GPR52/CRE Luciferase Reporter HEK293 Cell Line

The GPR52/CRE Luciferase Reporter HEK293 Cell Line is an engineered HEK293 cell line that expresses the stably integrated human GPR52 (G protein-coupled receptor 52, NM_005684) and firefly luciferase under the control of cAMP response elements (CRE). GPR52 exhibits intrinsic activity due to the extracellular loop 2 (ECL2) of the receptor, which acts as a tethered agonist within the ligand binding pocket. This cell line has been validated by assessing the reduction in activity by inverse agonists and by reversing the effect of inverse agonists using an agonist. Figure1. Illustration of decreased intrinsic GPR52 activity caused by an inverse agonist, and reversal of this effect by an agonist in GPR52/CRE Luciferase Reporter HEK293 Cell Line. Interested in screening and profiling inhibitors, blocking antibodies, or activators of MC4R without the need to purchase and license the cell line? Check out our Cell-Based Assays for Screening & Profiling. GPR52 is an orphan G protein-coupled receptor (GPCR) that is conserved among vertebrates and is mainly found in the human brain, especially in areas such as the striatum, nucleus accumbens, and medial prefrontal cortex. It belongs to the Class A (rhodopsin-like) GPCR family and is noted for its high basal constitutive activity, which allows it to signal through the Gs pathway to increase intracellular cAMP levels even without an external ligand. The importance of GPR52 in human disease relates to its function linking the dopaminergic and glutamatergic systems. It is co-expressed with dopamine D2 receptors in striatal medium spiny neurons but has opposing intracellular effects, leading to its recognition as a significant therapeutic target for neuropsychiatric and neurodegenerative disorders. Activation of GPR52 presents a potential non-dopaminergic approach for addressing the positive, negative, and cognitive symptoms of schizophrenia, and its capability to influence huntingtin protein levels makes it a candidate for Huntington's disease treatments.