The focus of our research is to understand how cells in multicellular organisms such as mammals acquire their identity to become specialized cells, such as bone-forming cells (osteocytes), bone-resorbing cells (osteoclasts), cartilage-forming cells (chondrocytes), or fat-forming cells (adipocytes). Over the last two decades, our laboratory has identified several key intrinsic factors and their related signaling pathways that are required for skeletal homeostasis. Namely: TGFbeta-Vimentin-ATF4 in mesenchymal stem cells; ATF4-Ihh in chondrocytes; ATF4-Osteocalcin and ATF4-Rankl in osteoblasts; ATF4-Hop2 in committed osteoblasts, and Hop2-C/EBP in committed adipocytes. Our current work focuses on defining the mechanisms by which ATF4 in cartilage controls the transcription of Rankl and Mmp13 to regulate the transition of cartilage to bone. Our ultimate is to translate the knowledge gained from such research into developing better and more efficient care plans for people suffer from skeletal diseases including dwarfing conditions, bony nonunion, fracture repair and osteoporosis.
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