My research is focused on the gap-junction protein Connexin43 (Cx43) as a regulator of intracellular signaling activated by therapeutic, hormonal and mechanical stimuli in osteocytes. A fundamental part of these investigations has been the generation and characterization of a genetically modified mouse model in which connexin43 has been deleted exclusively from osteocytes. Using this mouse model, I am studying the requirement of Cx43 for the survival of osteocytes and the effect of osteocyte apoptosis on bone formation and resorption.
