Description
Single-nucleotide polymorphisms (SNPs) can impact GPCR drug response at different stages of the GPCR life cycle starting from the altered expression, folding, stability, cell surface tracking, or localization (i.e. receptor-integrity-based), in the interaction with ligands impacting efficacy, potency, selectivity, modality, or kinetics (i.e. ligand-based), impact basal activity, functional selectivity, activation kinetics, internalization, or desensitization (i.e. signalling-based), as well as affecting di-/oligomerization, homo-/heteromerisation, transactivation, or other membrane interactions (i.e. interaction-based). A mutation’s effect might only become apparent in specific circumstances, tissues, or moments, so that each GPCR variant requires functional characterization as a prerequisite to understanding the link to a given phenotype. Various technologies (Zhang and Xie, 2012) have been employed to study GPCRs to our better understanding of receptor pharmacology covering diverse aspects of the GPCR life cycle. BRET: bioluminescence resonance energy transfer; FRET: Förster/ fluorescence resonance energy transfer; SpIDA: Spatial Intensity Distribution Analysis; TIRF: total internal reflection fluorescence microscopy; FCS: Fluorescence correlation spectroscopy; BN-PAGE: blue native-polyacrylamide gel electrophoresis; Co-IP: co-immunoprecipitation; ELISA: enzyme-linked immunosorbent assay; SPR: surface plasmon resonance; cAMP: cyclic adenosine monophosphate; GTPγS: guanosine 5'-O-[gamma-thio]triphosphate); ELISA: enzyme-linked immunosorbent assay.
| Date made available | 2021 |
|---|---|
| Publisher | Zenodo |