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Titlebook: Cytotoxic Effector Mechanisms; Eckhard R. Podack Conference proceedings 1989 The Editor(s) (if applicable) and The Author(s), under exclus

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Clinical Features of Aplastic Anaemiaomplex C5b-9 (.-. 1986): . Assembly of C5b-9 begins with proteolytic conversion of C5 to C5b by the C5 convertases formed as a consequence of complement activation. Development of a transient binding site for C6 leads to formation of a stable C5b-6 dimer. Subsequent binding of C7 and formation of C5
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Aplastic Anemia — A Stem Cell Disorder?hemotaxis, protein turnover in tissues, endocytosis and exocytosis, or tumorigenesis (. 1984). In addition, there is also considerable evidence that cellular proteases play an important role in cell-mediated cytotoxicity: T-cell killing can be inhibited by diisopropylfluorophosphate (DFP) or PMSF (.
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Clinical Features of Aplastic Anaemiaies using aged sheep erythrocytes as a target cell suggested a minor role for C9 in this process (. 1968; . and . 1969), the prevailing view now is that the formation of stable cytolytic complexes in fresh erythrocytes or bacteria absolutely requires the presence of C9. There is still, however, cons
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Der Grosse Augenblick und der Kreis der Zeit. 1900), but only in the last decade has progress been made in understanding the nature of this phenomenon. It has become evident that the complement sequence is inhibited species-specifically on the membrane at two steps at least (. et al. 1986), thus protecting the erythrocytes against the complem
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Cytotoxic Effector Mechanisms978-3-642-73911-8Series ISSN 0070-217X Series E-ISSN 2196-9965
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