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Researchers in the Levine Lab investigate bone and mineral metabolism, including disorders of parathyroid development, vitamin D homeostasis, and mechanisms for G-protein-coupled signal transduction. The laboratory has identified or characterized the molecular genetic basis for a number of clinical disorders of bone and mineral metabolism and advanced understanding of the role of transmembrane signaling in regulating cellular activity.
The lab has extensive research experience analyzing gene targets and transcriptional regulation, as well as in investigations of osteoporosis, vitamin D insufficiency, and pharmacological modulators of bone remodeling, including parathyroid hormone analogs, sclerostin antagonists, and bisphosphonates.
Additional research interests in the Levine Lab extend to the molecular basis for embryological development of the parathyroid glands.
Employing translational and basic research, work in the Levine Lab has led to the identification of the molecular and genetic bases of several conditions and disease mechanisms:
- Albright hereditary osteodystrophy
- Progressive osseous heteroplasia
- McCune Albright syndrome
- Novel forms of vitamin D-dependent rickets due to inactivation of CYP2R1
- The principal 25-hydroxylase
- Over-activity of CYP3A4, an important enzyme involved in the metabolism of many steroids and drugs.
Michael A. Levine, MD, FAAP, FACP, MACE
Medical Director, Center for Bone Health
Dr. Levine has an active laboratory research program that complements and extends his clinical studies. He has identified the molecular basis of several inherited disorders of mineral metabolism. His research interests extend to the molecular basis for embryological development of the parathyroid glands.