ArticleMolecular and cellular biology2000
Differential mechanisms of LEF/TCF family-dependent transcriptional activation by beta-catenin and plakoglobin.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 179 citations in OpenAlex.
- Adipocyte-specific ablation of plakoglobin in mice does not affect adiposity but results in sexual-dimorphic effects on weight gain.Physiological reports · 2025Article
- Junction Plakoglobin - A Dual-Role Player in Cancer Biology.International journal of surgery (London, England) · 2025Review
- Plakoglobin does not participate in endothelial barrier stabilization mediated by cAMP.Scientific reports · 2025Article
- miR-195-5p as Regulator of γ-Catenin and Desmosome Junctions in Colorectal Cancer.International journal of molecular sciences · 2023Article
- WNT5A inhibition alters the malignant peripheral nerve sheath tumor microenvironment and enhances tumor growth.Oncogene · 2021Article
- Cleavage of Desmosomal Cadherins Promotes γ-Catenin Degradation and Benefits Wnt Signaling in Coxsackievirus B3-Induced Destruction of Cardiomyocytes.Frontiers in microbiology · 2020Article
- The epithelial-mesenchymal transition induced by transcription factor LEF-1 is independent of β-catenin.Biochemistry and biophysics reports · 2018Article
- Genetics of and pathogenic mechanisms in arrhythmogenic right ventricular cardiomyopathy.Biophysical reviews · 2018Review
- Opposite Interplay Between the Canonical WNT/β-Catenin Pathway and PPAR Gamma: A Potential Therapeutic Target in Gliomas.Neuroscience bulletin · 2018Review
- The canonical way to make a heart: β-catenin and plakoglobin in heart development and remodeling.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- A C-terminally truncated form of β-catenin acts as a novel regulator of Wnt/β-catenin signaling in planarians.PLoS genetics · 2017Article
- Beyond cell-cell adhesion: Plakoglobin and the regulation of tumorigenesis and metastasis.Oncotarget · 2017Review
- Interactions between PPAR Gamma and the Canonical Wnt/Beta-Catenin Pathway in Type 2 Diabetes and Colon Cancer.PPAR research · 2017Review
- Alzheimer Disease: Crosstalk between the Canonical Wnt/Beta-Catenin Pathway and PPARs Alpha and Gamma.Frontiers in neuroscience · 2016Review
- Beyond β-catenin: prospects for a larger catenin network in the nucleus.Nature reviews. Molecular cell biology · 2016Review
- Opposite Interplay between PPAR Gamma and Canonical Wnt/Beta-Catenin Pathway in Amyotrophic Lateral Sclerosis.Frontiers in neurology · 2016Review
- Mice with Hepatic Loss of the Desmosomal Protein γ-Catenin Are Prone to Cholestatic Injury and Chemical Carcinogenesis.The American journal of pathology · 2015Article
- The cellular prion protein PrPc is a partner of the Wnt pathway in intestinal epithelial cells.Molecular biology of the cell · 2015Article
- Neuronal development is promoted by weakened intrinsic antioxidant defences due to epigenetic repression of Nrf2.Nature communications · 2015Article
- Janus-faces of NME-oncoprotein interactions.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
beta-Catenin and plakoglobin are highly homologous components of cell-cell adherens junctions linking cadherin receptors to the actin cytoskeleton. beta-Catenin, in addition, activates transcription by forming a complex with LEF/TCF family transcription factors in the nucleus. Plakoglobin can also bind to LEF-1 and, when overexpressed in mammalian cells, enhances LEF-1-directed transcription. Plakoglobin overexpression, however, results in the elevation and nuclear translocation of endogenous beta-catenin. We show here, by DNA mobility shift analysis, that the formation of a plakoglobin-LEF/TCF-DNA complex in vitro is very inefficient compared to a complex containing beta-catenin-LEF-DNA. Moreover, in plakoglobin-transfected cells plakoglobin-LEF/TCF-DNA complexes were not formed; rather, the endogenous beta-catenin, whose level is elevated by plakoglobin transfection, formed a beta-catenin-LEF-DNA complex. Removal of the N- and C-terminal domains of both beta-catenin and plakoglobin (leaving the armadillo repeat domain intact) induced plakoglobin-LEF-DNA complex formation and also enhanced beta-catenin-LEF-DNA complexing, both with in vitro-translated components and in transfected cells. Transfection with these truncated catenins increased endogenous beta-catenin levels, but the truncated catenins acted as dominant-negative inhibitors of beta-catenin-driven transcription by forming transcriptionally inactive complexes with LEF-1. When these catenin mutants were prevented from entering the nucleus, by their fusion to the connexin transmembrane domain, they indirectly activated transcription by increasing endogenous beta-catenin levels. These results suggest that overexpression of plakoglobin does not directly activate transcription and that formation of catenin-LEF-DNA complexes is negatively regulated by the catenin N- and C-terminal domains.
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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.