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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.
Cell Death Regulation in Health and Disease - Part C, Volume 353 in the International Review of Cell and Molecular Biology series, reviews and details current advances in cell and molecular biology. The IRCMB series maintains the highest standard by publishing timely topics authored by prominent cell and molecular biologists, with this release covering Developmental and seasonal regulation of neural cell death in birds, Post-translational modifications in cell death regulation, The role of cell death in tissue regeneration and fibrosis, Crosstalk between the apoptosis and autophagy signaling pathways, IP3 receptor signal integration in cell death and survival decisions, and more. Provides a comprehensive collection of front-of-the line research in the field of cell death regulation Authored by established and active cell and molecular biologists drawn from international sources Includes only invited review articles, covering selected topics in many different organisms and disease settings
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
Cell death is one of the fundamental processes by which normal development is modulated, and the importance of both necrosis and apoptosis in a number of pathologies has generated intense interest from researchers in many fields. This timely book covers both the proteins that are produced by dying cells and the proteins that signal cells to initiate cell death.Cell Death Proteins provides an overview of the explosive interest in cellular death. Six review papers, written by researchers at the forefront of this rapidly moving field, focus on proteins that promote, signal, and inhibit cell death. Major players involved in the cell death cascade and its controls are covered, including cell cycle checkpoints, the function of interleukin-1J converting enzyme, the role of IGF-I receptor, the Bcl-2 family of proteins, viral inhibitors of apoptosis, and p53-dependent apoptosis.
The 2002 Nobel Prize in Physiology or Medicine was awarded to Sydney Brenner, H. Robert Horvitz, and John E. Sulston for their seminal discoveries concerning "genetic regulation of organ development and programmed cell death." This clearly marked the prime importance of understanding the molecular mechanisms controlling cell death. The 1 st International Symposium on Programmed Cell Death was held in the Shanghai Science Center of the Chinese Academy of Sciences on September 8-12, 1996. A number of key issues in apoptosis were discussed at the meeting, and progress in major areas of apopto sis research was summarized by expert participants at the meeting and published by Plenum Publishing Corporation as a book entitled Programmed Cell Death. In the last six years, we have witnessed a real explosion in our knowledge on how cells undergo apoptosis, thereby participating in various developmental and pathophysiological processes. At this ever exciting time, we organized the 2nd International Symposium on Programmed Cell Death.
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.
Cell Death Regulation in Health and Disease - Part B, Volume 352, the latest release in the International Review of Cell and Molecular Biology, reviews and details current advances in cell and molecular biology. Chapters in this updated release include Regulation of cell death signaling in insects, Bcl-2 family proteins, Cell death signaling in prokaryotes, Parthanatos in neurodegenerative diseases, Cell death regulation in yeast, Mutual regulation of autophagy and necroptosis, Therapeutic inhibition of cell death by autophagy induction, and Necroptosis in neurodegenerative diseases. Provides a comprehensive collection of front-of-the line research in the field of cell death regulation Authored by established and active cell and molecular biologists drawn from international sources Presents only invited review articles, covering selected topics in many different organisms and disease settings
The second edition of this encyclopedia presents over 400 biologically important signaling molecules and the content is built on the core concepts of their functions along with early findings written by some of the world’s foremost experts. The molecules are described by recognized leaders in each molecule. The interactions of these single molecules in signal transduction networks will also be explored. This encyclopedia marks a new era in overview of current cellular signaling molecules for the specialist and the interested non-specialist alike. Currently, there are more than 30,000 genes in human genome. However, not all the proteins encoded by these genes work equally in order to maintain homeostasis. Understanding the important signaling molecules as completely as possible will significantly improve our research-based teaching and scientific capabilities.
One of the major goals of researchers in the field of apoptosis is to identify targets for novel therapies in cancer, AIDS, and Alzheimer’s disease. Understanding the molecular mechanisms of the various components of the apoptotic pathways is the first step to reaching this goal. The 2002 Nobel Prize in Physiology or Medicine was awarded to Sydney Brenner (United Kingdom), H. Robert Horvitz (US) and John E. Sulston (UK) "for their discoveries concerning genetic regulation of organ development and programmed cell death." Cell death is a fundamental aspect of embryonic development, normal cellular turnover and maintenance of homeostasis (maintaining a stable, constant environment) on the one hand, and aging and disease on the other. This volume addresses the significant advances with the techniques that are being used to analyze cell death. This volume provides the necessary, trusted methods to carry out this research on these latest therapeutic techniques. Once researchers understand the molecular mechanisms of the apoptotic pathways, they can begin to develop new therapies Presents key methods on studying tumors and how these cancer cells evade cell death Eliminates searching through many different sources to avoid pitfalls so the same mistakes are not made over and over