Target intelligence / Profile preview

Vezatin, adherens junctions transmembrane protein (VEZT)

Target
VEZT
Molecular classification
Adherens junction protein, Transmembrane protein, Other
01

Overview

Vezatin, adherens junctions transmembrane protein (VEZT), is a two-pass transmembrane protein crucial for the formation and maintenance of adherens junctions, particularly in epithelial cells[1][2]. Vezatin forms part of the cadherin-catenin complex, facilitating stable cell–cell contacts by co-localizing with E-cadherin and β-catenin at adherens junctions. The protein is also involved in the maturation and stabilization of neuromuscular synapses by directly binding to acetylcholine receptors (AChRs), and it interacts with several cytoskeletal and signaling proteins, including myosin VIIA, radixin, and Arf6[3]. Its biological importance is highlighted in embryonic development, maintenance of epithelial integrity, and neuronal synaptic function. Pathologically, VEZT acts as a tumor suppressor in several cancers, with downregulation linked primarily to promoter hypermethylation and microRNA-mediated repression, especially in gastric cancer[2]. Additionally, genetic variants in VEZT are associated with increased susceptibility to endometriosis, and alterations in its neuronal expression can modulate synaptic activity and seizure susceptibility[2][3]. Currently, there are no known drugs targeting VEZT directly, and its role in therapeutic interventions remains under investigation.

Other names
VEZTDKFZP761C241VezatinVezatin, adherens junctions transmembrane protein
02

Biological functions

Cell–cell adhesionFormation and maintenance of adherens junctionsRegulation of cytoskeletal organizationMaturation of neuromuscular synapsesModulation of neuronal synaptic transmission
03

Disease associations

Cancer (notably gastric cancer as a potential tumor suppressor)EndometriosisEpilepsyOther (general developmental disorders involving cell adhesion)
04

Biomarkers

Decreased VEZT expression as a potential biomarker in gastric cancer (linked to promoter hypermethylation)[2]Genetic polymorphisms associated with risk for endometriosis[2]

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