Our lab uses functional genomics and molecular biology approaches to uncover how chromatin-modifying enzymes and scaffolding proteins regulate gene expression in cells. While genomics (the sequencing side) reveals what is in the genome, functional genomics asks how that information gets used: which genes are turned on or off in a given context, how transcription factors, chromatin remodelers, and other regulatory proteins physically interact with DNA and each other to control gene expression, and what happens when a gene or protein-protein interaction is disrupted. We use tools like CRISPR editing, degron systems (AID/dTAG) for rapid protein depletion, immunoprecipitation–mass spectrometry, RNA-seq, ATAC-seq, ChIP-seq/CUT&RUN, HiChIP, cellular phenotypic assays, single-cell genomics, and computational modeling. Together, these approaches let us trace how protein interactions on chromatin shape gene expression and, ultimately, cell behavior.

A central question driving our lab is specificity: how do regulatory protein complexes know where to go in the genome, and when? Human cells encode more than a thousand transcription factors and hundreds of chromatin regulators, yet each complex must find the right partners and reach the right genes at the right time. We think nuclear scaffolding proteins are a key part of this specificity. Our goal is to decode the molecular logic of nuclear scaffolds and learn how they direct chromatin complexes to their targets in both normal and diseased cells.

These principles apply across cell types, but we are especially interested in what happens when they break down in cancer. In cancer, many of the most consequential changes happen not in the DNA sequence itself but in how proteins assemble on chromatin. Transcription factors, co-activators, and chromatin remodelers form complex regulatory networks, and when these networks go awry, cells can switch on oncogenic programs or silence tumor suppressors. We are especially focused on pancreatic cancer, which has the lowest five-year relative survival rate of all major cancers. Although the first RAS-targeted therapy was approved in 2026 for previously treated metastatic pancreatic cancer, durable treatment options remain limited. By systematically mapping the chromatin interactions that cancer cells depend on to survive and grow, we aim to uncover new therapeutic vulnerabilities that are invisible to DNA sequencing alone.