Associate Professor, Eppley Institute
Ph.D. - University of Texas, M.D. Anderson Cancer Center and Health Science Center at Houston
Apoptosis is a cellular program that removes unwanted or damaged cells in order to ensure proper development and maintain tissue homeostasis. Deregulation of apoptosis contributes to the etiology of degenerative diseases and cancer. During apoptosis, upstream pathways initiated by various stimuli converge onto mitochondria, which release apoptogenic factors and cause cell death. We are interested in the regulation of this mitochondria-dependent cell death pathway. In particular, we focus on two major upstream regulators of this pathway, the Bcl2 family members and calcium. Experiments are being carried out to investigate how Bid, Bim, Bax and other pro-apoptotic Bcl2 family members receive upstream signals and relay the signals to mitochondria. We hope to identify cellular mechanisms that either positively or negatively regulate this signal transduction pathway. Since calcium level is deregulated during apoptosis induced by multiple stimuli, and on the other hand, elevated intracellular calcium is known to damage mitochondria, we would also like to delineate the pathways that lead to calcium deregulation and mitochondrial damage. Our goal in these studies is to uncover the molecular details of how signals from the cell surface or the nucleus are transmitted to mitochondria and eventually lead to the destruction of the cell.
E-Mail: Xu Luo