In healthy adults, cell adhesion is tightly regulated and migration of most cell types is limited, unless stimulated by infection or wounding. Initiation of migration depends upon recognition of changes in the protein environment by individual cells.
I am interested in molecules that detect matrix markers of tissue damage and result in cell mobilisation. The interaction of cells with fresh matrix causes membrane protrusion, formation of new cell adhesions and disassembly by endocytosis of existing attachment points; each of these must occur in a polarised fashion.
Initiation and suppression of cell migration are equally important; failure in the former would result in healing defects, failure of the latter would result in tumour formation.
Therefore I use cell-based biochemical and imaging techniques to examine the temporal and spatial regulation of migration signals, thus resolving the molecular mechanism of intrinsic repair mechanisms.