ArticleMolecular biology of the cell2026
Wnt signaling is modulated by the buffer-like properties of cadherins.
Article in Molecular biology of the cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
β-catenin is a critical effector of the Wnt pathway and a key component of the cadherin complex. Whether Wnt-regulated cytoplasmic β-catenin interacts with the cadherin-associated pool under physiological conditions is unclear. Using a cell line depleted of N- and E-cadherins, we demonstrate that cadherin-depleted cells exhibit lower levels of basal b-catenin that plateau to a similar level as the parental line with Wnt3a stimulation. The cadherin-depleted line exhibits significantly enhanced levels of Wnt signaling by comparison to its parental control; these effects are reversed by wild-type E-cadherin but not E-cadherin with disrupted b-catenin-binding. Enhanced Wnt signaling in the cadherin-depleted line is consistent with a previous study showing that Wnt pathway activation correlates with fold changes in β-catenin levels, rather than the absolute concentration. Our mathematical modeling suggests a mechanism in which β-catenin binding to cadherins acts as a sink to maintain elevated cytoplasmic b-catenin levels in the face of b-catenin destruction complex activity, and also limits pathway response. Our bioinformatic analysis reveals a correlation between elevated Wnt target gene expression and E-cadherin loss in a Wnt-driven model of thyroid cancer. Our results have relevance for tumorigenesis, as cadherin loss is commonly associated with poor prognosis and increased metastatic potential.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.