Transmembrane protein 230 (TMEM230)

Transmembrane protein 230 (TMEM230) is a small vertebrate-conserved transmembrane protein found in secretory and recycling vesicles, particularly those in neurons[5][4]. TMEM230 is implicated in synaptic vesicle trafficking, endosomal recycling, and has a key role in regulating blood vessel sprouting and integrity[1][2][3]. Elevated TMEM230 expression drives the migration, adhesion, and extracellular matrix remodeling of glioblastoma cells, promotes abnormal vascularization, and supports tumor expansion by modulating angiogenesis and vascular mimicry[1][2]. Mutations in TMEM230 have been associated with autosomal dominant Parkinson's disease, where they disrupt vesicle trafficking and mitochondrial function, trigger caspase-dependent apoptosis, and modulate disease pathogenesis, potentially via interplay with other PD-linked proteins like PINK1 and parkin[3][4]. TMEM230 is emerging as a potential therapeutic target in cancer (mainly glioblastoma) and neurodegenerative disease, though no specific drugs currently exist that directly target it[5][1][2][3][4].

Other names

C20orf30HSPC274dJ1116H23.2.1UNQ2432/PRO4992UPF0414 transmembrane protein C20orf30TMEM230[5][4]

Not established for drugs, due to lack of specific interacting compounds. - In cellular function studies, gene knockdown (reduction of TMEM230) inhibits tumor migration, adhesion, and growth; upregulation promotes vascular mimicry and angiogenesis in glioblastoma[1][2]. - In Parkinson’s disease models, pathogenic mutations impact vesicular trafficking, mitochondrial function, and apoptosis via PARP1 cleavage and ROS/caspase pathways[3][4].