Search:

Product Information All Elsevier Sites   Advanced Product Search
SiteStat.jsp
BBA - Molecular Cell Research - Autophagy

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research BBA - Molecular Cell Research
External linkAutophagy
Volume 1793, Issue 9,  Pages 1395-1532 (September 2009)
Edited by G. Kroemer and J.-C. Martinou

Although autophagy, as it occurs in human cells, has first been viewed as a mechanism of cellular self-destruction, now the notion emerges that autophagy constitutes a homeostatic process that, after stress, guarantees for the optimal restoration of the equilibrium state at the cellular and organismal levels. The future will tell whether this paradigm shift is definitive or whether the pendulum will swing back and reveal an essential role for autophagy in the pathogenic loss of some human cell types, in specific diseases

Image

Guido Kroemer, M.D. Ph.D. Research Director, INSERM, Institut Gustave Roussy, Villejuif, France. Guido Kroemer is currently a research director at the French Medical Research Council (INSERM), and the director of the Research Unit "Apoptosis, Cancer and Immunity" at the Institut Gustave Roussy located in Villejuif, near Paris, France. Prior to joining the INSERM (1993), Dr. Kroemer was a senior scientist of the European Community at the Spanish National Research Council (CSIC), at the National Center of Molecular Biology (1990–1992), and at the National Center of Biotechnology (1993). Dr. Kroemer did his post-doctoral training in the Collège de France, Nogent-sur-Marne (1988–1989) and at the University of Innsbruck, Austria, after receiving his Ph.D./M.D. degree at the same university in 1985. He also holds a Ph.D. in biology (Autonomous University of Madrid, 1992). Guido Kroemer's team discovered in 1994 that mitochondrial membrane permeabilization is a critical step in programmed cell death. His current research focuses on pathogenic derangements of programmed cell death, the pathophysiology of autophagy, the molecular perturbations of cancer cell apoptosis, the pharmacological induction of apoptosis, and the role of immunogenic cell death in anticancer therapy. Guido Kroemer is the most cited scientist worldwide in the field of cell death as well as in the area of mitochondrial research. He is member of EMBO, German Academy of Sciences (Leopoldina), Academia Europaea, and European Academy of Sciences and Arts. He received the 2006 Descartes Prize, the highest scientific distinction of the European Union, for his fundamental discoveries in the field of programmed cell death (apoptosis). He also received one of the Grands Prix from the French Academy of Sciences in 2007, as well as the Carus Medal from the German Academy of Sciences.

Back to top
Image

Jean-Claude Martinou, M.D., Ph.D. Jean-Claude Martinou is currently a professor and the head of the Department of Cell Biology at the University of Geneva, Switzerland. After specializing in hematology in Toulouse, France in 1986, Dr. Martinou completed his Ph.D. at the CNRS in Toulouse and a post-doc at Washington University Medical School in St-Louis, USA. In 1990, he moved to Switzerland and worked at Geneva University to study the molecular mechanisms of neuronal apoptosis. In 1992, he joined the pharmaceutical industry and became the director of the Neurobiology Division at Glaxo Institute for Molecular Biology (1996–1997) and at Serono Pharmaceutical Research Institute in Geneva (1998–2000). In 1992, Dr. Martinou's team was the first to report an anti-apoptotic function of Bcl-2 in neurons, during development and under pathological conditions. This finding suggested that the cell death program was conserved among cell types and that its inhibition could be beneficial in several pathologies. Since then he has been interested in understanding the molecular mechanisms of Bcl-2 family members, in particular at the mitochondrial level. In 1997 his group reported the ability of Bax, a pro-apoptotic member of the Bcl-2 family, to form pores in lipid planar bilayers. Dr. Martinou's team is now trying to decipher the mechanisms by which Bax triggers the permeabilization of the outer mitochondrial membrane during apoptosis.

Back to top


  
Printer-friendly version   Printer-friendly version