Protein Kinase-mediated Decisions Between Life and Death
Protein Kinase-mediated Decisions Between Life and Death

Author: Ayse Basak Engin

Publisher: Springer Nature

Published: 2021-02-04

Total Pages: 415

ISBN-13: 3030498441

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Protein phosphorylation via protein kinases is an inevitable process that alters physiological and pathological functions of the cells. Thus, protein kinases play key roles in the regulation of cell life or death decisions. Protein kinases are frequently a driving factor in a variety of human diseases including aging and cellular senescence, immune system and endothelial dysfunctions, cancers, insulin resistance, cholestasis and neurodegenerative diseases, as well as bacterial resistance in persistent infections. Recent developments in quantitative proteomics provide important opinions on kinase inhibitor selectivity and their modes of action in the biological context. Protein Kinase-mediated Decisions Between Life and Death aims to have the reader catch insights about up-to-date opinions on “Protein Kinases” related pathways that threaten human health and life. As “Protein Kinases” are related to many health problems, clinicians, basic science researchers and students need this information. Chapter “Signal Transduction in Immune Cells and Protein Kinases” is available open access under a Creative Commons Attribution 4.0 International License via link.springer.com.

Molecular Regulation of Receptor Interacting Protein Kinase 3 Induced Cell-death in Physiology and Disease
Molecular Regulation of Receptor Interacting Protein Kinase 3 Induced Cell-death in Physiology and Disease

Author: Kartik Gupta

Publisher:

Published: 2021

Total Pages: 0

ISBN-13:

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Programmed cell-death (PCD) refers to a collection of related biological pathways that dismantle cells using an underlying genetic program. Necroptosis is a form of PCD regulated by receptor interacting protein kinase (RIP/RIPK) family member RIPK3 and RIPK1. Despite our knowledge on necroptosis signaling, we do not fully understand the decision-making processes that favor necroptosis over other forms of PCD. In my thesis, I describe how the dynamic regulation of RIPK3 is linked to its role in cell-death decision making and also its extracellular role.I first report that cells respond to impending necroptosis by expelling RIPK3 in extra-cellular vesicles (EVs) including exosomes. Curiously, these EVs were also associated with increased lysosomal cargo proteins and greater numbers. This led us to postulate and identify a role of RIPK3 in MLKL dependent endosomal to lysosomal switch of EV biogenesis as a result of calcium influx. I then report the identification of a phosphorylation that is directly linked to RIPK3 protein stability during G2/M phases of the cell cycle. RIPK3 is constantly degraded by the ripoptosome which is physiologically assembled in mitosis. We discovered that S369 phosphorylation on RIPK3 by Polo-like kinase 1 during mitosis antagonizes access of ripoptosome (a complex that cleaves RIPK3), enabling this association in mitosis and elevated RIPK3 levels. Together, this solves a long-standing puzzle in the field on how RIPK3 can co-exist with the ripoptosome. RIPK3 levels are also elevated in abdominal aortic aneurysms (AAA)-a vascular disease in which the aorta undergoes pathological expansion due to the loss of vascular smooth muscle cells (SMCs) through necroptosis. Based on these data and previous work from lab members, I hypothesized that PKCÎþ mediated STAT activation causes increased Ripk3 expression via an enhancer element. Ongoing studies demonstrate that upon attenuation of this element, AAA can be rescued. In conclusion, with the help of my colleagues, I demonstrate three ways in which cellular levels of RIPK3 are regulated in physiological processes such as cell-cycle and also in diseases such as AAA. The fundamental understanding of RIPK3 biology opens avenues for therapeutic targeting of this unique cell-death factor.

Mechanisms of Cell Death
Mechanisms of Cell Death

Author: Zahra Zakeri

Publisher:

Published: 1999

Total Pages: 236

ISBN-13:

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Contains papers from a July 1998 conference held at the Queens College Campus of the City University of New York. Papers are arranged in sections on mechanisms and general considerations, programmed (developmental) cell death, and cell death and pathological and clinical situations. Specific topics

Molecular Mechanisms in Visual Transduction
Molecular Mechanisms in Visual Transduction

Author: D.G. Stavenga

Publisher: Elsevier

Published: 2000-11-30

Total Pages: 597

ISBN-13: 0080536778

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Molecular mechanisms in visual transduction is presently one of the most intensely studied areas in the field of signal transduction research in biological cells. Because the sense of vision plays a primary role in animal biology, and thus has been subject to long evolutionary development, the molecular and cellular mechanisms underlying vision have a high degree of sensitivity and versatility. The aims of visual transduction research are firstto determine which molecules participate, and then to understand how they act in concert to produce the exquisite electrical responses of the photoreceptor cells.Since the 1940s [1] we have known that rod vision begins with the capture of a quantum of energy, a photon, by a visual pigment molecule, rhodopsin. As the function of photon absorption is to convert the visual pigment molecule into a G-protein activating state, the structural details of the visual pigments must beexplained from the perspective of their role in activating their specific G-proteins. Thus, Chapters 1-3 of this Handbook extensively cover the physico-chemical molecular characteristics of the vertebrate rhodopsins. Following photoconversion and G-protein activation, the phototransduction cascade leads to modifications of the population of closed and open ion channels in the photoreceptor plasma membrane, and thereby to the electrical response. The nature of the channels of vertebrate photoreceptors is examined in Chapter 4, and Chapter 5 integrates the present body of knowledge of the activation steps in the cascade into a quantitative framework. Once the phototransduction cascade is activated, it must be subsequently silenced. The various molecular mechanisms participating in inactivation aretreated in Chapters 1-4 and especially Chapter 5. Molecular biology is now an indispensable tool in signal transduction studies. Numerous vertebrate (Chapter 6) and invertebrate (Chapter 7) visual pigments have been characterized and cloned. The genetics and evolutionary aspects of this great subfamily of G-protein activating receptors are intriguing as they present a natural probe for the intimate relationship between structure and function of the visual pigments. Understanding the spectral characteristics from the molecular composition can be expected to

Stress-Activated Protein Kinases
Stress-Activated Protein Kinases

Author: Francesc Posas

Publisher: Springer Science & Business Media

Published: 2008-01-24

Total Pages: 322

ISBN-13: 3540755691

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In this book leading researchers in the field discuss the state-of-the-art of many aspects of SAPK signaling in various systems from yeast to mammals. These include various chapters on regulatory mechanisms as well as the contribution of the SAPK signaling pathways to processes such as gene expression, metabolism, cell cycle regulation, immune responses and tumorigenesis. Written by international experts, the book will appeal to cell biologists and biochemists.

The Inflammasomes
The Inflammasomes

Author: Isabelle Couillin

Publisher: Springer Science & Business Media

Published: 2011-07-02

Total Pages: 233

ISBN-13: 3034801483

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The inflammasome was first described in 2002 as a molecular complex activating proinflammatory caspases and therefore regulating the maturation and biological activities of cytokines such as IL-1 and IL-18. This finding was substantiated by the identification of several mutations in the cias1 gene, encoding the human NLRP3 protein, responsible for several autoinflammatory disorders such as the Muckle Wells syndrome. Since, the interest for this complex has constantly increased and several inflammasome complexes with different specificities have been described. These inflammasomes sense a wide variety of pathogens and danger signals and are key players in the inflammatory response. With the contributions of leading international experts in the field, this book provides an extensive overview of the current knowledge of inflammasome biology and their role in health and disease.

Apoptosis
Apoptosis

Author: Douglas R. Green

Publisher: Cambridge University Press

Published: 2011-08-22

Total Pages: 470

ISBN-13: 1139498738

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Apoptosis, or cell death, can be pathological, a sign of disease and damage, or physiological, a process essential for normal health. This book, with contributions from experts in the field, provides a timely compilation of reviews of mechanisms of apoptosis. The book is organized into three convenient sections. The first section explores the different processes of cell death and how they relate to one another. The second section focuses on organ-specific apoptosis-related diseases. The third section explores cell death in non-mammalian organisms, such as plants. This comprehensive text is a must-read for all researchers and scholars interested in apoptosis.

Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging
Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging

Author: M. A. Hayat

Publisher: Academic Press

Published: 2016-12-28

Total Pages: 431

ISBN-13: 0128094273

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Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging is an eleven volume series that discusses in detail all aspects of autophagy machinery in the context of health, cancer, and other pathologies. Autophagy maintains homeostasis during starvation or stress conditions by balancing the synthesis of cellular components and their deregulation by autophagy. This series discusses the characterization of autophagosome-enriched vaccines and its efficacy in cancer immunotherapy. Autophagy serves to maintain healthy cells, tissues, and organs, but also promotes cancer survival and growth of established tumors. Impaired or deregulated autophagy can also contribute to disease pathogenesis. Understanding the importance and necessity of the role of autophagy in health and disease is vital for the studies of cancer, aging, neurodegeneration, immunology, and infectious diseases. Comprehensive and forward-thinking, these books offer a valuable guide to cellular processes while also inciting researchers to explore their potentially important connections. Presents the most advanced information regarding the role of the autophagic system in life and death Examines whether autophagy acts fundamentally as a cell survivor or cell death pathway or both Introduces new, more effective therapeutic strategies in the development of targeted drugs and programmed cell death, providing information that will aid in preventing detrimental inflammation Features recent advancements in the molecular mechanisms underlying a large number of genetic and epigenetic diseases and abnormalities, including atherosclerosis and CNS tumors, and their development and treatment Includes chapters authored by leaders in the field around the globe—the broadest, most expert coverage available

Insulin Action
Insulin Action

Author: Ashok K. Srivastava

Publisher: Springer Science & Business Media

Published: 1998-05-31

Total Pages: 206

ISBN-13: 9780792381136

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In 1996 the 75th anniversary of the discovery of insulin was celebrated at the University of Toronto, the scene of that discovery in 1921. This volume was stimulated by the scientific program which was staged at that time and brought together much of the world's best talent to discuss and analyze the most recent developments in our understanding of pancreatic function, insulin secretion, the interaction of insulin with its target tissues, the mechanism of insulin action at the cellular level, and the defects which underlie both Type I (insulin-dependent diabetes mellitus, IDDM) and Type II (noninsulin-dependent diabetes mellitus, NIDDM) forms of the disease. We have chosen to focus the present volume on work related to insulin action.