Paul Lampe

Dr. Paul Lampe received a B.A. from Carleton College and a Ph.D. in Biochemistry from the University of Minnesota. Since 1995, he has been on the faculty of the Fred Hutchinson Cancer Research Center in Seattle, Washington and the University of Washington, and is presently cohead of the Translational Research Program. Dr. Lampe has studied how gap junctions are regulated for over 30 years and has published over 115 articles in peer-reviewed journals.

The Lampe Laboratory at the Fred Hutchinson Cancer Research Center, investigates the control of cell growth at the cell biological level to mechanistically connect gap junction regulation with wound repair responses in skin, hypoxic events in the heart and cell cycle, as well as the control of cell growth and how the relationship is disrupted during carcinogenesis. Gap junctions allow diffusion of small molecules (<1000 MW) between adjacent cells via matched cell-to-cell membrane channels. Vertebrate gap junctions are composed of proteins derived from the connexin gene family and the Laboratory’s results indicate that gap junction formation and degradation are highly regulated via protein kinases at various stages of wound repair. Gap junctions are highly dynamic and are created and degraded within minutes to hours. The Lampe Laboratory data indicates kinases such as Akt, PKA, PKC, CK1, cdc2/cyclin B, MAPK and others, regulate specific steps of gap junction protein export, assembly, channel gating (opening and closing of the channels) and size and degradation. During the first 48 hours of wound repair, at least 4 kinases are sequentially activated to facilitate a coordinated cellular response via proliferation and migration. Paul Lampe’s Laboratory has studied the functional consequences of these phosphorylation events in terms of the level of intercellular communication, proliferation, migration and interaction with other key regulatory proteins, and has concluded that gap junctions play key roles in initiating wound repair and migration, followed by their downregulation to permit cellular proliferation in normal skin. This work has been continuously funded by the National Institutes of Health for the last 18 years.