Regulator of G-protein signaling 16 (RGS16)

Regulator of G-protein signaling 16 (RGS16) is a member of the small B/R4 subfamily of the RGS protein family, which act as GTPase-activating proteins (GAPs) to accelerate GTP hydrolysis on G protein α subunits, terminating signaling mediated by G protein-coupled receptors (GPCRs)[1][2][3][5][7]. RGS16 has a conserved RGS homology domain and influences both classical GPCR signaling and non-classical pathways, such as MAPK, PI3K/AKT, RhoA, and CXCR4, implicating it in immune regulation, inflammatory response, tumorigenesis, metabolic homeostasis, and circadian rhythm control[1][2][5][7]. Its expression varies across tissues—including retina, pituitary, bone marrow, and liver—and is modulated by post-translational modifications like phosphorylation and palmitoylation[2][7]. Dysregulation of RGS16 contributes to several diseases, notably cancer, inflammation, metabolic disorders, and more, and serves as a potential biomarker and therapeutic target in several malignancies[1][2][4][5][7]. No approved drugs selectively target RGS16, although its modulation can affect response to therapies targeting its downstream pathways[2].

Other names

RGS16RGSRRGS-rhRGS-rA28-RGS14A28-RGS14PRetinal-specific RGSRetinally abundant regulator of G-protein signalingRGS-R

Enhancement of GTP hydrolysis by G protein α subunit to terminate GPCR signaling[1][2][3][5]. Modulation of non-classical MAPK, PI3K/AKT, RhoA, and CXCR4 signaling pathways, affecting cellular responses[1][2].