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Adhesion G protein-coupled receptor B3 (ADGRB3), also known as BAI3, is a member of the adhesion GPCR family with a large extracellular domain responsible for cell–cell adhesion and signaling[1][3][4][5]. Highly expressed in the brain, ADGRB3 is crucial for synaptic development, dendritic morphogenesis, and the elimination of redundant synapses, impacting circuit refinement essential for motor learning and cognition[1][2]. It interacts with secreted C1q-like proteins to regulate synaptic density, and its disruption is implicated in neurodevelopmental disorders[1][2]. Beyond the nervous system, ADGRB3 mediates myoblast fusion in muscle and modulates metabolic and angiogenic pathways[1][3][5]. Aberrant ADGRB3 expression or genomic alteration is linked to certain malignancies (lung, breast, ovarian, gastric, prostate) and vascular or metabolic diseases including insulin regulation and venous thromboembolism[1][3][5]. No drugs currently target ADGRB3 directly, but its roles in diverse physiological and pathological processes are under investigation as potential therapeutic opportunities.
Not established—ADGRB3 is considered an orphan receptor (no approved drugs directly targeting it); Signal regulation via tethered agonist after autoproteolytic cleavage within the GAIN domain; Binds secreted C1q-like proteins; modulates synaptic density and insulin secretion through downstream signaling.
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