These two kinases are found in the same tissue and cell types, exist in similar subcellular regions, phosphorylate similar substrates and are thought to exert redundancy in signal transduction. However, we hypothesize that their must be specificity in signaling between these two kinases and that their specific signals are likely to be integrated to modulate a specific biological response that governs cell growth. Our work with Src focuses on a substrate that is a binding partner for Src. We are currently engaged in trying to understand the molecular mechanism by which AFAP-110 transmits signals from Src that lead to the disruption of actin filaments. This may be a fundamentally important concept for cancer research, as the one thing all cancer cells have in common is a change in cell shape.
Cellular shape is governed by the cytoskeleton, of which actin filaments play a predominant role.
Our work with Yes is focused on understanding the unique signals sent by Yes and not Src. We have discovered that Yes is differentially regulated, compared to Src and we are trying to understand the mechanism for Yes regulation. This may be important, as colon cancer patients who have an activated Yes oncogene have a very poor prognosis. In addition, we have identified a tyrosine phosphorylated protein that specifically binds to Yes and not Src. It is possible that this protein may modulate Yes-specific signaling events.