Senior Scientist and Principal Investigator: Mike Forte
The Forte lab is exploring the use of small molecule inhibitors of the mitochondrial calcium efflux pathway and their use as therapies in a variety of devastating human diseases.
Mike Forte firstname.lastname@example.org
B.S., University of Notre Dame, 1973
Ph.D., University of Washington, 1978
I was raised in Seattle, WA and graduated summa cum laude from the University of Notre Dame. Missing the Northwest, I decided to return to the Seattle for my graduate training in the Dept. of Genetics at the University of Washington. My thesis project focused on initial attempts to understand chromosome structure using yeast as an experimental model. After finishing my Ph.D. work, my attention turned to something new, and I spent four years in the laboratory of Dr. Ching Kung at the University of Wisconsin in Madison, WI as a postdoctoral fellow. My projects there focused on trying to understand the molecular basis of a variety of ion channel mutants that had been generated in the protozoan Paramecium. My first faculty position was in the Dept. of Biology at Case Western Reserve University in Cleveland, OH where I continued to work on Paramecium but became fascinated by trying to understand the nature of the protein conformational changes driven by voltage changes in ion channels. For a number of years, we modeled these changes within the context of a mitochondrial protein, exploiting the powerful genetics available in the yeast system. While at Case, I began my work on cell signaling in Drosophila, which eventually focused on the mechanisms responsible for synaptic growth. In 1986, I jumped at the chance to move back to the Northwest and was a founding member of the Vollum Institute. Currently, my lab is trying to understand the role of mitochondria in cellular Ca2+ homeostasis.
Justina Šileikytė email@example.com
B.Sc., Vilnius University, Lithuania, 2007
M.Sc., Vilnius University, Lithuania, 2009
Ph.D., University of Padova, Italy, 2013
While a master student in Biophysics at Vilnius University, Lithuania, I was awarded an Erasmus Fellowship that allowed me to spend time in the laboratory of Dr. F. Ricchelli at the University of Padova, Italy. At this point, I began my studies on the mitochondrial permeability pore (PTP), an inner mitochondrial membrane channel involved in numerous pathologies, by investigating a specific outer membrane protein, TSPO, and its role in the regulation of PTP activity. After obtaining my MSc degree, I enrolled as a PhD student in the Cellular Biology Program at the University of Padova and continued my studies on the PTP with Dr. Ricchelli and Dr. P. Bernardi. Meantime, I got interested in High Throughput Screening of small molecule libraries and took part in an NIH-funded program of Drs. Forte and Bernardi aimed at identifying novel inhibitors of the PTP. Recently, I have joined Mike Forte's lab in order to support characterization as well as target identification campaign of these molecules.
The Forte laboratory currently focuses on the role played by mitochondria in cellular Ca2+ homeostasis and cell death. For these studies the lab uses genetic, biochemical and pharmacological analysis in mammalian systems. Most of these studies focus on the physiological role of a specific mitochondrial Ca2+ efflux pathway known as the mitochondrial permeability transition pore (PTP). By generating specific lines of mutant mice, the lab has demonstrated that the repression of PTP opening confers stunning resistance to cell death in mouse models of some of the most therapeutically challenging human diseases. In a complimentary set of studies, a battery of potent small molecule inhibitors of the mitochondrial Ca2+ efflux have been identified. The current studies center on the use of these inhibitors as tools to identify yet unresolved biochemical components of the PTP, and on their use as therapies for a variety of devastating human diseases in which altered mitochondrial Ca2+ handling have been implicated.
Shutting down the Pore
Prolonged opening of the mitochondrial permeability transition pore (PTP) causes mitochondrial dysfunction and promotes cell death. It is implicated in a variety of the most therapeutically challenging human diseases and is a target of interest for novel therapeutics.
Vollum Institute, OHSU
3181 SW Sam Jackson Park Rd.
Mail code L474 (regular mail)
Dock 4, Vollum Rm. 3402B (express mail)
Portland, OR 97239-3098