biography
“I study the fundamental mechanisms of cell death because, ironically, cell death is key to life.” – Don Newmeyer, Ph.D.
Dr. Newmeyer is currently a Professor of LIAI's Cellular
Immunology division, and has served on the LIAI faculty since 1994. Dr.
Newmeyer's research focuses on the functioning of apoptosis, or
programmed cell death, and the role of mitochondria during the process.
Dr. Newmeyer received his B.S. in physics and his M.S. in mathematics
from Drexel University in 1976. In 1980, he received an M.S. in
biophysics from the University of Rochester, followed by his Ph.D. in
biophysics in 1983. That same year, Dr. Newmeyer began his postdoctoral
work at the Biocenter of the University of Basel in Basel, Switzerland.
In 1985, he returned to the U.S. to begin a postdoctoral fellowship
with the University of California, San Diego in its Biology Department.
From 1989 to 1994, Dr. Newmeyer worked as an assistant staff scientist
at the La Jolla Cancer Research Institute.
Dr. Newmeyer received the Newcomen Award for Excellence in Chemistry and Physics from Drexel University in 1976.
research focus
Cells in the body can undergo a process of suicide, called programmed
cell death or apoptosis. This process is important for the normal
development of the body plan in embryos, as well as for maintaining the
size of adult organs and regulating the normal function of the immune
system. Furthermore, a number of diseases, including cancer, AIDS, and
autoimmune disorders, involve the improper control of this cell death
process.
The Newmeyer laboratory is investigating the detailed mechanisms of
programmed cell death that operate inside the cell. In particular, the
team is examining how mitochondria-the "energy factory" in the cell-
play a critical role in the apoptotic cell death program. A basic
understanding of this process will likely suggest new approaches for
the treatment of diseases that involve the inappropriate death or
survival of certain types of cells.
selected publications
Caspase-independent mitochondrial cell death results from loss of respiration, not cytotoxic protein release. Mol Biol Cell. 2009
Opa1-mediated cristae opening is Bax/Bak and BH3 dependent, required for apoptosis, and independent of Bak oligomerization. Mol Cell. 2008
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