Emilia Galperin, PhD

My lab studies the functional cross-talk between endocytic and signaling cellular machineries. Endocytosis is a mechanism by which cells remove plasma membrane proteins, ligands, nutrients, lipids, and other molecules from the cell surface to the cell interior. Endocytosis also provides spatial and temporal control of signaling. However, there are gaps in our knowledge of the mechanisms of endocytosis cross-talk with signaling cascades. Our focus is on the extracellular signal-regulated kinases 1 and 2 (ERK1/2) signaling pathway that plays an essential role in several critical steps of embryonic development and tumor progression. The ERK1/2 pathway controls cellular functions such as apoptosis, motility, proliferation, and differentiation. Although kinases and phosphatases of this pathway have been studied extensively and targeted therapeutically, the mechanisms that determine the signal specificity and orchestrate the diverse biological outcomes of ERK1/2 signaling are still poorly understood. Scaffold proteins are critical players in the ERK1/2 signaling pathway. They integrate incoming signals and deliver signaling specificity. Yet, the mechanisms of their action are still not fully understood. Our goal is to uncover how scaffold proteins regulate ERK1/2 signals in the various biological processes.

Current studies in my lab aim to determine the mechanisms underlying the ability of the scaffold protein, Shoc2, to accelerate ERK1/2 signals. Shoc2 protein is essential for embryonic development and a critical regulator of ERK1/2 activity. We found that Shoc2 creates a signaling hub that regulates ERK's developmental signals in a spatio-temporal manner. To provide a detailed understanding of how Shoc2 is involved in determining the specificity of ERK1/2 signaling outcomes, we employ state-of-the-art innovative microscopy, genetic (zebrafish model), molecular, and cellular approaches. Our research will contribute to the advancement of novel therapeutic strategies and innovations for developmental disorders and cancer progression and potentially result in improved therapies with low toxicity.