Rad and Gem-like GTP-binding protein 2 (REM2)

Rad and Gem-like GTP-binding protein 2 (REM2) is a member of the RGK (Rad, Gem, Rem, Kir) subfamily of small Ras-like GTPases, primarily expressed in the brain[1][2][3]. REM2 protein contains regions for both intrinsic disorder and a functional GTPase domain, with unique sequence variations that result in low GTP hydrolysis activity compared to canonical Ras GTPases[2]. REM2 acts as a key cytosolic signaling molecule that transduces neuronal activity—particularly through calcium influx—into structural and functional changes in neurons, regulating synapse formation, inhibiting dendritic branching, and modulating gene expression[2][3]. REM2 interacts with numerous proteins including voltage-gated calcium channels, calmodulin, and 14-3-3 proteins, influencing neuronal excitability and morphogenesis[1][2][3]. Its signaling is distinct from traditional GTPase switches, being controlled in part by post-translational modifications rather than classic GAP/GEF cycling[2]. REM2 does not have a confirmed role as a drug target, and no direct interacting drugs, mechanisms of drug action, biomarkers, or safety concerns have been described to date[1][2][3]. Its biological roles position it as an important regulator of brain development and synaptic plasticity, but its involvement in specific diseases or therapeutic applications is not established.

Other names

REM2GTP-binding protein REM 2FLJ38964RAS (RAD and GEM)-like GTP binding 2RAS-like GTP binding 2Rad and Gem-related 2 (rat homolog)rad and Gem-like GTP-binding protein 2