Graduate Students and Postdoctoral Scholars in the lab are working on 3 areas of research: immune cell signaling,  immune dysfunction and protein regulation.

Immune cell signaling, particularly the earliest signaling events that occur at the membrane, starting with receptor ligation and the activation of the membrane-proximal protein tyrosine kinases (i.e. Src, Lyn, Fyn, Hck, Fgr, Syk). We also focus on how receptor ligation influences signal output, how networks of kinases and phosphatases are mobilized specifically in response to different types of stimuli, and how negative feedback processes restrain inflammation. 

Our lab studies how myeloid cells discriminate between inflammatory ligands to promote different types of responses, and how different basal states can bias the response of myeloid cells to pro-inflammatory stimuli. Immune cells can become dysfunctional by circumventing regulatory signaling blockades to create dysfunctional hyperinflammatory or immunosuppressive polarization states. Identifying the mechanisms driving these dysfunctional states will help us identify key events or lynchpin proteins that may be therapeutically modulated to treat patients with autoimmune disease and cancer.

Protein Regulation, Structure, and Dynamics: We study the fundamental mechanisms by which signaling proteins are activated and inhibited: protein-protein interactions, localization, and energetic constraints. We have used structure, biophysics and structure-guided mutagenesis to test questions about protein dynamics, allosteric regulation, and dimer formation in membrane-proximal signaling proteins. Most recently, we are investigating the role of dimerization in the tyrosine kinase Csk, the master negative regulator of the Src-family kinases.

View publications here.

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