Non-canonical Autophagy: Mechanisms and Pathophysiological Implications outlines the differences between ‘canonical’ and ‘non-canonical’ forms of autophagy, highlighting the discoveries concerning the molecular mechanisms underlying these unconventional forms of autophagy and the advancements in pathophysiological features of ‘non-canonical’ autophagy. Non-canonical Autophagy: Mechanisms and Pathophysiological Implications also discusses all the forms ‘non-canonical’ autophagy and the complexity of autophagy-dependent cell death as the challenges and pitfalls in the development of clinically viable modulators of autophagy. This book aims to give readers a better understanding of mechanisms underlying ‘non-canonical’ autophagy so that they can interpret biological effects of autophagy correctly and identify reliable novel and effective treatment strategies. Presents the most advanced information regarding the molecular mechanism underlying non-canonical autophagy Outlines the increasing evidence regarding the involvement of non-canonical autophagy in multiple physiological and pathological processes Discusses the therapeutic potential of autophagy modulators and the obstacles that have limited their development
|Author||: Paula Maldonado Villavicencio|
|Release Date||: 2019|
|Pages||: 329 pages|
Autophagy in Health and Disease offers an overview of the latest research in autophagy with a translational emphasis. This publication takes scientific research in autophagy a step further and offers integrated content with advancements in autophagy from cell biology and biochemical research to clinical treatments. A necessary reference for the bookshelf of medical and scientific researchers and students, Autophagy in Health and Disease presents high quality, reputable information on autophagy, allowing the reader quick access to the most applicable information. Discusses current understanding of the roles of autophagy in health and disease Covers the background of autophagy, the development of tools and therapeutics to measure and modulate autophagy, and autophagy in tissues and disease processes Features an accompanying website with figures and tables
What is autophagy? Why would neurons or other brain cells digest parts of themselves through autophagy? How can autophagy save the lives of cells under some conditions, but act as a culprit or accomplice to cell death in others? How does dysfunction of autophagy contribute to neurological diseases and can it be repaired or restored? This book addresses these questions and provide an expert view of the emerging concepts in autophagy research, focusing on autophagic processes and regulation in neurons. Current experimental evidence for both evolutionarily conserved and specialized regulatory mechanisms for autophagy in the mammalian nervous system will be presented. Advances in our understanding of the complex interplay of autophagy induction and downregulation will be discussed in relation to the critical balance needed to modulate neuroprotection versus neurodegeneration in the context of neurological diseases including Alzheimer's, Parkinson's, Huntington's, ischemic-hypoxic and lysosomal diseases.
The cyclic purine nucleotides 3’,5’-cAMP and 3’,5’-cGMP are well-established second messengers. cGMP has recently been covered in a volume of the Handbook of Experimental Pharmacology (volume 191). In addition to 3’,5’-cAMP and 3’,5’-cGMP, so-called non-canonical cyclic nucleotides exist. These comprise the cyclic pyrimidine nucleotides 3’,5’-cCMP and 3’,5’-cUMP, the purine nucleotide 3’,5’-cIMP, the 2’,3’-nucleoside monophosphates and cyclic dinucleotides. In this volume of the Handbook of Pharmacology, word-leading experts in the field summarize our current knowledge on these non-canonical cyclic nucleotides, discuss open questions, future research directions and the pharmacotherapeutic implications. Special emphasis will be given to the emerging roles of 3’,5’-cCMP and 3’,5’-cUMP as second messengers with regard to generators, effectors, biological functions, inactivation and bacterial toxins. The role of 3’,5’-cIMP as potential second messenger will also be critically discussed. Furthermore, we will consider transport of cyclic nucleotides and their potential role as first messengers. The role of the cyclic dinucleotide cGAMP in the immune system will covered, too. Lastly, the book will present important methodological aspects ranging from mass-spectrometric methods for cyclic nucleotide detection to the synthesis of nucleotide analogs as experimental tools and holistic methods for analysis of cyclic nucleotide effects.
This volume details a comprehensive and extensive set of protocols for the study of autophagy in vitro and in vivo. Chapters focus on mammals, various model organisms, and provide protocols for the study of autophagy-related processes outside of the canonical autophagy pathways. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Authoritative and cutting-edge, Autophagy: Methods and Protocols aims to ensure successful results in the further study of this vital field.
|Author||: Nikolai Gorbunov,E. Marion Schneider|
|Publisher||: BoD – Books on Demand|
|Release Date||: 2016-11-10|
|ISBN 10||: 9535127268|
|Pages||: 526 pages|
Autophagy in Current Trends in Cellular Physiology and Pathology is addressed to one of the fundamental molecular mechanisms - autophagy- evolutionarily adopted by cells for processing of unnecessary or malfunctioned constituents and shaping intracellular structures, adjusting them to environmental conditions, aging, disease, neoplasia, and damages over their life period. Particular attention is paid to autophagy-mediated barrier processes of selective sequestration and recycling of impaired organelles and degradation of invading microorganisms, that is, the processes sustaining intrinsic resistance to stress, tissue degeneration, toxic exposures, and infections. The presented topics encompass personal experience and visions of the chapter contributors and the editors; the book chapters include a broad analysis of literature on biology of autophagy.
This book discusses novel concepts and discoveries concerning the regulation of innate immunity by autophagy and autophagy-related proteins. In the past decade, there have been major advances in our understanding of the molecular mechanisms of autophagy and its physiological functions. This book highlights emerging studies on the underlying mechanisms of autophagy regulation of innate immunity, including inflammation, antiviral immunity and anti-bacterial responses and the signaling pathways that prompt or inhibit the initiation and progression of related diseases. It also offers new ideas and strategies for future drugs based on manipulating autophagy, especially selective autophagy mediated by cargo receptors. Providing a comprehensive overview of the autophagy regulation of innate immunity, it is a valuable resource for graduate students and researchers in the fields of immunology, cell biology and translational medicine.
|Author||: Robert Weissert,Fabienne Brilot|
|Publisher||: Frontiers Media SA|
|Release Date||: 2017-11-23|
|ISBN 10||: 2889453472|
|Pages||: 329 pages|
Over the last years it has become evident that many neurological diseases of the central nervous system (CNS) are induced by a specific adaptive immune response directed against molecules expressed on CNS-resident cells. Well-recognized examples are anti-N-Methyl-D-Aspartate Receptor (NMDAR) encephalitis which is characterized by the presence of antibodies against neuron-expressed NMDAR, or neuromyelitis optica (NMO), induced by antibodies to astrocyte-expressed aquaporin-4. Many more examples exist, and antibodies, and T or/and B cells have increasingly been associated with CNS disease. Often the symptoms of these diseases have not been typically reported to have an immune aetiology. Beside classical neurological symptoms like ataxia, vision disturbance, and motor or sensory symptoms, these can include cognitive disturbances, behavioral abnormalities, or/and epileptic seizures. Although much has been learned regarding the pathophysiology of prototypic examples of these disorders, there are still major gaps in our understanding of their biology. This may be due to the fact that they are rare diseases, and their therapies are still very limited. This research topic includes contributions addressing the analysis of the adaptive immune response driving disease including target antigens, molecular epitope mapping, and factors involved in the disease pathogenesis such as complement activation cascades, genetic and genomic regulation, as well as environmental triggers. Diagnostic criteria and methods, and treatment are also discussed. The overall aim of the volume is to review progress in our pathophysiological understanding of immune-mediated CNS disorders in order to advance diagnostic and therapeutic approaches, and ultimately improve outcomes for patients.
This book is a collection of selected and relevant research, concerning the developments within the Cell Death field of study. Each contribution comes as a separate chapter complete in itself but directly related to the books topics and objectives. The target audience comprises scholars and specialists in the field.
|Author||: Fabiola Osorio,Bart Everts|
|Publisher||: Frontiers Media SA|
|Release Date||: 2019-12-09|
|ISBN 10||: 2889632288|
|Pages||: 329 pages|
Starting in the early 1970s, a type of programmed cell death called apoptosis began to receive attention. Over the next three decades, research in this area continued at an accelerated rate. In the early 1990s, a second type of programmed cell death, autophagy, came into focus. Autophagy has been studied in mammalian cells for many years. The recen
|Release Date||: 1877|
|Pages||: 329 pages|
|Author||: Randie Hee Kim|
|Release Date||: 2009|
|Pages||: 258 pages|
Many individual aspects of the dynamics and assembly of biological membranes have been studied in great detail. Cell biological approaches, advanced genetics, biophysics and biochemistry have greatly contributed to an increase in our knowledge in this field.lt is obvious however, that the three major membrane constituents - lipids, proteins and carbohydrates- are studied, in most cases separately and that a coherent overview of the various aspects of membrane biogenesis is not readily available. The NATO Advanced Study Institute on "New Perspectives in the Dynamics of Assembly of Biomembranes" intended to provide such an overview: it was set up to teach students and specialists the achievements obtained in the various research areas and to try and integrate the numerous aspects of membrane assembly into a coherent framework. The articles in here reflect this. Statting with detailed contributions on phospholipid structure, dynamics, organization and biogenesis, an up to date overview of the basic, lipidic backbone of biomembranes is given. Extensive progress is made in the research on membrane protein biosynthesis. In particular the post- and co-translational modification processes of proteins, the mechanisms of protein translocation and the sorting mechanisms which are necessary to direct proteins to their final, intra - or extracellular destination have been characterized in detail. Modern genetic approaches were indispensable in this research area: gene cloning, hybrid protein construction, site directed mutagenesis and sequencing techniques elucidated many functional aspects of specific nucleic acid and amino acid sequences.
Autophagy is a fundamental biological process that enables cells to autodigest their own cytosol during starvation and other forms of stress. It has a growing spectrum of acknowledged roles in immunity, aging, development, neurodegeneration, and cancer biology. An immunological role of autophagy was first recognized with the discovery of autophagy’s ability to sanitize the cellular interior by killing intracellular microbes. Since then, the repertoire of autophagy’s roles in immunity has been vastly expanded to include a diverse but interconnected portfolio of regulatory and effector functions. Autophagy is an effector of Th1/Th2 polarization; it fuels MHC II presentation of cytosolic (self and microbial) antigens; it shapes central tolerance; it affects B and T cell homeostasis; it acts both as an effector and a regulator of Toll-like receptor and other innate immunity receptor signaling; and it may help ward off chronic inflammatory disease in humans. With such a multitude of innate and adaptive immunity functions, the study of autophagy in immunity is one of the most rapidly growing fields of contemporary immunological research. This book introduces the reader to the fundamentals of autophagy, guides a novice and the well-informed reader alike through different immunological aspects of autophagy as well as the countermeasures used by highly adapted pathogens to fight autophagy, and provides the expert with the latest, up-to-date information on the specifics of the leading edge of autophagy research in infection and immunity.
Autophagy principally serves an adaptive function to protect organisms against diverse human pathologies, including cancer and neurodegeneration. Recent developments using in vitro, ex vivo and in vivo models show the involvement of the autophagy pathway in immunity and inflammation. Moreover, direct interactions between autophagy proteins and immune signalling molecules have also been demonstrated. Defects in autophagy - similar to cancer, neurodegenerative diseases and aging - through autophagy gene mutation and/or microbial antagonism, may underlie the pathogenesis of many infectious diseases and inflammatory syndromes. In spite of the increasing awareness of the importance of autophagy in these pathophysiological conditions, this process remains underestimated and is often overlooked. As a consequence, its role in the initiation, stability, maintenance, and progression of these diseases are still poorly understood. This book reviews the recent advances regarding the functions of the autophagy pathway and autophagy proteins in immunity and inflammation, focusing on their role in self-nonself distinction, their implications in innate and adaptive immune responses and their dysregulation in the pathology of certain inflammatory and autoimmune diseases.
This book series consists of 3 volumes covering the basic science (Volume 1), clinical science (Volume 2) and the technology and methodology (Volume 3) of autophagy. Volume 1 focuses on the biology of autophagy, including the signaling pathways, regulating processes and biological functions. Autophagy is a fundamental physiological process in eukaryotic cells. It not only regulates normal cellular homeostasis, and organ development and function, but also plays an important role in the pathogenesis of a wide range of human diseases. Thanks to the rapid development of molecular biology and omic technologies, research on autophagy has boomed in recent decades, and more and more cellular and animal models and state-of the-art technologies are being used to shed light on the complexity of signaling networks involved in the autophagic process. Further, its involvement in biological functions and the pathogenesis of various diseases has attracted increased attention around the globe. Presenting cutting-edge knowledge, this book series is a useful reference resource for researchers and clinicians who are working on or interested in autophagy.
Burkholderia pseudomallei and B. mallei, causes melioidosis and glanders, respectively, which are two endemic infectious diseases in many parts of the world. The recent reports of glanders outbreaks in horses in Pakistan and Bahrain and the increasing incidence of human melioidosis in Thailand and other tropical regions have resulted in increased research efforts to prevent these diseases. Moreover, both B. mallei and B. pseudomallei exhibit an intriguing intracellular life cycle including the induction of actin tail formation and cell fusion and thereby have developed as model organisms in infection biology. This Research Topic summarizes recent progress to understand these pathogens at the molecular level, with emphasis in their virulence traits, host pathogen interactions, population structure and potential targets for therapeutic intervention and vaccine development.