Laurent Dejean, Ph.D.
Office Location: Science 1, Room 356
Office Phone: 559.278.2008
Dr. Dejean earned his Ph.D. in Biochemistry and Cell Biology from the University of Bordeaux 2. He has done post-doctoral research at the University of Barcelona and worked as a research assistant and faculty member at New York University. He joined the chemistry faculty at Fresno State in 2011.
Areas of Specialty
Mitochondria are organelles involved in both life and death processes within all eukaryotic cells. These organelles release pro-death mediators during early apoptosis; and this release represents the commitment step of programmed cell death. The Bcl-2 family of proteins is a key regulator of the mitochondrial response to apoptotic signals. This family contains both pro- (Bax and Bak) and anti- (Bcl-2 and Bcl-xL) apoptotic members. All these proteins eventually localize to mitochondria and finely regulate the release of apoptotic mediators. The focus of my research is to understand the mechanisms that underlie and control this release of mitochondrial proteins during both physiological and pathophysiological conditions.
The upregulation of the anti-apoptotic Bcl-2 and/or Bcl-xL leads to a resistance to apoptosis associated with tumor formation. Mimicking this status through Bcl-2 or Bcl-xL overexpression induces the inhibition of mitochondrial permeabilization. Interestingly however, Bcl-2 or Bcl-xL overexpression leads to an increase of Bax in the mitochondrial outer membrane. Thus, Bcl-2 and Bcl-xL seem to antagonize Bax in healthy cells, but these proteins may become “partners in crime” to eliminate tumors by allowing the accumulation of Bax at the mitochondria. The objectives of our laboratory are then to investigate the molecular mechanisms through which Bcl-2 and Bcl-xL capture Bax at the mitochondria and how this phenomenon could allow to specifically kill cancer cells. We will more particularly study the effects of Bcl-2/xL expression levels on mitochondrial Bax interactome. Finally, the influence of Bcl-2/xL binding capacity to Bax on cell bioenergetics will also be investigated as metabolic alterations are a common feature in several types of tumors.