EHD3 (EH domain-containing protein 3) is a member of the EHD family of ATP-dependent membrane remodeling proteins that regulate endocytic membrane trafficking and recycling pathways
[1]. EHD3 localizes predominantly to recycling tubular and vesicular membrane structures and interacts with the closely related isoform EHD1, supporting transport processes within the endosomal system
[1]. Mechanistically, EHD3 participates in endosome-to-recycling compartment and early endosome-to-Golgi trafficking, thereby contributing to receptor recycling, cargo sorting, and maintenance of Golgi morphology
[2][3]. Through these trafficking functions, EHD3 influences the intracellular distribution of membrane proteins and helps preserve endosomal network organization
[2][3]. In disease-associated models, EHD3 has attracted attention because its expression is frequently lost in gliomas, where restoration of EHD3 suppresses cellular proliferation and promotes cell-cycle arrest and apoptosis, supporting a tumor-suppressive role linked to vesicular trafficking regulation
[4]. EHD3 is also implicated in cardiac membrane protein trafficking and has been reported to undergo differential regulation in heart failure, highlighting the importance of endocytic recycling pathways in cardiovascular biology
[5]. Compared with related isoforms, EHD3 exhibits functional specialization despite its high sequence similarity to EHD1; experimental studies indicate that EHD1 primarily promotes membrane vesiculation, whereas EHD3 preferentially supports the stabilization and tubulation of tubular recycling endosomes
[6]. Consequently, EHD3 serves as a valuable experimental target for investigating endosomal recycling, membrane remodeling, Golgi-directed transport, and trafficking-dependent disease mechanisms
[2][4][6].