Vesicle amine transport protein 1 (VAT1)

Vesicle amine transport protein 1 (VAT1) is an abundant integral membrane protein of cholinergic synaptic vesicles that is involved in the storage and release of neurotransmitters at nerve terminals[1][3]. VAT1 belongs to the NADPH-dependent quinone oxidoreductase family, participating in vesicular and phospholipid transport, and also appears to have oxidoreductase activity against quinone substrates[2][1]. It dynamically associates with cellular membranes in response to signaling events and is implicated in multiple cellular processes, including mitochondrial fusion and cell migration[2][1]. Overexpression of VAT1 is associated with higher malignancy and migration potential in gliomas, making it a potential prognostic marker and therapeutic target in certain cancers; it also has biological and pathological roles in neurodevelopment and neurodegeneration[1][3]. VAT1 can interact with small molecules such as (–)-epigallocatechin-3-gallate (EGCg), which may modulate its function[1]. VAT1 is the canonical and widely used abbreviation. VAT1 is not a classical vesicular neurotransmitter transporter but a vesicle-associated protein with oxidoreductase and lipid transport activities. Listed aliases represent commonly used names in biological databases and literature[1][3]. No approved therapeutic drugs currently target VAT1, but research compounds (such as EGCg) demonstrate direct protein binding[1]. VAT1 is considered a protein-coding gene and is notably upregulated in certain high-grade cancers, supporting its potential target status in oncology and neurobiology[1].

Other names

Synaptic vesicle membrane protein VAT-1 homologVATIFLJ20230membrane protein of cholinergic synaptic vesiclesvesicle amine transport protein 1 homolog (T. californica)VAT1_HUMAN

Modulation of lipid transport and oxidoreductase signaling via protein binding (e.g., EGCg binding to VAT1)