"High Noise to Signal: Lessons from a Reported Tumor Suppressor"

Venue: MSI Small Lecture Theatre

Host:  Dr David Murray

Abstract

Cellular and organismal growth depend heavily on the PI3K/Akt signaling pathway. Dysregulation of the pathway is observed in cancer, overgrowth disorders, and metabolic disease. The mechanisms that ensure the timely activation and inactivation of Akt are therefore critical to organismal homeostasis and therapeutically relevant in the treatment of disease. In the first part of my talk, I will describe the mechanism by which Akt is turned on by PIP3, the signaling lipid generated by growth factor-mediated activation of PI3K. In the second part, I will present evidence that PHLPP, a phosphatase previously reported to inactivate Akt, is, in fact, a pseudophosphatase and that cancer genomics do not support a role for PHLPP in cancer. Finally, I will present some evolutionary clues as to the real biological function of PHLPP.