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  • 1
    Online Resource
    Online Resource
    Basel :S. Karger AG,
    Keywords: Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (184 pages)
    Edition: 1st ed.
    ISBN: 9783318003253
    Series Statement: Progress in Tumor Research Series ; v.35
    Language: English
    Note: Intro -- Contents -- Preface -- Multiple Genes Governing Biological Functions in the Genetic Backgrounds of LaboratoryMice and Asian Wild Mice -- Overview of Transgenic and Gene Knockout Mice -- Alkylation Carcinogenesis in Mice with Altered Levels of DNA Repair Methyltransferase -- Cancer Predisposition inMutantMice Defective in the XPC DNA Repair Gene -- Myeloid Leukemia: Disease Genes and MouseModels -- Genetic and Epigenetic Susceptibility to Endogenous Retrovirus-Induced Lymphomas in SL Mice -- Inheritance of Pulmonary Adenoma Susceptibility in Mice -- TSC2 GeneMutant (Eker) Rat Model of a Mendelian Dominantly Inherited Cancer -- Apc Gene KnockoutMice as a Model for Familial Adenomatous Polyposis -- A Rat Model System for Predisposition to Stomach Cancer -- Genetic and Hormonal Regulation of Murine Hepatocarcinogenesis -- Genetics of Skin Tumor Promotion -- The Genetic Components of Susceptibility to Breast Cancer in the Rat -- Author Index.
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  • 2
    Online Resource
    Online Resource
    Basel :S. Karger AG,
    Keywords: Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (265 pages)
    Edition: 1st ed.
    ISBN: 9783318011982
    Series Statement: Progress in Tumor Research Series ; v.38
    DDC: 616.99/4 s 612/.115
    Language: English
    Note: Cover -- Contents -- Preface -- References -- Mammalian Transglutaminases: A Family Portrait -- Introduction -- Keratinocyte Transglutaminase (TGM1) -- Nomenclature -- Site of Expression -- Promoter -- Inducers and Suppressors -- TG1 Protein -- Functions -- Disease -- Accession Number -- Tissue Transglutaminase (TGM2) -- Nomenclature -- Site of Expression -- Promoter -- Inducers and Suppressors -- TG2 Protein -- Functions -- Disease -- Accession Number -- Epidermal Transglutaminase (TGM3) -- Nomenclature -- Site of Expression -- Promoter -- Inducers and Suppressors -- TG3 Protein -- Functions -- Disease -- Accession Number -- Transglutaminase 4 (TGM4) -- Nomenclature -- Site of Expression -- Promoter -- Inducers and Suppressors -- TG4 Protein -- Functions -- Disease -- Accession Number -- Transglutaminase 5 (TGM5) -- Nomenclature -- Site of Expression -- Promoter -- Inducers and Suppressors -- TG5 Protein -- Functions -- Disease -- Accession Number -- Transglutaminase 6 (TGM6) -- Nomenclature -- Site of expression -- TG6 Protein -- Functions -- Accession Number -- Transglutaminase 7 (TGM7) -- Nomenclature -- Site of Expression -- Promoter -- Accession Number -- Factor XIII A1 Subunit (F13A1) -- Nomenclature -- Site of Expression -- Promoter -- Inducers and Suppressors -- F13A1 Protein -- Functions -- Disease -- Accession Number -- Band 4.2 (EPB4.2) -- Nomenclature -- Site of Expression -- Band 4.2 Protein -- Functions -- Disease -- Accession Number -- Resources for TGs Research -- Anti-TG2 Antibodies -- A. Calbiochem -- B. Lab Vision -- C. Novus Biologicals -- Anti-TG3 Antibody -- Immundiagnostik -- Anti-TG5 Antibody -- Orbigen, Inc. -- Anti-Factor XIIIa -- Lab Vision -- Anti-Erythrocyte Membrane Protein Band 4.2 (EPB4.2) Antibody -- Orbigen, Inc. -- Anti-Isopeptide Antibody -- Novus Biologicals -- References. , Structure-Function Relationships of Transglutaminases - A Contemporary View -- The Inherent Chemical Reactivity of Carboxamido and Thiol Functional Groups in Proteins -- Waterproof Activated Cysteines Make Transglutaminases - In Theory -- The Genes and Expression of Human TGases -- Regulators of TGases -- Enigmatic Secretion of TGases -- The Solved TGases Structures -- TGase Domain Structure -- Structural Correlates of Transglutamination -- Activation of Latent TGases -- Purine Nucleotide Binding and Hydrolysis by TGases -- G-Protein Signaling by TGase 2 -- Disulfide Exchange and Regulation Through Thiol Modifications -- NonCatalytic Interactions of TGase 2 -- Concluding Remarks -- Acknowledgments -- References -- Transglutaminases and Their Substrates -- Introduction -- The Members of TGase's Family -- TGases Substrates -- Conclusions -- References -- Type 2 Transglutaminase and Cell Death -- 'Tissue' Transglutaminase or Type 2 -- Role of TG2 in Cellular Functions -- Effects of TG2 Deletion in Mice -- Is TG2 a Proapoptotic or Prosurvival Protein? -- Is TG2 Involved in Autophagy? -- TG2 and Cell Death in Pathological Settings -- Neurodegenerative Diseases -- Liver Pathologies -- Conclusions -- References -- Transglutaminase and Cell-Survival Signaling -- Introduction -- TGase-2 as a cross-linker enzyme -- TGase-2 Activates RhoA by Transamidation -- TGase-2 as G-Protein Signal Transducer -- TGase-2 as Cell-Survival Factor -- TGase-2 Is Activated under Stressing Conditions -- TGase-2 as Inducer of Neuronal Differentiation -- References -- Transglutaminases in Wound Healing and Inflammation -- Introduction -- Cutaneous Wound Healing -- Role of Transglutaminases in Skin Morphogenesis and Cutaneous Wound Healing -- Genetically Modified Mice for Investigating the Role of Transglutaminases in Wound Healing. , General Role of TG2 in Cell-Matrix Interactions Significant in Wound Repair -- Multiple Activities and Regulation of TG2 -- Externalization of TG2 during Cell Stress and TG2-Associated Cell Death -- Role of TG2 in Matrix Synthesis and Degradation -- Matrix Structural Role of TG2 -- Role of TG2 in Cell Migration -- Role of TG2 in the Inflammatory Response -- TG2 and Activation of Phospholipase A2 -- TG2 and Inflammatory Conditions -- Wound Healing and Fibrosis in the Kidney -- Aberrant Wound Healing in the Kidney Leading to Progressive Renal Scarring -- The Role of TG2 in Wound Healing and Scarring in the Kidney -- TG2 in Progressive Renal Scarring -- Dual Approach to Transglutaminase-Based Wound Repair: Transglutaminase as a Novel Molecular Target and as a Biocatalyst for Tissue Engineering -- Conclusions -- Acknowledgments -- References -- Transglutaminases in Epidermis -- Introduction -- Epidermal Differentiation -- Keratinocyte Transglutaminases -- Transglutaminase Type 1 -- Regulation of TG1 Level and Activity -- Transglutaminase Type 3 -- Transglutaminase Type 5 -- Transglutaminases in Skin Disease -- Transglutaminase Function in Epidermis -- Acknowledgments -- References -- Tissue Transglutaminase (TG2) in Cancer Biology -- Introduction -- TG2 as Antiapoptotic Factor -- The Connection between TG2, Drug Resistance and Metastasis -- TG2 Expression in Drug-Resistant Cells -- TG2 Expression in Metastatic Cancer Cells -- TG2 and Integrin-Mediated Signaling -- TG2 and Carcinogenesis -- Conclusion -- References -- Transglutaminases in Neurodegenerative Disorders -- Introduction -- TGs in Development of the Nervous System -- TGs in Neuronal Apoptosis -- TGs in Neurodegeneration -- Huntingtont's Disease -- Alzheimert's Disease -- Parkinsont's Disease -- Amyotrophic Lateral Sclerosis -- Injury of the Nervous System -- Conclusions -- References. , Tissue Transglutaminase and Celiac Disease -- General Concepts on Celiac Disease -- The Discovery that Tissue Transglutaminase is the Main Autoantigen in CD: New Tool for CD Diagnosis -- tTG is Upregulated and Catalitically Active in CD Intestinal Mucosa -- tTG Deamidating Activity Can Trigger Immune Response to Gliadin -- Substrate Specificity of tTG Towards Gluten Peptides -- tTG Transamidating Activity Seems to be Responsible for Autoimmunity in CD -- Potential Role of Anti-tTG Antibodies in CD Pathogenesis -- Conclusions -- References -- Transglutaminases as Biotechnological Tools -- Biomedicine -- Cosmetics -- Food -- Seafood Products -- Meat Products -- Dairy Products -- Soy Products -- Cereal-Based Products -- Edible Films -- Nutritional Aspects of TGase-cross-linked Proteins -- Leather and Textile Industries -- Analytical Biotechnology Applications -- Other Applications -- Conclusions -- References -- Extracellular Transglutaminase: Factor XIII -- Introduction -- Gene and Expression of Factor XIII -- Structure of Factor XIII -- Sushi Domains in Factor XIIIB -- Functions of Factor XIII -- TGase-Related Diseases -- Factor XIII-Related Diseases -- Polymorphisms of Factor XIII and Thrombosis -- Clinical Features of Congenital Factor XIII Deficiency -- Molecular Defects in Congenital Factor XIII Deficiency -- Animal Model of Factor XIII Deficiency -- Factor XIII Replacement Therapy -- References -- Transglutaminases of Lower Organisms -- Introduction -- TGs and Their Homologs Involved in Protein Cross-Linking -- TG in Growth and Development -- Gene Sequence Analysis of TGs -- Amino Acid Residues Involved in Transamidation Activity of Thioredoxins and PDIs -- Conclusion -- Acknowledgments -- References -- Transglutaminases of Higher, Lower Plants and Fungi -- Introduction -- Possible Roles of Plant TGases. , Structural Role in Cytoskeleton and Cell Wall -- TGases in Chloroplasts -- TGases in Programmed Cell Death -- Light Sensitivity of TGase in Higher Plants -- Light and Salt Stress Effects on TGase Activity in Algae -- Plant and Animal TGases Recognize Each Other's Substrates -- The First Plant TGase -- The First Mammalian-Type TGase of Slime Molds -- Biotechnological Aspects -- Acknowledgments -- References -- Author Index -- Subject Index -- A -- B -- C -- D -- E -- F -- G -- H -- I -- K -- L -- M -- N -- P -- R -- S -- T -- W -- Y.
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  • 3
    Online Resource
    Online Resource
    Osnabrück : Universität Osnabrück - FB3 Erziehungs- und Kulturwissenschaften - Lehrstuhl für Berufs- und Wirtschaftspädagogik
    Keywords: Forschungsbericht ; Berufsbildung ; Globalisierung
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource (200 Seiten, 3,40 MB) , Illustrationen, Diagramme, Karten
    Language: German , English
    Note: Förderkennzeichen BMBF 01BE17018A-B , Verbundnummer 01183314 , Sprache der Kurzfassungen: Deutsch, Englisch
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  • 4
    Electronic Resource
    Electronic Resource
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 88 (2000), S. 4085-4090 
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Epitaxy of high-quality GaN on sapphire requires a rather sophisticated substrate preparation prior to the GaN epilayer growth, namely nitridation of the substrate's surface, growth of a GaN nucleation layer at a relative low temperature, and reduction of the defect density of this layer by a subsequent annealing step. For studying both, the detailed mechanisms of this complex procedure and its growth parameter dependencies, we attached an in situ spectroscopic ellipsometer to a nitride metal-organic vapor phase epitaxy reactor. First, the high-temperature dielectric function of GaN was measured using samples from different suppliers. Based on these data, the effect of growth parameter variations on the crystal quality of GaN epilayers could be monitored in situ. In particular, we determined the threshold temperature and the duration of the substrate nitridation under ammonia as well as the thermal threshold and duration of the nucleation layer transformation. Additionally, based on the in situ measurements a qualitative estimate for the crystalline quality of the nucleation layer and the epilayer is provided. Finally, the surface roughness of differently prepared GaN layers was evaluated by using the high-energy spectroscopic range of our vacuum-ultraviolet ellipsometer (3.5–9.0 eV). © 2000 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary 1 It was shown recently that stimulation of cardiac muscarinic M2-receptors revealed an enhanced negative inotropic response in isolated rat left atria after exposure to hypochlorite-induced oxidative stress. This phenomenon was not observed after stimulation of the cardiac A1-receptor, which like the M2-receptor is coupled to Gi-proteins. Since even the contractile response to M3-receptor stimulation was not amplified in the rat portal vein, we hypothesized a M2-receptor specificity of this hypochlorite-induced enhancement. 2 The present study was performed in order to investigate whether the sympathoinhibitory response to presynaptically located M2-receptor stimulation would also be modified after exposure to hypochlorite in the rat tail artery. We applied electrical field stimulation (EFS) in order to mimic sympathetic neurotransmission. 3 EFS increased the vascular tone frequency-dependently (0.3–4 Hz). EFS-induced vasoconstriction could be attenuated by acetylcholine (30 nm−1 μm) in a concentration-dependent manner. Hypochlorite (10 and 100 μm) did not affect the sympathoinhibitory effect of acetylcholine (100 nm). 4 In conclusion, in contrast to cardiac M2-receptors, hypochlorite did not amplify the sympathoinhibitory effects of presynaptic M2-receptors. The different responsiveness between neuronal and cardiac M2-receptors to hypochlorite may be explained by the different G-protein subunits involved in the activation of the underlying signalling cascade.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1365-2494
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: To determine the impacts of climate change and defoliation on the community structure and plant diversity of a semi-natural temperate grassland, monoliths of a permanent grassland were exposed to ambient or elevated atmospheric CO2 concentrations (ambient + 235 ppmv) and temperature (ambient + 3°C) from October 1998 to December 2000. The monoliths were subjected to two different cutting frequencies, either two or six cuts per year. The grassland community structure changed during the course of the experiment and was more responsive to changes in management than to changes in climate. Increased cutting frequency stimulated plant diversity by enhancing the number of forb species, but plant diversity was not significantly affected by climate change. The contribution of individual plant species to the vegetation cover revealed species-specific responses to climate change and cutting frequency, but for most species significant interactions between climate change and cutting frequency were present. There were no clear-cut effects of treatments on the total annual yield and the proportion of forbs present, as significant interactions between climate change and cutting frequency occurred. It is concluded that differential grassland management will modify plant species-specific responses to climate change and resulting changes in the botanical composition of mixed-species, temperate grasslands.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 35 (2005), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The linear model of maturation of IFN-γ-producing cells from a proliferative pool of type 2 cytokine-producing T cells represents a fundamental shift in interpreting how changes in cytokine production by T cell populations are regulated. A major tenet of this model is antigen-independent, bystander proliferation of type 2 T cells and their maturation to IFN-γ+ cells. Both clinical observations and prevailing theories of immune system development in asthma are consistent with this highly interpretative in vitro model, which allows unambiguous characterization of the modulation of the intrinsic features of T cell proliferation and differentiation by environmental and genetic factors. Hypotheses based on the linear model of T cell maturation are readily testable and should lead to a greater understanding of not only allergen-specific responses, but also the non-specific, bystander effects associated with specific responses to allergens or pathogens. Topics to be discussed in the context of the linear model of T cell maturation in this review include: (1) allergic responses to an inciting allergen that may enhance sensitivity to subsequent yet different allergens; (2) dampening the preferential accumulation of type 2 T cells during a typical immune response against viral and bacterial pathogens; (3) allergen-independent sensitization in asthmatics: (4) the ‘hygiene hypothesis’ for the reported increased allergy development in industrialized countries; (5) elevated IFN-γ levels in asthmatics, in addition to the expected high levels of type 2 cytokines; (6) testing the effects of inflammatory mediators, as well as various anti-inflammation therapies on T cell maturation; and (7) testing the influence of gene variation on T cell maturation.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Rationale Asthmatic airway remodelling is characterized by myofibroblast hyperplasia and subbasement membrane collagen deposition. We hypothesized that cytokines and growth factors implicated in asthmatic airway remodelling are increased in bronchoalveolar lavage (BAL) fluid of asthmatics after segmental allergen challenge (SAC), and that these growth factors and cytokines increase α-smooth muscle actin (α-SMA) and collagen III synthesis by human lung fibroblasts (HLFs).Methods Transforming growth factor (TGF)-β1, TGF-β2, IL-4 and IL-13 levels were measured in BAL fluid from 10 asthmatics and 9 non-asthmatic controls at baseline and then 1 day, 1 week and 2 weeks after SAC. Confluent cultures of HLFs were stimulated by exogenous addition of TGF-β1, TGF-β2, IL-4 or IL-13 (concentration range 0.01–10 ng/mL) over 48 h. Collagen III was measured in culture supernates and α-SMA in cell lysates by Western blot.Results At baseline, there was no difference in BAL fluid concentrations of TGF-β1, IL-4 and IL-13 between asthmatics and controls; however, non-asthmatics had higher concentrations of total TGF-β2. In asthmatics, BAL fluid concentrations of all four factors increased significantly 1 day after SAC. TGF-β1, TGF-β2 and IL-13 concentrations returned to baseline by 1 week after SAC, but BAL fluid IL-4 concentration remained elevated for at least 2 weeks. TGF-β1, TGF-β2 and IL-4 significantly increased α-SMA in fibroblasts, but only IL-4 caused corresponding increases in collagen III synthesis. IL-13 had no direct effects on collagen III synthesis and α-SMA expression.Conclusions Because IL-4 caused a dose-dependent increase in α-SMA and collagen III synthesis, it may be an important cytokine mediating asthmatic airway remodelling. TGF-β1 and TGF-β2 may also play a role in airway remodelling by stimulating phenotypic change of fibroblasts to myofibroblasts. Additionally, collagen III synthesis appears to be independent of myofibroblast phenotype and is apparently regulated by different growth factors and cytokines.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 16 (1986), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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