GPCRs represents the largest class of the cell-surface receptors that are targeted by ~35% of the currently marketed drugs. Downstream signaling cascades orchestrated by GPCRs are finely tuned by three primary effectors: heterotrimeric G Proteins, which initiate signaling; G protein-coupled receptor kinases (GRKs), that phosphorylates the receptor; and arrestins, which further couples to an agonist-occupied and phosphorylated receptor to initiate a broad spectrum of cellular signaling pathways independent of the G proteins.

Our current focus lies in studying different GPCRs and how their membrane environment fine-tunes GPCR signaling downstream. Specifically, we aim to address the following questions:

1. How phospholipids, a major component of the lipid bilayer orchestrates the structure and function of GPCRs?

2. What are the structural and molecular determinants of GPCR-GRK interaction and signaling?

To study this, we are using a combination of biophysical, biochemical, and structural biology approach. By deciphering the intricate crosstalk between GPCRs, GRKs, and phospholipids, we seek to reveal new regulatory mechanisms that could inform innovative therapeutic strategies targeting GPCR signaling.