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"We are a cell biology laboratory interested in gaining a better understanding of the molecular regulation of endocytosis and its integration within wider cell signaling and metabolic homeostasis.
Recently, our collaborative efforts identified the molecular basis of the NAK kinase-mediated phosphorylation of the most abundant clathrin adaptor, AP2 (link to paper). We showed that AP2 phosphorylation not only leads to changes in its interactome, but is a major decision point in clathrin-mediated endocytosis, capable of affecting its rates.
We are building on these findings by exploring systematically and mechanistically how kinases and phosphatases regulate clathrin-mediated endocytosis. We focus on NAK kinases, which are also recent drug development targets for neuropathic pain, and were linked by GWAS to an increased neurodegeneration risk."
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