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  • 1
    Online Resource
    Online Resource
    Correlation between the exposure of aromatic chromophores at the surface of the Fc domains of immunoglobulin G and their ability to bind complement
    American Chemical Society (ACS) ; 1977
    In:  Biochemistry Vol. 16, No. 2 ( 1977-01-25), p. 233-240
    Details
    In: Biochemistry, American Chemical Society (ACS), Vol. 16, No. 2 ( 1977-01-25), p. 233-240
    Type of Medium: Online Resource
    ISSN: 0006-2960 , 1520-4995
    URL: Article
    DOI: 10.1021/bi00621a012
    RVK:
    WA 15000
    Language: English
    Publisher: American Chemical Society (ACS)
    Publication Date: 1977
    detail.hit.zdb_id: 1472258-6
    SSG: 12
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  • 2
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    Online Resource
    Binding Site of Human IgG Subclasses and Their Domains for Fc Receptors of Activated Murine T Cells
    The American Association of Immunologists ; 1977
    In:  The Journal of Immunology Vol. 119, No. 3 ( 1977-09-01), p. 1077-1083
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 119, No. 3 ( 1977-09-01), p. 1077-1083
    Abstract: A subpopulation of activated murine T cells (25%) were found to bear Fc receptors for mouse, rabbit, and human IgG. Studies, by rosette inhibition and indirect immunofluorescence, of their specificity for human IgG subclasses have shown that these receptors bound nonaggregated IgG1, IgG2, and IgG3 in a comparable fashion, but did not bind IgG4. The binding site has been localized exclusively to the Fc region and the binding capacity of this fragment was not affected by mild reduction. Binding of the Fc fragment of IgG4 could not be demonstrated. Using isolated Cγ2 and Cγ3 (pFc′) domains from IgG1 and a Cγ3-derived fragment (Fc′), a major binding site was localized to the Cγ3 domain between residues Gln342 and His433. A 10-fold molar excess of Cγ3 dimer over native Fc was, however, required to show comparable activity. The monomeric Cγ2 domain was 10-fold less active than the Cγ3 fragment. Human urine β2-microglobulin was not cytophilic. These data are discussed and it is suggested that the Cγ2 and Cγ3 domains may contribute to the formation of a cooperative binding site through quaternary interdomain interactions. By redistribution experiments, it was demonstrated that the three human IgG subclasses shown to be cytophilic share common or linked receptors, which were not associated with the H-2 alloantigens.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.119.3.1077
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1977
    detail.hit.zdb_id: 1475085-5
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  • 3
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    Online Resource
    Epidermal Growth Factor Receptor and Transforming Growth Factor β Signaling Pathways Cooperate To Mediate Chlamydia Pathogenesis
    American Society for Microbiology ; 2020
    In:  Infection and Immunity Vol. 88, No. 4 ( 2020-03-23)
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 88, No. 4 ( 2020-03-23)
    Abstract: Human genital Chlamydia infection is a major public health concern due to the serious reproductive system complications. Chlamydia binds several receptor tyrosine kinases (RTKs) on host cells, including the epidermal growth factor receptor (EGFR), and activates cellular signaling cascades for host invasion, cytoskeletal remodeling, optimal inclusion development, and induction of pathogenic epithelial-mesenchyme transition (EMT). Chlamydia also upregulates transforming growth factor beta (TGF-β) expression, whose signaling pathway synergizes with the EGFR cascade, but its role in infectivity, inclusions, and EMT induction is unknown. We hypothesized that the EGFR and TGF-β signaling pathways cooperate during chlamydial infection for optimal inclusion development and stable EMT induction. The results revealed that Chlamydia upregulated TGF-β expression as early as 6 h postinfection of epithelial cells and stimulated both the EGFR and TGF-β signaling pathways. Inhibition of either the EGFR or TGF-βR1 signaling substantially reduced inclusion development; however, the combined inhibition of both EGFR and TGF-βR1 signaling reduced inclusions by over 90% and prevented EMT induction. Importantly, EGFR inhibition suppressed TGF-β expression, and an inhibitory thrombospondin-1 (Tsp1)-based peptide inhibited chlamydia-induced EMT, revealing a major source of active TGF-β during infection. Finally, TGF-βR signaling inhibition suppressed the expression of transforming acidic coiled-coil protein-3 (TACC3), which stabilizes EGFR signaling, suggesting reciprocal regulation between TGF-β and EGFR signaling during chlamydial infection. Thus, RTK-mediated host invasion by chlamydia upregulated TGF-β expression and signaling, which cooperated with other cellular signaling cascades and cytoskeletal remodeling to support optimal inclusion development and EMT induction. This finding may provide new targets for chlamydial disease biomarkers and prevention.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00819-19
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2020
    detail.hit.zdb_id: 1483247-1
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  • 4
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    Online Resource
    Molecular Pathogenesis of Chlamydia Disease Complications: Epithelial-Mesenchymal Transition and Fibrosis
    American Society for Microbiology ; 2018
    In:  Infection and Immunity Vol. 86, No. 1 ( 2018-01)
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 86, No. 1 ( 2018-01)
    Abstract: The reproductive system complications of genital chlamydial infection include fallopian tube fibrosis and tubal factor infertility. However, the molecular pathogenesis of these complications remains poorly understood. The induction of pathogenic epithelial-mesenchymal transition (EMT) through microRNA (miRNA) dysregulation was recently proposed as the pathogenic basis of chlamydial complications. Focusing on fibrogenesis, we investigated the hypothesis that chlamydia-induced fibrosis is caused by EMT-driven generation of myofibroblasts, the effector cells of fibrosis that produce excessive extracellular matrix (ECM) proteins. The results revealed that the targets of a major category of altered miRNAs during chlamydial infection are key components of the pathophysiological process of fibrogenesis; these target molecules include collagen types I, III, and IV, transforming growth factor β (TGF-β), TGF-β receptor 1 (TGF-βR1), connective tissue growth factor (CTGF), E-cadherin, SRY-box 7 (SOX7), and NFAT (nuclear factor of activated T cells) kinase dual-specificity tyrosine (Y) phosphorylation-regulated kinase 1a (Dyrk1a). Chlamydial induction of EMT resulted in the generation of α-smooth muscle actin (α-SMA)-positive myofibroblasts that produced ECM proteins, including collagen types I and III and fibronectin. Furthermore, the inhibition of EMT prevented the generation of myofibroblasts and production of ECM proteins during chlamydial infection. These findings may provide useful avenues for targeting EMT or specific components of the EMT pathways as a therapeutic intervention strategy to prevent chlamydia-related complications.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00585-17
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2018
    detail.hit.zdb_id: 1483247-1
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