ArticleJournal of cell science2015
α-Catenin phosphorylation promotes intercellular adhesion through a dual-kinase mechanism.
Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 57 citations in OpenAlex.
- An intrinsically disordered region mediates RNA-binding selectivity and cellular activities of LARP6.Nature communications · 2026Article
- Intact Mass Profiling Reveals Phospho-Proteoforms of the Catenins (85-110 kDa) Regulated by Actomyosin Contractility.Angewandte Chemie (International ed. in English) · 2025Article
- Phosphoproteomics unveils the signaling dynamics in neuronal cells stimulated with insulin and insulin-like growth factors.Cell communication and signaling : CCS · 2025Article
- UBE2O-mediated ubiquitylation directs cytoplasmic CTNNA1 to promote cell-to-ECM adhesions.EMBO reports · 2025Article
- α-catenin phosphorylation is actomyosin-sensitive and required for epithelial barrier functions through Afadin.bioRxiv : the preprint server for biology · 2025Article
- Mechanism of trypsin-mediated differentiation of pancreatic progenitor cells into functional islet-like clusters.World journal of diabetes · 2025Article
- α-catenin phosphorylation is elevated during mitosis to resist apical rounding and epithelial barrier leak.Biology open · 2025Article
- Article
- Toll-like receptor signalling via IRAK4 affects epithelial integrity and tightness through regulation of junctional tension.Development (Cambridge, England) · 2023Article
- α-Catenin acetylation is essential for its stability and blocks its tumor suppressor effects in breast cancer through Yap1.Cancer gene therapy · 2023Article
- Proteomics and phosphoproteomics of failing human left ventricle identifies dilated cardiomyopathy-associated phosphorylation of CTNNA3.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Depletion of the RNA-binding protein PURA triggers changes in posttranscriptional gene regulation and loss of P-bodies.Nucleic acids research · 2023Article
- The α-Catenin mechanosensing M region is required for cell adhesion during tissue morphogenesis.The Journal of cell biology · 2023Article
- Tuning Epithelial Cell-Cell Adhesion and Collective Dynamics with Functional DNA-E-Cadherin Hybrid Linkers.Nano letters · 2022Article
- Rac1-PAK1 regulation of Rab11 cycling promotes junction destabilization.The Journal of cell biology · 2021Article
- Proteomic characterization of GSK3β knockout shows altered cell adhesion and metabolic pathway utilisation in colorectal cancer cells.PloS one · 2021Article
- Novel somatic variants in CTNNA1 gene in Iranian patients with diffuse gastric cancer.Gastroenterology and hepatology from bed to bench · 2021Article
- Article
- Protein phosphatase 1 activity controls a balance between collective and single cell modes of migration.eLife · 2020Article
- Afadin regulates actomyosin organization through αE-catenin at adherens junctions.The Journal of cell biology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
The cadherin-catenin adhesion complex is a key contributor to epithelial tissue stability and dynamic cell movements during development and tissue renewal. How this complex is regulated to accomplish these functions is not fully understood. We identified several phosphorylation sites in mammalian αE-catenin (also known as catenin α-1) and Drosophila α-Catenin within a flexible linker located between the middle (M)-region and the carboxy-terminal actin-binding domain. We show that this phospho-linker (P-linker) is the main phosphorylated region of α-catenin in cells and is sequentially modified at casein kinase 2 and 1 consensus sites. In Drosophila, the P-linker is required for normal α-catenin function during development and collective cell migration, although no obvious defects were found in cadherin-catenin complex assembly or adherens junction formation. In mammalian cells, non-phosphorylatable forms of α-catenin showed defects in intercellular adhesion using a mechanical dispersion assay. Epithelial sheets expressing phosphomimetic forms of α-catenin showed faster and more coordinated migrations after scratch wounding. These findings suggest that phosphorylation and dephosphorylation of the α-catenin P-linker are required for normal cadherin-catenin complex function in Drosophila and mammalian cells.
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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.