Titlebook: Complement; Hans J. Müller-Eberhard,Peter A. Miescher Book 1985 Springer-Verlag Berlin Heidelberg 1985 Komplement.bacteria.blood.genetics.

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Overview: 978-3-540-15075-6978-3-642-82416-6

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https://doi.org/10.1007/978-3-211-09463-1nce to infection. Two primary pathways of activation are known, the classical and alternative, which are each subject to a variety of intrinsic and extrinsic controls. Both pathways proceed initially by the sequential self-assembly of multimacromolecular enzyme complexes. C4 consists of three polype

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https://doi.org/10.1007/978-3-030-11175-5e. For example, structure analyses have progressed to a point that detailed features of these The number designation used throughout the text for amino acid residues is that of the human C3a sequence unless otherwise stated factors have been elucidated at the molecular level. The molecules in questi

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https://doi.org/10.1007/978-3-658-29957-6mely the cleavage of C3 into its two primary fragments C3a and C3b. This reaction can be brought about by a number of enzymes but physiologically it is principally caused by the two homologous enzymes which are generated as a consequence of complement activation. These are the two C3 convertases of