B.A., Chemistry, Southern Illinois University at Carbondale. 1972
Ph.D., Physical Chemistry, Stanford University, 1977.
NIH postdoctoral fellow, Cell and Molecular Biology, The Biological Laboratories,Harvard University, 1977-81
Princeton University, Biology Department, 1981-88
The Worcester Foundation for Experimental Biology, 1988-97
University of Massachusetts Medical School,1989-present
Mechanochemical Signal Transduction, Muscular Dystrophy
Cells modulate their internal stiffness (cortical tension) in response to external forces, such as the stiffness or chemical composition of their extracellular environment. Poorly understood signaling pathways downstream of mechanical stimulation regulate cell growth, survival and differentiation. Increased stiffness of the extracellular matrix (ECM) can promote tumor growth or lead to increased size (hypertrophy) of muscles. Cross-talk between these growth and survival pathways is limits some cancer treatments, resulting in choices between cancer reoccurrence and heart failure.
Our laboratory is interested in how the signaling and cytoskeletal proteins at the plasma membrane transduce signals arising from extracellular force into cellular responses. We have linked membrane proteins known for their roles in muscular dystrophies to signaling pathways understood best for their roles during tumor cell growth and migration. We are finding both similarities and differences between these pathways in tumor and other nonmuscle cells versus skeletal muscle and heart cells. We aim to both increase our basic understanding of stiffness-sensing biochemical sensing and to identify cell type-specific interactions that can be targeted for chemotherapeutics and muscular dystrophies.
Kay Son, Ph.D.
Tara Smith, M.S.