Intermedilysin-receptor interactions during assembly of the pore complex: assembly intermediates increase host cell susceptibility to complement-mediated lysis.
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Risk of non-Hodgkin lymphoma in association with germline variation in complement genes.
(66/225)
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How to polymerize in order to survive.
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Resistance of Escherichia coli to osmotically introduced complement component C9.
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Investigation into the action of osmotically introduced C9 in Escherichia coli (in the absence of any other complement components) revealed that C9 could inhibit inner membrane respiration and cause a decrease in the viability of cells that were normally complement sensitive. This effect is analogous to the loss of inner membrane function and viability due to the assembly of the C5b-9 complex on these cells. Complement-resistant cells showed no such inhibition of respiration or loss of viability when subjected to the osmotic introduction of C9. The reason for this failure of C9 to affect complement-resistant cells was explored to determine whether this resistance to C9 was due to an inability of proteins in general to be osmotically introduced into the complement-resistant cells. The protein toxins melittin and colicin E1 were showed to be able to kill these complement-resistant cells (as well as complement-sensitive cells) when osmotically introduced into the periplasm. Therefore, cellular resistance to osmotically introduced C9 is not due to an inability of proteins to be introduced into the cells and may be related to a mechanism of cellular resistance to the C5b-9 complex. (+info)
Molecular cloning and characterization of a paramyosin from Clonorchis sinensis.
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Functionally active complement proteins C6 and C7 detected in C6- and C7-deficient individuals.
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Two sensitive sandwich ELISAs based on monoclonal antibodies directed to native C6 and C7 allowed the detection and quantitation of these complement proteins in 20 out of 37 serum samples from individuals who had previously been classified as deficient in these proteins as assessed by immunochemical and/or functional assays. Furthermore, serum from four C6-deficient and one combined C6-/C7-deficient individual showed an increase in the terminal complement complex (TCC) and a decrease in native C6 and C7 after complement activation as assayed by specific ELISAs. Despite their (incomplete) deficiencies, these individuals therefore possess functionally active terminal complement proteins with respect to their ability to generate the TCC. As these individuals have no history of a susceptibility to neisserial infections, even low concentrations of functionally active C6 and C7 may provide sufficient protection against those micro-organisms whose destruction requires TCC formation. (+info)
Complement component C3 binds to activated normal platelets without preceding proteolytic activation and promotes binding to complement receptor 1.
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Topology of the membrane-bound form of complement protein C9 probed by glycosylation mapping, anti-peptide antibody binding, and disulfide modification.
(72/225)
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