta-catenin activity is thought to occur via a cytoplasmatic multiprotein complex that includes the serine/threonine kinase glycogen synthase kinase-3beta (GSK-3beta) that phosphorylates beta-catenin, marking it for degradation by the proteasome. Here, we provide evidence showing that GSK-3beta has a nuclear function in downregulating the activity of beta-catenin. Using colorectal cell lines that express a mutant form of beta-catenin, which cannot be phosphorylated by GSK-3beta and ectopically expressed mutant beta-catenin protein, we show that nuclear GSK-3beta functions in a mechanism that does not involve beta-catenin phosphorylation to reduce the levels of Wnt signalling. We show that GSK-3beta enters the nucleus, forms a complex with beta-catenin and lowers the levels of beta-catenin/TCF-dependent transcription in a mechanism that involves GSK-3beta-Axin binding.

Indexed as

beta CateninCadherinsCell LineCell Line, TumorCell NucleusColorectal NeoplasmsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansModels, BiologicalPhosphorylationProteasome Endopeptidase ComplexProtein BindingSignal TransductionTranscription, GeneticWnt Proteinsbeta CateninCadherinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanProteasome Endopeptidase ComplexWnt Proteins

Identifiers

PMID18223684
OpenAlexW1992379971

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.