The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index.
β-Catenin destruction complex: insights and questions from a structural perspective
Abstract
At the heart of the canonical Wnt signaling pathway is the beta-catenin destruction complex, which functions in the absence of Wnt signaling to keep the cytosolic and nuclear levels of beta-catenin very low by promoting the phosphorylation and ubiquitination of beta-catenin. Structural studies, combined with other experimental approaches, have begun to provide important insights into the mechanism of the destruction complex. We suggest a working model for the destruction complex based on the existing structural and experimental data, and focus on the questions that this model and other studies have raised about the function of the complex in both the normal and Wnt-inhibited states.
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“Next, the β-catenin proteins undergo proteasomal destruction [259, 260], which is greatly accelerated by the presence of IDRs in addition to the bound ubiquitin signal [262].”
From Intrinsically disordered proteins play diverse roles in cell signaling (2022) · cites this paper as [260]
In the citing paper
“Prior to Wnt signaling, the transcription factor β-catenin is maintained at low levels by the β-catenin destruction complex, which is an assembly of the 852 residue mostly disordered scaffold protein axin, the 2,843 residue massively disordered protein adenomatous polyposis coli (APC), and the three mostly structured proteins β-catenin, casein kinase Ia (CKI-a), and glycogen synthetase kinase 3b (”
From Intrinsically disordered proteins play diverse roles in cell signaling (2022) · cites this paper as [260]
In the citing paper
“The two kinases phosphorylate residues within a long IDR at β-catenin’s amino terminus [259, 260].”
From Intrinsically disordered proteins play diverse roles in cell signaling (2022) · cites this paper as [260]
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Metadata
- Authors
- Kimelman, D., & Xu, W.
- Affiliations
- University of Washington (US)
- Corresponding author
- Kimelman, D
- ORCID
- Venue
- Oncogene
- Published
- 2006-12-04
- Volume
- 25
- Issue
- 57
- Pages
- 7482-7491
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2072335762
- Cited by
- 628
- References
- 72
- Citations by year
- 2026: 8 · 2025: 21 · 2024: 23 · 2023: 27 · 2022: 41 · 2021: 52 · 2020: 19 · 2019: 25 · 2018: 37 · 2017: 40 · 2016: 28 · 2015: 36 · 2014: 51 · 2013: 33 · 2012: 40
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (CA 90351, R01CA090351)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD027262, HD27262)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- β-catenin destruction complex, Wnt/β-catenin signaling, β-catenin phosphorylation, β-catenin ubiquitination, protein complex structure, Wnt signaling inhibition
- MeSH terms
- Animals, Cell Nucleus, Colonic Neoplasms, Cytosol, Humans, Models, Biological, Phosphorylation, Protein Conformation, Stem Cells, Ubiquitin, beta Catenin
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