Tullio Pozzan
University of Padua
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Primary Section: 23, Physiology and Pharmacology Secondary Section: 22, Cellular and Developmental Biology Membership Type:
International Member
(elected 2006)
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Biosketch
Tullio Pozzan is presently Emeritus Professor at the University of Padova and Emeritus Researchers of the Italian National Research Council. Dr. Pozzan is known for it contributions to the development of numerous methods for the study of second messenger signaling in living cells and for his studies on the role of mitochondria in Ca2+ signaling processes. Dr. Pozzan was born in Venice, went to Padova to study Medicine where he graduated in 1973. Soon after graduation he started to work on the mechanism of mitochondrial ion fluxes. In 1977 he moved to Cambridge (UK) as a postdoctoral fellow where he started a life long collaboration with Roger Y. Tsien (Nobel laureate in Chemistry in 2008). They developed together the first intracellularly trappable fluorescent Ca2+ indicators and they demonstrated the importance of Ca2+ signaling in leukocyte activation. Back in Padova in 1981, he created an independent group and he developed the first genetically encoded targeted Ca2+ and l cAMP sensors. He has been President of the European Cell Biology, Organization, he is member of the National Academy of Sciences since 2006, of the Royal Society of Canada and of the Royal Society of London and of the Accademia dei Lincei.
Research Interests
Tullio Pozzan group is presently focused on the study of Ca2+ and CAMP signaling in different pathophysiological conditions, in particular in mouse models of Alzheimer disease and of cardiac dysfunctions. His lab continues the development of novel approaches to investigate the dynamics of second messenger levels in live cells in situ and in vivo with special interest for the involvement of mitochondria. To this end they have recently developed novel genetically encoded fluorescent probes for Ca2+ and cAMP that allow to investigate the subcellular distribution of these signals not only is isolated cells, but also in intact anesthetized mouse models. These novel approaches have led to the understanding of the modification of mitochondrial functionality in mouse models of genetic forms of Alzheimer, in the uncovering of the mechanisms leading to intracellular Ca2+ and cAMP microdomains generation and their importance in key pathophysiological processes such as apoptosis, autophagy and cardiac cell dysfunctions.
