RASSLs and DREADDs are families of designer G-protein-coupled receptors (GPCRs) built specifically to allow for precise spatiotemporal control of GPCR signaling in vivo. These engineered GPCRs, called RASSLs (receptors<unk><unk>  by<unk><unk> s), are unresponsive to endogenous<unk> s but can be<unk>  by nanomolar concentrations of pharmacologically inert, drug-like small molecules. Currently, RASSLs exist for the interrogation of several GPCR signaling pathways, including those<unk>  by Gs, Gi, Gq, Golf and β-arrestin. A major cause for success of RASSL resources has been open exchange of DNA constructs, and RASSL related resources. The hM4Di-DREADD's inhibitory effects are a result of the CNO's stimulation and resulting activation of the G-protein inwardly rectifying potassium (GIRK) channels. This causes hyperpolarization of the targeted neuronal cell and thus attenuates subsequent activity.
Receptor activated solely by a synthetic ligand
GABAA receptor negative allosteric modulator
Protein kinase inhibitor
Cysteine-rich secretory protein
TP53-inducible glycolysis and apoptosis regulator
GABAA receptor positive allosteric modulator
Tumor M2-PK
CCR5 receptor antagonist