Recent Special Issues of CDD
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2009
July: Special Issue on Molecular mechanisms of autophagy in mammals
The growing importance of autophagy is clearly demonstrated by the exponentially increasing number of publications in this area. Although autophagy was initially classified as a form of cell death, it is now generally accepted that this is not the case.Autophagy mostly promotes cell health and survival and, only under peculiar conditions, can it result in cellular death. In the first issue of 2009, Cell Death and Differentiation published nine reviews on the topic of Autophagy in Aging, Disease and Death. These are now followed by six other papers covering more specific aspects on the complex regulation of this process and its crosstalk with apoptosis and other essential cellular functions such as energy production, vesicular traffic and cellular immunity.
March: Special Issue on Cell death mechanisms
Although cell death occurs in many different ways, it uses several common and evolutionarily conserved mechanisms. These control distinct forms of cell demise ranging from necrosis and excitotoxicity to autophagy and apoptosis. This review series comprises state-of the art reviews, which summarise our knowledge of basic mechanisms of cell death in a context of different pathological processes. Articles, written by the leaders in the field, present a comprehensive picture of cell-death routines and their role in shaping diseases. This collection of papers should serve as a key resource to researchers in cell biology, neurobiology, oncology, biochemistry and pharmacology.
January: Special Issue on Autophagy in Aging, Disease and Death
Autophagy ('self-eating') is one of the most intriguing phenomena in cell biology. It is a process by which the cellular content is digested by the lysosomal machinery. Autophagy is functionally related to a diverse range of stress responses, including cell death. In this special issue of Cell Death & Differentiation, prominent scientists review the basic physiology of autophagy, as well as its implications for health and disease, in infection, immune responses, cancer, a range of organ-specific pathologies,and in age-related disorders.
Top of page2008
July: Special issue to celebrate Richard Lockshin's 70th Birthday
More than 40 years have elapsed since Richard Lockshin first coined the expression "programmed cell death" (PCD) when he deciphered the basic rules that govern the destruction of intersegmental muscle cells during silkworm development. Richard Lockshin launched the pioneering idea that PCD would be controlled by a combination of cell-extrinsic and cell-intrinsic factors, yet would be executed through a plethora of catabolic reactions from inside the self-destroying cell. A compendium of comprehensive review articles discusses the phylogeny, as well as the ever more sophisticated regulation of PCD in a variety of model organisms. This collection of state-of-the-art reviews should interest researchers in all areas of cell biology.
April: Special Issue on The biology of Hypoxia-inducible factors
Multi-cellular organisms have evolved multiple mechanisms to respond to decreased oxygen levels (hypoxia). These physiological responses are invoked to maintain oxygen homeostasis. Hypoxia is also a critical feature of many diseases including ischemia and cancer. Hypoxia inducible factors (HIFs) are transcription factors which provide a molecular basis for the physiological and pathophysiological consequences of hypoxia. In this issue of CDD, several reviews focus on the regulators and biological consequences of HIF activation.
February: Special Issue on Immunity
Cell death is essential for effective immunity.Cells of the adapive immune system are heavily selected during development and those that fail to make the grade,the majority of developing T- and B-lymphocytes,undergo apoptosis. Apoptosis is also used to control the size of mature lympocyte populations,to eliminate autoreachive lymphoctes and is a major mechanism of killing by CTL and NK cells.In this issue of CDD, several reviews focus on the role of death,at the cellular level,in immunity.
January: Special Issue on Tumor stress, cell death and the ensuing immune response
The mechanistic and phenomenological characteristics of cell death play a major role in shaping the immune response. This review series included state-of-the art reviews on the relationship between cell death and the immune system. Comprehensive articles discuss how the stress, agony and demise of virus-infected or transformed cells can determine whether the innate and cognate immune systems are activated or suppressed. Moreover, the question how cell death of immune effectors can regulate immune responses is discussed. This compendium of comprehensive review articles should serve as a key resource to researchers in immunology, cell biology, oncology, virology and pharmacology.
Top of page2007
July: Special issue on Cellular and molecular mechanisms of tissue damage and repair
For multicellular organisms, the process of death is inseparable from life. The process of cell death occurs continuously and is a fundamental mechanism for development and, perversely, for survival. To date, at least 10 distinct modes of homeostatic cell death (e.g. anoikis, autophagy, caspase-independent apoptosis, Wallerian degeneration, excitotoxicity, cornification etc.) have been identified. Further understanding of death mechanisms could lead to an improvement of our knowledge of survival and protection and, therefore, in our understanding of the aetiology of certain diseases. This special issue comprises a collection of papers written by some of the renowned speakers at the Academia Europaea & Klaus Tschira Foundation's international symposium in March 2007.
January: Special Issue on Caspases
Caspases are cysteine proteases that are essential for executing apoptosis. In recent years it has become clear that in addition to their role in apoptosis, many caspases have pleiotropic functions. This review series includes comprehensive articles by experts in the caspase field, and covers the basic biology of caspases, their mechanisms of activation, cellular substrates, natural and synthetic inhibitors, apoptotic and non-apoptotic functions and role in inflammation and immunity. This compendium of up-to-date articles should serve as a key resource to researchers in biochemistry/enzymology, cell biology, cancer biology, immunology, virology and drug discovery.
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March: The Endoplasmic Reticulum
This special issue features a collection of reviews on the endoplasmic reticulum (ER), dysfunction of which has been implicated in multiple major human diseases, including diabetes and neurodegenerative diseases. These reviews provide unique insights into the physiological role of, and the mechanisms behind, the endoplasmic reticulum stress response, as well as possible targets for the treatment of human diseases involving ER stress.
May: NF-κB and Cell Death
NF-κB is a key transcription factor that controls both cell death and cell life, including proliferation and differentiation. Deregulation of NF-κB is implicated in all major diseases including cancer, inflammation and AIDS. Thus both fundamental biologists and clinicians must be aware of the physiological regulation and pathological deviations of NF-κB. This series of reviews is a must read for cell biologists, oncologists, immunologists, haematologists and virologists.
June: p53
The tumor suppressor p53 is a fundamental transcription factor regulating life and death of cells in response to a number of stimuli and particularly in response to genotoxic damage. Loss of p53 expression is observed in a large number of tumours, and plays a major role in tumour development and response to therapy. The recent identification of related genes poses new questions on what is now recognised as a p53 transcription factor family. It is fundamental that both researchers and clinicians are aware of the recent knowledge on the molecular mechanisms involved in p53 family regulation and on the pathways they regulate, both in physiological and pathological conditions.
August: Special Issue in Honour of Stanley J. Korsmeyer
Bcl-2 family members are subdivided into BH3-only proteins, Bax/Bak-like killers and Bcl-2-like survival factors that interact with each other to integrate survival and death signals in higher eukaryotes. Some family members might also regulate cell cycle progression, DNA damage control and metabolic processes. Although mutations of Bcl-2 family members are rare in cancer, their crucial impact on the life-death decision of a cell makes them attractive targets for anticancer therapy, especially in chemoresistant tumor cells which are often insensitive to apoptotic death stimuli. This review series provides an update on our current knowledge about the mode of actions and intervening possibilities of Bcl-2 family members, the regulation of caspase-dependent and -independent signaling pathways, the role of mitochondria and the ER in apoptosis execution and the evolutionary conservation of death signaling pathways across species. It honours Stanley J. Korsmeyer who largely contributed to all these topics in the last two decades.
Top of page2005
June: Translational Control in Cell Death
August Supplement: Retroviruses and Apoptosis
August: Dependence Receptors
September: Nobel Prize Winners
November Supplement: Autophagy
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