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The ability of cells to sense and respond to changes in oxygenation underlies a multitude of developmental, physiological, and pathological processes. This volume provides a comprehensive compendium of experimental approaches to the study of oxygen sensing in 48 chapters that are written by leaders in their fields.
This book covers a wide biological range of problems regarding oxygen sensing in tissues. Oxygen sensing is defined as a process in which 02 reacts with different cellular components to avoid hypoxic cell damages. Oxygen sensing contributes to auxiliary mechanisms which help bacteria, invertebrates, vertebrates, and mammalians to survive and withstand hypoxic sensations. For the first time, experts from different disciplines have cooperated in examining various biological systems exhibiting this phenomenon.
Proceedings of the XIVth International Symposium on Arterial Chemoreception, held June 24-28, 1999, in Philadelphia, Pennsylvania. This volume, containing the proceedings of the fourteenth biannual ISAC meeting presents a new departure from their traditional focus on arterial chemoreceptors and their functions, in the expansion to include the study and discussion of oxygen sensing in other tissues and cells, and the genes involved. Bringing together scientists from cellular and systemic boundaries of physiology, working at the interface of cellular and molecular biology, this book, containing new physiological and biochemical perspectives.
This book represents an updated review of the physiology of the carotid body chemoreceptors. It contains results in the topics at the frontiers of future developments in O2-sensing in chemoreceptor cells. Additionally, this volume provides data from studies carried out in other O2-sensing tissues including pulmonary vasculature and erythropoietin producing cells. It is a prime source of information and a guideline for arterial chemoreception researchers.
This book describes the methods of analysis and determination of oxidants and oxidative stress in biological systems. Reviews and protocols on select methods of analysis of ROS, RNS, oxygen, redox status, and oxidative stress in biological systems are described in detail. It is an essential resource for both novices and experts in the field of oxidant and oxidative stress biology.
Erythropoiesis represents a vital physiologic process that can be adjusted to combat compromised oxygen availability, otherwise known as hypoxia. The canonical response to adapt to hypoxia is mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1). When oxygen is available HIFalpha subunits are hydroxylated by prolyl hydroxylase enzymes (PHD1-3) to allow for binding to the von Hippel-Lindau (VHL) tumour suppressor protein, which serves as the substrate recognition subunit of an E3-ubiquitin ligase complex that ultimately targets proteins for proteasome-mediated degradation. The work presented in this thesis demonstrates a novel role of VHL in recruiting DCNL1 to initiate E3-ubiquitin ligase enzymatic activity which, in essence, allows for the degradation of HIFalpha to commence. In hypoxia, hydroxylation does not take place and as a result HIFalpha can promote the transactivation of a repertoire of genes that aid in adaptation to hypoxia including one which encodes the glycoprotein hormone erythropoietin (EPO). EPO binds to EPO receptor (EPOR) expressed on erythroid progenitor cells to promote their proliferation and differentiation into red blood cells. An erythroid specific oxygen sensing pathway is elucidated in this thesis wherein EPOR is hydroxylated by PHD3 to promote VHL-mediated degradation in a manner analogous to HIFalpha. Combined, these findings build upon our fundamental understanding of how cells detect and counter hypoxic stress.