Gadd45 Stress Sensor Genes Springer. Este artículo no está disponible.Gadd45 Stress Sensor Genes Springer

This second edition is fully updated throughout and covers the emerging evidence that indicates that the Gadd45 family of proteins plays a unique and critical role as sensors of stress, including genotoxic, physiological, and oncogenic stress.  It sheds light on the complex cellular stress response, encompassing myriad molecular pathways with a plethora of regulators and effectors.

The GADD45 stress response genes encode small (18 kd) nuclear/cytoplasmic proteins.  These genes are rapidly induced by a wide variety of endogenous and exogenous stress stimuli. Despite marked similarities, Gadd45 genes are regulated differentially and exhibit functional diversity.  Gadd45 proteins respond to physiological and oncogenic stress, and are implicated in cell cycle arrest, DNA demethylation and repair, apoptosis, cell survival, genomic stability, and inflammation.

The purpose of this book is to provide a comprehensive overview of the unique global role that Gadd45 proteins play as stress sensors and the molecular pathways involved.

M. Raza Zaidi is an Associate Professor at the Fels Cancer Institute for Personalized Medicine and the Department of Cancer and Cellular Biology, Lewis Katz School of Medicine at Temple University (Philadelphia, PA, USA). He is also a member of the Blood Cell Development and Function Program of the Fox Chase Cancer Center. Raza received his PhD in Biochemistry and Molecular Biology from Robert Wood Johnson Medical School, Rutgers University (NJ), followed by a Postdoctoral Fellowship at the National Cancer Institute (NCI), National Institutes of Health (Bethesda, MD). The overarching goal of his research program is to understand the molecular underpinnings of cutaneous pathogenesis with a specific focus on delineating the molecular mechanisms of ultraviolet radiation (UVR)-induced melanomagenesis. Within this context, his laboratory has ventured into the basic biology of melanoblast/melanocyte development and migration, melanin biogenesis, and inflammatory and immunosuppressive responses to UVR exposure in the skin microenvironment.

Dan Liebermann received a PhD degree in cancer genetics at the Weizmann Institute, Rehovoth, Israel.  His postdoctoral training was at the Stanford University School of Medicine (1980-1985).  He started his independent research career at the University of Pennsylvania in 1985. He moved to Temple University School of Medicine in 1993, where he is currently a Professor of Cancer and Cellular Biology and the Fels Cancer Institute for Personalized Medicine in Philadelphia, Pennsylvania. The central theme of his research program has been elucidating the molecular mechanisms that govern normal cell development and carcinogenesis, notably blood cell development, inflammation, leukemogenesis, and breast carcinogenesis. He has made major contributions in the area of hematopoietic cell differentiation, identifying and characterizing myeloid differentiation (MyD) primary response genes, which play important roles in terminal differentiation of hematopoietic cells. He has made discoveries of several novel genes, including the GADD45 family of stress response genes.