Development and regeneration require various kinds of intercellular signaling and adhesion molecules. Our research has been focused on regulatory mechanisms of such cell-cell interactions. Numerous intercellular signaling molecules are generated as membrane-anchored proteins, and they are subjected to proteolytic processing to liberate their extracellular domains (ectodomain shedding). Molecular bases that regulate the ectodomain shedding events are coming into focus. Evidence suggests that ADAM family proteases are involved in the ecotodmain shedding of various membrane proteins. We are currently studying roles of ADAM proteases in development and diseases, which will clarify physiological significance of ecdodomain shedding mediated by ADAM proteases.
Prof. Hiroshi Kawamoto
Assist. Prof. Kyoko Masuda
The major aim of our laboratory is to elucidate the molecular mechanisms that regulate cell fate decisions in the process of lineage restriction from multipotent hematopoietic stem cells to unipotent progenitors. A series of studies from our laboratory on early hematopoiesis have led to a fundamental redefinition of lymphoid progenitors as well as the ontogeny and phylogeny of T- and B-cell development. We thus have proposed our original model of hematopoiesis, namely “myeloid-based model”, in which myeloid potential is retained along with specification pathway towards erythroid, T, and B cell lineages. Among various events occurring during hematopoiesis, we are mainly focusing on the process towards the production of T cells.