ArticlePloS one2014
Cadherin cytoplasmic domains inhibit the cell surface localization of endogenous E-cadherin, blocking desmosome and tight junction formation and inducing cell dissociation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Migrating mesoderm cells self-organize into a dynamic meshwork structure during chick gastrulation.eLife · 2025Article
- Loss of Cell-Cell Contact Inhibits Cellular Differentiation of α-Catenin Knock Out P19 Embryonal Carcinoma Cells and Their Colonization into the Developing Mouse Embryos.Biotech (Basel (Switzerland)) · 2024Article
- Article
- Comparison of Fixation Methods for the Detection of Claudin 1 and E-Cadherin in Breast Cancer Cell Lines by Immunofluorescence.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Article
- E-cadherin loss in RMG-1 cells inhibits cell migration and its regulation by Rho GTPases.Biochemistry and biophysics reports · 2019Article
- Density-dependent ERK MAPK expression regulates MMP-9 and influences growth.Molecular and cellular biochemistry · 2019Article
- Nonmuscle myosin IIA is involved in recruitment of apical junction components through activation of α-catenin.Biology open · 2018Article
- Cadherins Interact With Synaptic Organizers to Promote Synaptic Differentiation.Frontiers in molecular neuroscience · 2018Article
- Snail1 expression in human colon cancer DLD-1 cells confers invasive properties without N-cadherin expression.Biochemistry and biophysics reports · 2016Article
- Cadherin 2/4 signaling via PTP1B and catenins is crucial for nucleokinesis during radial neuronal migration in the neocortex.Development (Cambridge, England) · 2016Article
- 293 cells express both epithelial as well as mesenchymal cell adhesion molecules.International journal of molecular medicine · 2016Article
- The N-cadherin cytoplasmic domain confers anchorage-independent growth and the loss of contact inhibition.Scientific reports · 2015Article
- E-cadherin cytoplasmic domain inhibits cell surface localization of endogenous cadherins and fusion of C2C12 myoblasts.Biology open · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The downregulation of E-cadherin function has fundamental consequences with respect to cancer progression, and occurs as part of the epithelial-mesenchymal transition (EMT). In this study, we show that the expression of the Discosoma sp. red fluorescent protein (DsRed)-tagged cadherin cytoplasmic domain in cells inhibited the cell surface localization of endogenous E-cadherin, leading to morphological changes, the inhibition of junctional assembly and cell dissociation. These changes were associated with increased cell migration, but were not accompanied by the down-regulation of epithelial markers and up-regulation of mesenchymal markers. Thus, these changes cannot be classified as EMT. The cadherin cytoplasmic domain interacted with β-catenin or plakoglobin, reducing the levels of β-catenin or plakoglobin associated with E-cadherin, and raising the possibility that β-catenin and plakoglobin sequestration by these constructs induced E-cadherin intracellular localization. Accordingly, a cytoplasmic domain construct bearing mutations that weakened the interactions with β-catenin or plakoglobin did not impair junction formation and adhesion, indicating that the interaction with β-catenin or plakoglobin was essential to the potential of the constructs. E-cadherin-α-catenin chimeras that did not require β-catenin or plakoglobin for their cell surface transport restored cell-cell adhesion and junction formation.
Indexed as
Identifiers
What OpenQuestion holds
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.