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Cellular Responses to Stress

Cellular Responses to Stress

Copyright Date: 1999
Pages: 184
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  • Book Info
    Cellular Responses to Stress
    Book Description:

    Cellular Responses to Stressbrings together a group of scientists who work on different but interrelated aspects of cellular stress responses. The book provides state-of-the-art information on the wide spectrum of ways in which cells can respond to different forms of stress induced by chemicals, oxidants, and DNA-damaging agents. Mechanisms are described that involve altered uptake and efflux of chemical agents, intracellular detoxification, and DNA damage responses. Many of these changes trigger a cascade of reactions mediated by stress-activated signaling pathways, which have the capacity to determine whether a cell will survive or die. The spectrum of topics covered in this book aims to provide a broad overview of our current knowledge of the different forms of adaptive response systems.

    It is hoped that this text will stimulate further research to establish the relative cellular role of specific response pathways and will enable us to gain a deeper understanding of the mechanisms that allow cells to live or die. This book will be valued by university researchers at all levels, industrial scientists in the pharmaceutical and biotechnology industries, and clinical researchers.

    Originally published in 1999.

    ThePrinceton Legacy Libraryuses the latest print-on-demand technology to again make available previously out-of-print books from the distinguished backlist of Princeton University Press. These paperback editions preserve the original texts of these important books while presenting them in durable paperback editions. The goal of the Princeton Legacy Library is to vastly increase access to the rich scholarly heritage found in the thousands of books published by Princeton University Press since its founding in 1905.

    eISBN: 978-1-4008-6504-8
    Subjects: Biological Sciences

Table of Contents

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  1. Front Matter
    (pp. i-iv)
  2. Table of Contents
    (pp. v-vi)
  3. Preface
    (pp. vii-viii)
    C.P. Downes, C.R. Wolf and D.P. Lane
  4. Abbreviations
    (pp. ix-xii)
  5. 1 Signal transduction by the c-Jun N-terminal kinase
    (pp. 1-12)
    Roger J. Davis

    Mitogen-activated protein kinases (MAP kinases) are established to be important mediators of intracellular signalling within cells. These protein kinases function within signalling pathways that are initiated by multiple mechanisms, including the activation of cell surface receptors. A major target of MAP kinase signalling is the regulation of gene expression. These properties implicate MAP kinases in developmental processes and in the response of cells to their environment, for example growth factors, cytokines or exposure to stress. Indeed, studies using both genetic and biochemical approaches have demonstrated the essential role of MAP kinases in mammals, insects, nematodes and plants.

    In mammals, three...

  6. 2 Roles of the AMP-activated/SNFI protein kinase family in the response to cellular stress
    (pp. 13-28)
    D. Grahame Hardie

    Although it is now well known that several protein kinase cascades are activated in response to different types of cellular stress [1], in most cases the intracellular signals that activate the cascades remain unknown. An exception to this is the mammalian AMP-activated protein kinase (AMPK) svstem [2,3], which is activated in response to stresses that deplete cellular energy charge via mechanisms that are now well understood. AMPK was discovered by its ability to regulate metabolic enzymes involved in lipid metabolism, and these remain its best characterized physiological targets [4], However, there are increasing indications, discussed below, that it also regulates...

  7. 3 Making the connection: coupling of stress-activated ERK/MAPK (extracellular-signal-regulated kinase/mitogen-activated protein kinase) core signalling modules to extracellular stimuli and biological responses
    (pp. 29-48)
    John M. Kyriakis

    Signal transduction networks which culminate in the activation of extracellular-signal-regulated kinases (ERKs)/mitogen-activated protein kinases (MAPKs) have been widely conserved in eukaryotic cell evolution (Fig. 1) [1,2]. At the heart of these networks are so-called ‘core signalling modules’, consisting of the ERKs/MAPKs that are activated by concomitant Tyr and Thr phosphorylation catalysed by members of the MAPK/ERK kinase (MEK) family. MEKs, in turn, are activated by Ser/Thr phosphorylation catalysed by protein kinases of several families collectively termed MAPK kinase kinases (MAPKKKs) [1,2]. The diversity of kinases with MAPKKK activity reflects the breadth of extracellular stimuli that can activate ERK/MAPK networks. The...

  8. 4 Stress-activated MAP kinase (mitogen-activated protein kinase) pathways of budding and fission yeasts
    (pp. 49-62)
    Jonathan B.A. Millar

    One of the most common responses of eukaryotic cells to growth-modulatory signals is the activation of one or more MAP (mitogen-

    Nomenclature: standard fission yeast nomenclature has been used throughout the review. An example is as follows: the pathway is designated STY1, the genesty l, cells bearing a wild-type genesty l+, mutant cellssty l-and the protein Sty l. activated protein) kinase cascades. Signal transduction through MAP kinase cascades involves sequential phosphorylation and activation of three distinct kinases: the MAP kinase kinase kinase (or MAPKKK), the MAP kinase kinase (or MAPKK) and the MAP kinase itself. Although...

  9. 5 Protein kinase cascades in intracellular signalling by interleukin-1 and tumour necrosis factor
    (pp. 63-78)
    Jeremy Saklatvala, Jon Dean and Andrew Finch

    Interleukin-1α (IL-1α), IL-βand tumour necrosis factor α (TNFα) are primary inflammatory cytokines that mediate many of the local and systemic features of inflammation [1,2]. They are produced mainly by monocytes and macrophages in response to a range of stimuli, including microbial products, immune complexes, activated T-cells and the

    To whom correspondence should be addressed. combined action of other cytokines, such as interferon 7, IL-2 and granulocyte/macrophage colony-stimulating factor. TNFβ, or lymphotoxin α, is made by activated T-lymphocytes. The IL-1s and TNFs have a highly similar, broad range of physiological effects and provide crucial signals by which activated mononuclear phagocytes...

  10. 6 Regulation of actin dynamics by stress-activated protein kinase 2 (SAPK2)-dependent phosphorylation of heat-shock protein of 27 kDa (Hsp27)
    (pp. 79-90)
    Jacques Landry and Jacques Huot

    SAPK2 (stress-activated protein kinase 2; also called p38a/β or RK) is a member of the still expanding family of mitogen-activated protein

    To whom correspondence should be addressed. kinases (MAP kinases) which have vital roles in transducing and orchestrating messages generated by a variety of growth factors, inflammatory cytokines and stressing agents [1–4]. Whereas the first group of MAP kinases characterized, represented by extracellular-signal-regulated kinases 1/2 (ERKl/2), have been shown mostly to be growth factor- or mitogen-activated kinases, SAPK2 (together with three other SAPKs) is mostly recognized as a stress-sensitive kinase. SAPK2 activation leads directly or indirectly via SAPK2-activated kinases...

  11. 7 DNA-dependent protein kinase and related proteins
    (pp. 91-104)
    Graeme C.M. Smith, Nullin Divechaf, Nicholas D. Lakin and Stephen P. Jackson

    The DNA-dependent protein kinase (DNA-PK) was first described as an activity in animal cell extracts that resulted in the phosphorylation of a variety of endogenous proteins, including the heat-shock protein Hsp90 [1]. Further studies revealed that DNA-PK must be bound to DNA before it can efficiently elicit its kinase activity [2–8]. Indeed, optimal substrates for DNA-PK are those that are DNA-binding proteins, suggesting that phosphorylation occurs most effectively when DNA-PK and its substrate are localized on the same DNA molecule. Initially, linearized double-stranded DNA molecules were thought to be the only activators of DNA-PK, although other types of DNA discontinuities...

  12. 8 Stress-induced activation of the heat-shock response: cell and molecular biology of heat-shock factors
    (pp. 105-118)
    Jose J. Cotto and Richard I. Morimoto

    Every cell responds to environmental, chemical and physiological stress through a rapid and preferential increase in expression of a highly conserved group of proteins known as the heat-shock proteins (Hsps). The cellular response to stress was discovered by Ritossa [1], who

    Present address: Department of Chemical Engineering, University of Texas at Austin, Austin, TX 78712, U.S.A.

    To whom correspondence should be addressed. observed an induction of specific chromosomal puffs in the polytene chromosomes ofDrosophila melanogasterupon exposure to elevated temperatures and chemical treatment. Concomitantly these treatments also caused a reduction in the number of pre-existing puffs, suggesting that the...

  13. 9 Transcriptional regulation via redox-sensitive iron—sulphur centres in an oxidative stress response
    (pp. 119-128)
    Bruce Demple, Elena Hidalgo and Huangen Ding

    Aerobic organisms must cope with the toxic side-effects of the oxygen upon which they depend. This toxicity is potentiated by various reactions, with the pivotal ones generating reactive derivatives that can damage key cellular components. These inadvertent toxicants include superoxide (O2-·), hydrogen peroxide and hydroxyl radical (·OH). Super-

    To whom correspondence should be addressed. oxide is formed through autoxidation reactions, such as the oxidation of reduced NADH oxidase by O2in mitochondria; other proteins throughout the cell are prone to similar superoxide-generating autoxidation [1,2]. The immune system produces O2-· deliberately by activating membrane-bound NADPH oxidase, which is part of the...

  14. 10 Adaptive responses to environmental chemicals
    (pp. 129-140)
    C.R. Wolf, G. Smith, A.G. Smith, K. Brown and C.J. Henderson

    Numerous organisms, particularly plants and micro-organisms, produce toxic chemicals as a defence against predators or in order to compete for nutrient sources. Therefore, as part of the evolutionary process, a complex spectrum of metabolic processes has arisen to combat their toxic effects [1]. Cytoprotection can be afforded by a range of different mechanisms, including those which affect drug accumulation by

    To whom correspondence should be addressed. preventing uptake or by accelerating efflux [2]. This is epitomized by the ATP-dependent transporters such as the multidrug-resistance transporters and the multidrug-resistance-related proteins. The next level of cellular defence is intracellular detoxification. A large...

  15. 11 Cellular response to cancer chemopreventive agents: contribution of the antioxidant responsive element to the adaptive response to oxidative and chemical stress
    (pp. 141-168)
    John D. Hayes, Elizabeth M. Ellis, Gordon E. Neal, David J. Harrison and Margaret M. Manson

    The administration of a chemical, or dietary components, to prevent the onset or to inhibit the progression of neoplastic disease is referred to as cancer chemoprevention [1]. This type of therapy has excited considerable interest as a powerful and, in ideal situations, a relatively harmless means of providing resistance against malignant disease. Individuals who will benefit most from chemoprevention are those who have an increased risk of developing malignancy, through inherited predisposition, their age, their sex or chronic exposure to factors known to cause carcinogenesis. Examples of chemoprevention include the use of non-steroidal anti-inflammatory drugs to treat patients with adenomatous...

  16. Index
    (pp. 169-171)