ArticleMolecular biology of the cell2020
Centrosomes are required for proper β-catenin processing and Wnt response.
Article in Molecular biology of the cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Centrosome-Signaling Pathway Crosstalk: A Core Hub From Cellular Homeostasis to Disease.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Sensing centrosome amplification: the interface between centriole duplication and autophagy.Nature communications · 2026Article
- Nuclear localization and transactivation of SYS-1/β-catenin is the result of serial gene duplications and subfunctionalizations.Cells & development · 2025Article
- Nucleation of the destruction complex on the centrosome accelerates degradation of β-catenin and regulates Wnt signal transmission.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- KIFC3 promotes proliferation, migration and invasion of esophageal squamous cell carcinoma cells by activating EMT and β-catenin signaling.World journal of gastrointestinal oncology · 2022Article
- Centrosomal enrichment and proteasomal degradation of SYS-1/β-catenin requires the microtubule motor dynein.Molecular biology of the cell · 2022Article
- Moonlighting at the Poles: Non-Canonical Functions of Centrosomes.Frontiers in cell and developmental biology · 2022Review
- Primary Cilia Formation Does Not Rely on WNT/β-Catenin Signaling.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Wnt/β-catenin signaling pathway is central to metazoan development and routinely dysregulated in cancer. Wnt/β-catenin signaling initiates transcriptional reprogramming upon stabilization of the transcription factor β-catenin, which is otherwise posttranslationally processed by a destruction complex and degraded by the proteasome. Since various Wnt signaling components are enriched at centrosomes, we examined the functional contribution of centrosomes to Wnt signaling, β-catenin regulation, and posttranslational modifications. In HEK293 cells depleted of centrosomes we find that β-catenin synthesis and degradation rates are unaffected but that the normal accumulation of β-catenin in response to Wnt signaling is attenuated. This is due to accumulation of a novel high-molecular-weight form of phosphorylated β-catenin that is constitutively degraded in the absence of Wnt. Wnt signaling operates by inhibiting the destruction complex and thereby reducing destruction complex-phosphorylated β-catenin, but high-molecular-weight β-catenin is unexpectedly increased by Wnt signaling. Therefore these studies have identified a pool of β-catenin effectively shielded from regulation by Wnt. We present a model whereby centrosomes prevent inappropriate β-catenin modifications that antagonize normal stabilization by Wnt signals.
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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.