Member Biography

My research program focuses on elucidating the molecular mechanisms of G protein-coupled receptor (GPCR) signaling, with an emphasis on how GPCR kinases (GRKs) and arrestins regulate signal transduction at the structural level. Using state-of-the-art approaches, including cryo-electron microscopy, X-ray crystallography, and advanced biophysical and biochemical methods, my laboratory dissects how GRK-dependent phosphorylation “barcodes” on GPCRs direct selective arrestin engagement and downstream signaling outcomes. Neurotensin receptor signaling in cancer. These mechanisms are highly relevant to cancer biology, as GPCRs frequently drive tumor cell proliferation, survival, and invasion. In particular, the neurotensin receptor 1 (NTSR1) is overexpressed in multiple cancers, including colorectal, pancreatic, prostate, and breast cancers, where it promotes oncogenic signaling, epithelial–mesenchymal transition, and metastatic behavior. Emerging evidence suggests that NTSR1 can signal through arrestin-dependent pathways in a biased manner, uncoupled from canonical G protein activation. By defining the structural determinants that govern NTSR1 phosphorylation, arrestin recruitment, and signaling bias, my work aims to identify new strategies to selectively modulate oncogenic GPCR signaling pathways in cancer. Chemokine receptors and ACKR3 in tumor progression and metastasis. In parallel, my laboratory investigates the structural and molecular basis of chemokine receptor signaling in cancer, with a particular focus on atypical chemokine receptor 3 (ACKR3/CXCR7). ACKR3 is highly expressed in many solid tumors and the tumor microenvironment, where it regulates chemokine availability, cell migration, angiogenesis, and metastatic dissemination. Unlike canonical chemokine receptors, ACKR3 signals primarily through arrestin-dependent mechanisms rather than heterotrimeric G proteins, making it a powerful model for dissecting noncanonical GPCR signaling pathways that are increasingly recognized as drivers of tumor progression. Our work focuses on how GRK-mediated phosphorylation patterns control arrestin activation, receptor trafficking, and downstream signaling in ACKR3 and related chemokine receptors. By resolving high-resolution structures of chemokine receptor–arrestin–downstream effector complexes and defining their functional signaling states, we aim to uncover new opportunities for targeting chemokine-driven tumor growth, immune modulation, and metastasis with greater precision.

Post-doctoral Fellowship - Purdue University, West Lafayette, IN 2022

Post-doctoral Fellowship - University of Michigan, Ann Arbor MI 2017

Post-doctoral Fellowship - Vanderbilt University, Nashville TN 2016

Ph.D. - Vanderbilt University, Nashville TN 2015