Target intelligence / Profile preview

Nectin cell adhesion molecule 3 (NECTIN3)

Target
NECTIN3
Molecular classification
Immunoglobulin superfamily (IgSF) member, Cell adhesion molecule, Single-pass type I membrane protein, Adherens junction protein
01

Overview

Nectin cell adhesion molecule 3 (NECTIN3) is a single-pass type I membrane glycoprotein in the immunoglobulin superfamily, functioning as a Ca2+-independent cell adhesion molecule primarily at adherens junctions[1][3][5]. It contains three extracellular Ig-like domains, a transmembrane region, and a cytoplasmic tail that interacts with afadin to connect to the actin cytoskeleton. NECTIN3 forms both homophilic and heterophilic interactions, notably with other nectins (e.g., NECTIN1, NECTIN2), contributing to the establishment and maintenance of adherens junctions in epithelial, neural, and other tissues[1][3][5]. It is essential for tissue architecture, synapse formation, axonal guidance, morphogenesis, and various developmental processes. Mutations can cause congenital malformations, especially affecting the eye and orofacial region, and animal models reveal roles in fertility and neural patterning[5]. While NECTIN3 is regarded as a potential tissue integrity and morphogenesis modulator, it is not currently a major direct therapeutic target.

Other names
Nectin-3PRR3PVRL3CD113PPR3PVRR3DKFZP566B0846CDw113Poliovirus receptor-related protein 3NECTIN-3poliovirus receptor-related 3poliovirus receptor-related protein 3
02

Biological functions

Cell–cell adhesion (Ca2+-independent)Formation and maintenance of adherens junctionsInteraction with afadin for cytoskeletal linkageAxon guidanceSynapse formationRegulation of cell proliferationDirectional cell motilityParticipation in morphogenesis of epithelial and neural tissues
03

Disease associations

Congenital ocular defects (involving ciliary body development)Infertility (notably male, from Sertoli-spermatid adhesion defects)Orofacial cleftsCombined oxidative phosphorylation deficiency 8Potential implications in cancer and neurodevelopmental disorders (inferred from family function and expression patterns)
04

Safety considerations

Disruption may lead to tissue integrity defectsGenetic mutations can cause developmental anomalies, particularly in eye and orofacial tissuesPotential off-target effects on tissue homeostasis if targeted therapeutically

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