ArticleThe Journal of biological chemistry2016
αT-Catenin Is a Constitutive Actin-binding α-Catenin That Directly Couples the Cadherin·Catenin Complex to Actin Filaments.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Clinical Variability Including Non-Dilated Left Ventricular and Dilated Cardiomyopathy in a Pedigree With an Intragenic CTNNA3 Copy Number Variation.Clinical genetics · 2026Article
- Conventional rigid 2D substrates cause complex contractile signals in monolayers of human induced pluripotent stem cell-derived cardiomyocytes.The Journal of physiology · 2022Article
- Adherens junction engagement regulates functional patterning of the cardiac pacemaker cell lineage.Developmental cell · 2021Article
- Vinculin anchors contractile actin to the cardiomyocyte adherens junction.Molecular biology of the cell · 2019Article
- Mechanical stability of αT-catenin and its activation by force for vinculin binding.Molecular biology of the cell · 2019Article
- The N-cadherin interactome in primary cardiomyocytes as defined using quantitative proximity proteomics.Journal of cell science · 2019Article
- Force-dependent allostery of the α-catenin actin-binding domain controls adherens junction dynamics and functions.Nature communications · 2018Article
- Cardiospecific deletion of αE-catenin leads to heart failure and lethality in mice.Pflugers Archiv : European journal of physiology · 2018Article
- α-Catenin Structure and Nanoscale Dynamics in Solution and in Complex with F-Actin.Biophysical journal · 2018Article
- α-Catenin-dependent cytoskeletal tension controls Yap activity in the heart.Development (Cambridge, England) · 2018Article
- Real-time TIRF observation of vinculin recruitment to stretched α-catenin by AFM.Scientific reports · 2018Article
- αT-catenin: A developmentally dispensable, disease-linked member of the α-catenin family.Tissue barriers · 2018Review
- Measuring Protein Binding to F-actin by Co-sedimentation.Journal of visualized experiments : JoVE · 2017Article
- Structural and functional characterization ofThe Journal of biological chemistry · 2017Article
- Distinct intramolecular interactions regulate autoinhibition of vinculin binding in αT-catenin and αE-catenin.The Journal of biological chemistryArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
α-Catenin is the primary link between the cadherin·catenin complex and the actin cytoskeleton. Mammalian αE-catenin is allosterically regulated: the monomer binds the β-catenin·cadherin complex, whereas the homodimer does not bind β-catenin but interacts with F-actin. As part of the cadherin·catenin complex, αE-catenin requires force to bind F-actin strongly. It is not known whether these properties are conserved across the mammalian α-catenin family. Here we show that αT (testes)-catenin, a protein unique to amniotes that is expressed predominantly in the heart, is a constitutive actin-binding α-catenin. We demonstrate that αT-catenin is primarily a monomer in solution and that αT-catenin monomer binds F-actin in cosedimentation assays as strongly as αE-catenin homodimer. The β-catenin·αT-catenin heterocomplex also binds F-actin with high affinity unlike the β-catenin·αE-catenin complex, indicating that αT-catenin can directly link the cadherin·catenin complex to the actin cytoskeleton. Finally, we show that a mutation in αT-catenin linked to arrhythmogenic right ventricular cardiomyopathy, V94D, promotes homodimerization, blocks β-catenin binding, and in cardiomyocytes disrupts localization at cell-cell contacts. Together, our data demonstrate that αT-catenin is a constitutively active actin-binding protein that can physically couple the cadherin·catenin complex to F-actin in the absence of tension. We speculate that these properties are optimized to meet the demands of cardiomyocyte adhesion.
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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.