My laboratory is interested in understanding the role of the calcium/calmodulin dependent protein kinase (CaMK) signaling cascade in cell biology and how its alterations contribute to disease. We use global and conditional knockout mouse models as well as pharmacological inhibitors to investigate the mechanisms by which one of the upstream kinases in the CaMK cascade, CaMKK2 along with its downstream kinases AMPK, CaMKI and CaMKIV, as well as targets regulate the fate and function of bone marrow-derived mesenchymal stem cells, bone cells and well as prostate cancer. CaMKK2 is over-expressed in prostate cancer and recent studies identify it to be a direct target of androgen receptor. We are interested in identifying the effects of CaMKK2 inhibition in prostate cancer-associated bone metastasis as well as establishing the identity of its downstream targets in prostate cancer as well as bone cells. Functional outcome of the manipulation of the CaMK cascade in age and cancer-associated osteoporosis is also special focus of our lab.
Pharm.D. - Duke University Medical Center, Durham, NC 2003-2007
Ph.D. - The Ohio State University, Columbus, OH 1997-2003
