ArticlePloS one2012
Competitive regulation of E-cadherin juxtamembrane domain degradation by p120-catenin binding and Hakai-mediated ubiquitination.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- F-actin organization excludes E-cadherin from the division furrow to ensure cytokinesis fidelity.Life science alliance · 2026Article
- Free apical surface hetero-cellular CDH1 homophilic binding is a major mediator of blastocyst-endometrium interaction in humans.Human reproduction (Oxford, England) · 2026Article
- Article
- The Lego hypothesis of tissue morphogenesis: stereotypic organization of parallel orientational cell adhesions for epithelial self-assembly.Biological reviews of the Cambridge Philosophical Society · 2025Review
- Beyond destruction: emerging roles of the E3 ubiquitin ligase Hakai.Cellular & molecular biology letters · 2025Review
- Trans-Compartmental Regulation of Tight Junction Barrier Function.Tissue barriers · 2023Review
- Degradation of p0071 and p120-catenin during adherens junction disassembly byFrontiers in cellular and infection microbiology · 2023Article
- Article
- Chronic Leptin Treatment Induces Epithelial-Mesenchymal Transition in MCF10A Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2022Article
- The Cross-Talk Between EGFR and E-Cadherin.Frontiers in cell and developmental biology · 2021Review
- Article
- E-cadherin Beyond Structure: A Signaling Hub in Colon Homeostasis and Disease.International journal of molecular sciences · 2019Review
- A central role for cadherin signaling in cancer.Experimental cell research · 2017Review
- Divergent roles of p120-catenin isoforms linked to altered cell viability, proliferation, and invasiveness in carcinogen-induced rat skin tumors.Molecular carcinogenesis · 2017Article
- Adherens Junctions on the Move-Membrane Trafficking of E-Cadherin.Cold Spring Harbor perspectives in biology · 2017Review
- Cell division orientation is coupled to cell-cell adhesion by the E-cadherin/LGN complex.Nature communications · 2017Article
- p120-catenin regulates VE-cadherin endocytosis and degradation induced by the Kaposi sarcoma-associated ubiquitin ligase K5.Molecular biology of the cell · 2017Article
- Epithelial-mesenchymal transition and nuclear β-catenin induced by conditional intestinal disruption of Cdh1 with Apc is E-cadherin EC1 domain dependent.Oncotarget · 2016Article
- Cell regulation by phosphotyrosine-targeted ubiquitin ligases.Molecular and cellular biology · 2015Review
- Protective role of p120-catenin in maintaining the integrity of adherens and tight junctions in ventilator-induced lung injury.Respiratory research · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
p120-Catenin binding to, and Hakai-mediated ubiquitination of the E-cadherin juxtamembrane domain (JMD) are thought to be involved in regulating E-cadherin internalization and degradation. However, the relationship between these two pathways is not understood. We targeted the E-cadherin JMD to mitochondria (WT-JMD) to isolate this domain from the plasma membrane and internalization, and to examine protein modifications and degradation. WT-JMD localized to mitochondria, but did not accumulate there except when proteasome activity was inhibited. We found WT-JMD was ubiquitinated, and arginine substitution of lysines at position 5 (K5R) and 83 (K83R) resulted in the stable accumulation of mutant JMD at mitochondria. p120-Catenin did not localize, or bind to WT-JMD even upon proteasome inhibition, whereas the K5,83R-JMD mutant bound and localized p120-catenin to mitochondria. Mutation of the p120-catenin binding site in combination with these lysine mutations inhibited p120-catenin binding, but did not decrease JMD stability or its accumulation at mitochondria. Thus, increased stability of JMD lysine mutants was due to inhibition of ubiquitination and not to p120-catenin binding. Finally, mutation of these critical lysines in full length E-cadherin had similar effects on protein stability as WT-JMD. Our results indicate that ubiquitination of the JMD inhibits p120-catenin binding, and targets E-cadherin for degradation.
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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.