Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

α-E-Catenin Inactivation Disrupts the Cardiomyocyte Adherens Junction, Resulting in Cardiomyopathy and Susceptibility to Wall Rupture

22 Aug 2006

Abstract excerpt

BACKGROUND: alpha-E-catenin is a cell adhesion protein, located within the adherens junction, thought to be essential in directly linking the cadherin-based adhesion complex to the actin cytoskeleton. Although alpha-E-catenin is expressed in the adherens junction of the cardiomyocyte intercalated disc, and perturbations in its expression are observed in models of dilated cardiomyopathy, its role in the myocardium...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cardiac Fibrosis and Remodeling
Share to Cardiovascular Effects of Exercise
Share to Wnt/β-catenin signaling in development and cancer

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 16923756
DOI: 10.1161/circulationaha.106.634469

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

α-E-Catenin Inactivation Disrupts the Cardiomyocyte Adherens Junction, Resulting in Cardiomyopathy and Susceptibility to Wall RupturePMID 16923756Read ↗

Loss of αT-catenin alters the hybrid adhering junctions in the heart and leads to dilated cardiomyopathy and ventricular arrhythmia following acute ischemia.Semantic proximity Read ↗

Heterozygous inactivation of the vinculin gene predisposes to stress-induced cardiomyopathy.Semantic proximity Read ↗

Cardiac-myocyte-specific excision of the vinculin gene disrupts cellular junctions, causing sudden death or dilated cardiomyopathy.Semantic proximity Read ↗

Unravelling the ultrastructural details of αT-catenin-deficient cell-cell contacts between heart muscle cells by the use of FIB-SEM.Semantic proximity Read ↗

Genetic inactivation of β-catenin is salubrious, whereas its activation is deleterious in desmoplakin cardiomyopathySemantic proximity Read ↗

Induced deletion of the N-cadherin gene in the heart leads to dissolution of the intercalated disc structure.Semantic proximity Read ↗

Cardiac Tissue-Restricted Deletion of Plakoglobin Results in Progressive Cardiomyopathy and Activation of β-Catenin SignalingSemantic proximity Read ↗

Loss of Cadherin-Binding Proteins β-Catenin and Plakoglobin in the Heart Leads to Gap Junction Remodeling and ArrhythmogenesisSemantic proximity Read ↗

Stabilised beta-catenin in postnatal ventricular myocardium leads to dilated cardiomyopathy and premature death.Semantic proximity Read ↗

Cardiac-specific ablation of Cypher leads to a severe form of dilated cardiomyopathy with premature death.Semantic proximity Read ↗

Cell-cell interaction in the heart via Wnt/ -catenin pathway after cardiac injurySemantic proximity Read ↗

Intercalated discs: cellular adhesion and signaling in heart health and diseasesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.