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We study the mechanisms by which anucleate blood platelets and their parent megakaryocytes respond to disease.

Blood platelets play critical roles in multiple processes and diseases, from their traditional function in hemostasis and would healing to inflammation, immunity, cancer metastasis and angiogenesis. There is evolving evidence that the molecular signature of platelets may be changed in disease conditions where these processes are altered. Our interests are in identifying the precise mechanisms utilized by platelets in adapting to the disease environment. 

To that end, we apply integrative strategies of omics-based discovery (from large clinical cohorts) paired with molecular, cellular, in-vivo and computational approaches for validation. Recent findings have outlined a number of heretofore unrecognized platelet mechanisms that are central to platelet response in disease. One such mechanism we identify is the unfolded protein response (UPR) significant in the platelet translational machinery, proper folding of proteins and protein homeostasis. Current focus of our research is directed toward a molecular understanding of the UPR and the broader integrated stress response in the platelet, and deciphering what fraction, if any, is derived from their parent megakaryocytes. Substantial additional effort is also directed at other platelet responses, including their cross-functional interactions with other immune cells.