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Members of the protein kinase C (PKC) family of Ser/Thr kinases are encoded by nine distinct but closely related genes, which give rise to more than 12 different protein isoforms via a mechanism of alternative RNA splicing. Most PKC proteins are ubiquitously expressed and participate in a plethora of functions in most cell types. A majority of PKC isoforms is also expressed in cells of the immune system in which they are involved in signal transduction downstream of a range of surface receptors, including the antigen receptors on T and B lymphocytes. PKC proteins are central to signal initiation and propagation, and to the regulation of processes leading to immune cell proliferation, differentiation, homing and survival. As a result, PKC proteins directly impact on the quality and quantity of immune responses and indirectly on the host resistance to pathogens and tendency to develop immune deficiencies and autoimmune diseases. A significant progress was made in recent years in understanding the regulation of PKC enzymes, their mechanism of action and their role in determining immunocyte behavior This volume reviews the most significant contributions made in the field of immune cell regulation by PKC enzymes. Several manuscripts are devoted to the role of distinct PKC isoforms in the regulation of selected immunocyte responses. Additional manuscripts review more general mechanisms of regulation of PKC enzymes, either by post-translational modifications, such as phosphorylation or controlled proteolysis, or by interaction with different binding proteins that may alter the conformation, activity and subcellular location of PKC. Both types of mechanisms can introduce conformational changes in the molecule, which may affect its ability to interact with cofactors, ATP, or substrates. This topic will be followed by a discussion on the positive and negative impact of individual PKC isoforms on cell cycle regulation. A second section of this volume concentrates on selected topics relevant to role of the novel PKC isoform, PKC-theta, in T lymphocyte function. PKC-theta plays important and some non-redundant roles in T cell activation and is a key isoform that recruits to the immunological synapse - the surface membrane area in T cells that comes in direct contact with antigen presenting cells. The immunological synapse is formed in T cells within seconds following the engagement of the TCR by a peptide-bound MHC molecule on the surface of antigen-presenting cells. It serves as a platform for receptors, adaptor proteins, and effector molecules, which assemble into multimolecular activation complexes required for signal transduction. The unique ability of PKC-theta to activate the NF-kB, AP-1 and NF-AT transcription factors is well established, and recent studies contributed essential information on the mechanisms involved in the recruitment of PKC-theta to the center of the immunological synapse and the nature of its substrates and the role of their phosphorylated forms in signal transduction. Additional review manuscripts will describe the unique behavior of PKC-theta in regulatory T cells and its role in the regulation of other cell populations, including those of the innate immune response. This volume brings together leading experts from different disciplines that review the most recent discoveries and offer new perspectives on the contributions of PKC isoforms to biochemical processes and signaling events in different immune cell populations and their impact on the overall host immune response.

T cell activation --- lymphocyte stimulation --- cell growth regulation --- Protein Kinase C --- signal transduction pathways

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Evolution. Phylogeny --- General ecology and biosociology --- Evolution (Biology) --- Ecology --- Ecology. --- ECO Ecology --- biodiversity --- biogeography --- climate and vegetation --- climates --- communities --- competition --- conservation --- demography --- diversity --- ecology --- ecosystems --- evolution --- genetics --- growth regulation --- handbooks --- history --- natural selection --- niche --- parasitism --- population --- population dynamics --- predation --- resource allocation --- speciation --- stability --- 574 --- Animal evolution --- Animals --- Biological evolution --- Darwinism --- Evolutionary biology --- Evolutionary science --- Origin of species --- Biology --- Evolution --- Biological fitness --- Homoplasy --- Natural selection --- Phylogeny --- Balance of nature --- Bionomics --- Ecological processes --- Ecological science --- Ecological sciences --- Environment --- Environmental biology --- Oecology --- Environmental sciences --- Population biology --- General ecology. Biocoenology. Hydrobiology. Biogeography --- Evolution (Biology). --- 574 General ecology. Biocoenology. Hydrobiology. Biogeography

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Leonard Hayflick and colleagues coined the term "cellular senescence" to describe the inevitable and irreversible proliferation arrest of primary human cells in culture. Specifically, Hayflick and coworkers reported the phenomenon of replicative senescence in primary human fibroblasts, showing that these cells can proliferate in vitro for about 55 population doublings before their proliferative capacity succumbs to irreversible proliferation arrest. Since those original observations, major advances in our understanding have come in several areas. We now know that several other triggers, in addition to proliferative exhaustion, can trigger the senescence program. One important class of senescence triggers, and a focus of this volume, are activated oncogenes in primary untransformed cells. There is now good evidence to indicate that senescence in response to this cue is a potent tumor suppressor mechanism, through its ability to block proliferation of incipient cancer cells. However, senescence is not simply a passive proliferation arrest that impacts only the senescent cell itself, but rather, senescent cells influence their environment and neighboring cells through an active secretory program. This secretory program appears to facilitate senescence as a tumor suppression process. Cellular Senescence and Tumor Suppression collects a number of chapters from leaders in the field to review the molecular basis of senescence and its physiological functions, with a particular emphasis on the role of senescence in tumor suppression.

Cancer cells - Growth - Regulation. --- Cancer cells --- Diseases --- Cell Physiological Processes --- Cell Aging --- Neoplasms --- Cell Physiological Phenomena --- Phenomena and Processes --- Medicine --- Oncology --- Health & Biological Sciences --- Growth --- Regulation --- Pathology, Cellular. --- Regulation. --- Cellular pathology --- Cytopathology --- Regulation of cancer cell growth --- Medicine. --- Cancer research. --- Human genetics. --- Pharmacology. --- Biomedicine. --- Cancer Research. --- Human Genetics. --- Pharmacology/Toxicology. --- Pathology --- Cytodiagnosis --- Biological control systems --- Cellular control mechanisms --- Oncology. --- Toxicology. --- Chemicals --- Pharmacology --- Poisoning --- Poisons --- Genetics --- Heredity, Human --- Human biology --- Physical anthropology --- Tumors --- Toxicology --- Drug effects --- Medical pharmacology --- Medical sciences --- Chemotherapy --- Drugs --- Pharmacy --- Cancer research --- Physiological effect

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Cell Cycle Control and Plant Development commences with an introductory chapter and is broadly divided into two parts. Part 1 details the basic cell machinery, with chapters covering cyclin-dependent kinases (CDKs), cyclins, CDK inhibitors, proteolysis, CDK phosphorylation, and E2F/DP transcription factors. Part 2, which describes the cell cycle and plant development, covers cell cycle activation, cell cycle control during leaf development, endoreduplication, the cell cycle and trichome, fruit and endosperm development, the hormonal control of cell division and environmental stress, and cell cycle exit.

Plant cell cycle. --- Cyclin-dependent kinases. --- Plant cells and tissues --- Plantes --- Kinases dépendantes des cyclines --- Growth --- Regulation. --- Cycle cellulaire --- Cellules et tissus --- Croissance --- Régularisation --- Plant cell cycle --- Cyclin-dependent kinases --- Regulation --- Plante --- plants --- Développement biologique --- biological development --- Différenciation cellulaire --- Cell differentiation --- Développement saisonnier --- Seasonal development --- Physiologie végétale --- Plant physiology --- Phosphorylation --- Transcription --- transcription --- Expression des gènes --- gene expression --- Mécanisme de défense --- Defence mechanisms --- Protéine recombinante --- Recombinant proteins --- Auxine --- Auxins --- 581.17 --- 581.14 --- Physiology of the cell --- Development --- 581.14 Development --- 581.17 Physiology of the cell --- Kinases dépendantes des cyclines --- Régularisation --- Plant tissues --- Cells --- Plant anatomy --- Tissues --- Biological rhythms in plants --- Cell cycle --- CDK proteins --- Cyclin-dependent protein kinases --- Protein kinases --- Growth&delete& --- transcription. --- Plant cells and tissues - Growth - Regulation

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There is no question that loss of cell cycle checkpoint regulation is an intrinsic characteristic of cancer. However, many tumors retain parallel checkpoint pathways that are activated by antitumor agents and facilitate therapeutic response. Failures in these therapy-linked checkpoint controls are closely associated with cancers that are highly resistant to therapeutic interventions. Checkpoint Controls and Targets in Cancer provides present-day mechanistic understandings of how multiple sets of proteins orchestrate cell cycle progression, discusses critical checkpoint controls that are evaded for cancer development, focuses on checkpoint pathways associated with antitumor effects, and identifies specific checkpoint regulators for targeting with small molecules in the clinical management of cancer. These aspects of cell cycle checkpoints are articulated critically by renowned experts from both academia and industry, and new concepts are forwarded that challenge existing dogmas. Collectively, Checkpoint Controls and Targets in Cancer provides a unique collection of insightful contributions, which are timely and offer significant interest and appeal to basic, translational and clinical scientists.

Antineoplastic agents -- Development. --- Cancer cells -- Growth -- Regulation. --- Cellular control mechanisms. --- Drug Resistance, Neoplasm --- Cell Cycle --- Pharmacology --- Cell Cycle Proteins --- Antineoplastic Agents --- Neoplasms --- Drug Therapy --- Proteins --- Biological Science Disciplines --- Therapeutics --- Cell Physiological Processes --- Diseases --- Therapeutic Uses --- Drug Resistance --- Amino Acids, Peptides, and Proteins --- Pharmacologic Actions --- Pharmacological Phenomena --- Analytical, Diagnostic and Therapeutic Techniques and Equipment --- Natural Science Disciplines --- Cell Physiological Phenomena --- Physiological Phenomena --- Chemicals and Drugs --- Disciplines and Occupations --- Phenomena and Processes --- Chemical Actions and Uses --- Oncology --- Public Health - General --- Animal Biochemistry --- Human Anatomy & Physiology --- Public Health --- Medicine --- Health & Biological Sciences --- Antineoplastic agents --- Cancer cells --- Development. --- Growth --- Regulation. --- Cell regulation --- Regulation of cancer cell growth --- Medicine. --- Cancer research. --- Pharmacology. --- Oncology. --- Biomedicine. --- Cancer Research. --- Pharmacology/Toxicology. --- Tumors --- Drug effects --- Medical pharmacology --- Medical sciences --- Chemicals --- Chemotherapy --- Drugs --- Pharmacy --- Cancer research --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Pathology --- Physicians --- Physiological effect --- Biological control systems --- Cell metabolism --- Cellular control mechanisms