Linking deep mutational scanning with engineered transcriptional reporters in human cell lines establishes a generalizable method for exploring pharmacogenomics, structure, and function across broad classes of drug receptors.

Serine and threonine phosphorylation sites work in concert to provide rapid and reproducible desensitization of the G-protein coupled receptor rhodopsin.

Multiple biochemical assays show that the topology of CCR5 and possibly other GPCRs may be inverted by ceramide or other sphingolipids through the process of regulated alternative translocation.

The adenosine A2a receptor couples to the heterotrimeric G protein Gs using both conserved contacts seen in other complexes and, in addition, novel contacts to the beta subunit of the G protein.

A combination of state-of-the-art biochemical, biophysical, and computational methods revealed that water molecules play a central role in signal propagation through G protein-coupled receptors.

A comprehensive approach to prediction of stabilizing mutations in G-protein coupled receptors yields high hit rate and crystal structures of 5HT2C in both active and inactive states.

Allosteric modulation in the M2 muscarinic receptor derives from a mix of interactions within and between the protomers of an oligomer.

Driving melanoma differentiation through G protein-coupled estrogen receptor signaling decreases proliferative capacity, decreases expression of the oncodriver and stem cell marker c-Myc, and increases the effectiveness of immunotherapy.

Cholesterol regulates cell-cell communication by activating the Hedgehog pathway, a central signaling system in development, regeneration and cancer.

The sodium leak NALCN channel functions as a core effector of GABA-B and D2 receptors that is used along with GIRK channels to regulate action potential firing in dopamine neurons.