Department of Biomedical and Applied Sciences
Indiana University School of Dentistry
United States of America
Ph.D. in Biochemistry and Molecular Biology, The University of Melbourne and St. Vincent’s Institute of Medical Research, Victoria, Australia. Postdoctoral Fellowship, Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Associate Research Scientist, Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, CT, USA.
The maintenance of bone mass in adult life depends upon the coordinated activities of both the osteoblasts, which make new bone, and the osteoclasts, the cells responsible for bone degradation. In skeletal diseases such as osteoporosis, Paget’s disease and hypercalcemia of malignancy, unregulated bone resorption by osteoclasts results in low bone mass, skeletal fragility and increased risk of bone fracture. The metabolic bone diseases and periodontitis also result in alveolar bone loss, tooth mobility and ultimately, tooth loss. Osteoclast adhesion and migration along the bone surface involves remodeling of its cytoskeleton and the assembly, organization and disassembly of specialized adhesion structures named podosomes. My laboratory is focused on identifying and characterizing key intracellular signaling proteins and protein complexes that are involved in regulating the attachment, migration and bone resorbing activity of osteoclasts. To this end, we are currently using a number of transgenic and knockout mice to investigate the role of specific tyrosine kinases, actin-regulatory proteins and GTP-binding/hydrolyzing proteins in regulating osteoclast function.
Huang S, Eleniste PP, Wayakanon K, Mandela P, Eipper BA, Mains RE, Allen MR, Bruzzaniti A. The Rho-GEF Kalirin regulates bone mass and the function of osteoblasts and osteoclasts. Bone. 2013 Dec 28. pii: S8756-3282(13)00545-0. doi: 10.1016/j.bone.2013.12.023. [Epub ahead of print] PubMed PMID: 24380811