BCL‐2 Protein Family: Essential Regulators of Cell Death

· Springer Science & Business Media
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145
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About this ebook

In this book, scientists pioneering the field have compiled a series of focused chapters to highlight the relevance of the BCL‐2 family of proteins in apoptosis, physiology and disease. An important focus of this volume is considering the potential TH ERA PEUT IC benefits of targeting apoptosis pathways in the context of human disease. Readers interested in understanding how a cell handles stress and the consequences of dysregulation of this process for human disease will find this book very valuable. It attempts to describe a fascinating area of research where physiology and biomedicine converge at different levels, revealing a trip from the molecular regulation of apoptosis to the impact of this process to the physiology of a whole organism.

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About the author

Claudio Hetz received his BA in Biotechnology Engineering from the University of Chile in 2000. In his PhD work with Claudio Soto at Serono Pharmaceutical Research Institute, Geneva, he showed that Prion pathogenesis involves endoplasmic reticulum stress responses and apoptosis. In 2004 he joined as a postdoctoral fellow Stanley Korsmeyer’s lab at Dana‐Farber Cancer Institute, a pioneer in the apoptosis field. Together they discovered new functions of the BCL‐2 family in organelle physiology. Dr. Hetz followed his projects in Laurie Glimcher’s lab at Harvard. During this period he expanded his studies on neurodegeneration, addressing the connection between apoptosis and the unfolded protein response in vivo. Since 2007 he is an Assistant Professor at the University of Chile and adjunct professor at Harvard. His lab uses animal models to investigate the signaling responses involved in protein misfolding disorders and the role of the BCL‐2 protein family in stress conditions. He was recently awarded with the TWAS‐ROLAC Young Scientist Prize, also as finalist with the Eppendorf and Science Award in Neurobiology, and other important recognitions.

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