Evidence map›Paper›PMID 41258755›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2025

GSK3β Regulates a Novel β-Catenin Degradation Pathway via the GID Complex in Wnt Signaling.

Masahiro Shimizu, Hiroshi Shibuya

Abstract read
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Chondroprotective Effects of Enzyme-Treated Extract fromInternational journal of molecular sciences · 2026
    Article
  2. Review
  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
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.

Masahiro ShimizuDepartment of Molecular Cell Biology, Institute of Integrated Research, Medical Research Laboratory, Institute of Science Tokyo, Tokyo, Japan.
Hiroshi ShibuyaDepartment of Molecular Cell Biology, Institute of Integrated Research, Medical Research Laboratory, Institute of Science Tokyo, Tokyo, Japan.

Funding

MEXT/JSPS KAKENHI 24K10280
6 · The paper itself

Abstract

The canonical Wnt signaling pathway plays a pivotal role in regulating cell proliferation, differentiation, and tissue homeostasis. These functions are largely regulated through the degradation of β-Catenin. Under Wnt-off conditions, β-Catenin is phosphorylated by the destruction complex, including GSK3β, and subsequently ubiquitinated by the E3 ligase βTrCP, leading to proteasomal degradation. In this study, we identified a regulatory mechanism in which suppression of GSK3β promotes β-Catenin degradation via the GID complex, a conserved multi-subunit E3 ubiquitin ligase. GSK3β knockdown increased β-Catenin ubiquitination and decreased its protein levels in both the cytoplasm and nucleus, independent of βTrCP. This degradation was rescued by knockdown of GID components MAEA and RMND5A, but not by suppression of βTrCP. Furthermore, Wnt stimulation promoted the interaction between GSK3β and the GID E3 ligases, disrupting the association between MAEA and β-Catenin and thereby stabilizing β-Catenin. Together, these findings reveal a GSK3β-dependent mechanism of β-Catenin regulation mediated by the GID complex.

Indexed as

beta CateninGlycogen Synthase Kinase 3 betaWnt Signaling PathwayHEK293 CellsHumansProteolysisUbiquitinationUbiquitin-Protein Ligasesbeta CateninGlycogen Synthase Kinase 3 betaGSK3B protein, humanUbiquitin-Protein Ligases

Identifiers

PMID41258755
PMCPMC12628731

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.