Target intelligence / Profile preview

Junctional adhesion molecule C (JAM3)

Target
JAM3
Molecular classification
Adhesion molecule, Tight junction protein, Immunoglobulin superfamily
01

Overview

Junctional adhesion molecule C (JAM3) is a 310-amino acid transmembrane glycoprotein (molecular weight ~35 kDa), belonging to the immunoglobulin superfamily adhesion molecules[6][3][2]. JAM3 contains two extracellular immunoglobulin-like domains, a single transmembrane segment, and a cytoplasmic tail with phosphorylation sites and a PDZ-binding motif[2][4]. It is primarily localized at tight junctions of endothelial and epithelial cells, where it regulates cell–cell adhesion, polarization, and barrier function[5][1][6]. JAM3 uniquely contributes to hematopoietic stem cell homing, vascular permeability, angiogenesis, and leukocyte–platelet adhesion during inflammation by interacting with integrin Mac-1 and other JAM family members[2][8][3]. Clinically, JAM3 mutations are associated with hemorrhagic destruction of the brain and congenital cataracts in rare syndromes[6]. Dysregulation of JAM3 is implicated in vascular disease, inflammation, and cancer progression[4][8].

Other names
JAM3JAM-CJunctional adhesion molecule 3Junctional adhesion molecule CJAMCJAM-3sJAM-CSoluble JAM-CUNQ859/PRO1868
02

Biological functions

Cell–cell adhesionTight junction formationRegulation of vascular permeabilityHoming and mobilization of hematopoietic stem and progenitor cellsModulation of inflammationRegulation of endothelial and epithelial cell polarity
03

Disease associations

InflammationCardiovascular disease (e.g., atherosclerosis)Autosomal recessive hemorrhagic destruction of the brain (rare pediatric syndrome)Pathologic angiogenesisCancer (associated with tumor progression, invasion, and angiogenesis)
04

Safety considerations

Loss-of-function mutations cause severe developmental syndromes with vascular and neurological symptoms[6]Therapeutic targeting could risk disruption of vascular integrity and immune cell migrationNotable risk for hemorrhagic complications due to disruption of endothelial barrier function[6]

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