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Complement-activating protein

Cytokines when bound to antigens initiate complement activation Proteins that can communicate between -sheet domains, immunoglobulin fold Table 35-4... [Pg.806]

STRUCTURE AND FUNCTION OF COBRA VENOM FACTOR, THE COMPLEMENT-ACTIVATING PROTEIN IN COBRA VENOM... [Pg.97]

C.-W. Vogel Cobra venom factor, the complement-activating protein of cobra venom. In Handbook of Natural Toxins, Vol. 5, Reptile and Amphibian Venoms. A. T. Tu, ed. Marcel Dekker, New York 1991, 147-188. [Pg.112]

G. Eggertsen, P. Lind, and J. Sjdquist Molecular characterization of the complement activating protein in the venom of the Indian cobra Naja n. siamensis). 1981. Mol. Immunol. 18, 125-133. [Pg.112]

Abramson, S., Hofistein, S.T. and Weissmann, G. (1982). Superoxide anion generation by human neutrophils exposed to monosodium urate. Effect of protein adsorption and complement activation. Arth. Rheum. 25, 174-180. [Pg.256]

TNF (17.5) Monocyte/macrophage, lymphocyte, neutrophil, endothelium, fibroblast, keratinocyte Activation of T and B cells, natural killer cells, neutrophils, and osteoblasts. Stimulation of endothelial cells to release chemotactic proteins, NO and PGI2. Tumoricidal activity. Induces fever, sleep, hepatic acute phase protein synthesis, catabolism, ACTH release. Lead to myocardial depression, hypotension/shock, hypercoagulability, and death. Stimulates production of IL-1, IL-6, IL-8, IFN-y, and H202. Suppression of cytochrome P-450, thyroglobulin, and lipoprotein lipase. Induces complement activation, release of eicosanoids, including PAF. Procoagulant activity. [Pg.59]

C5-derived peptide in serum. This molecule lacks anaphylatoxin activity (i.e. it cannot cause smooth muscle contraction), and its ability to cause che-motaxis in neutrophils is about 10-20 times lower than that of C5a. However, human serum also contains a heat-stable, anionic protein termed co-chemotaxin (relative molecular mass = 60 kDa), which acts in a concentration-dependent manner to permit C5a des Arg to act as a chemoattractant for neutrophils. Thus, C5a des Arg plus cochemotaxin working together probably account for most of the neutrophil chemoattractant activity in vivo following complement activation. The mechanism of action of cochemotaxin is unknown, but it may form a physical complex by attaching to a sialic acid residue on the oligosaccharide chain of C5a des Arg. Deglycosylation of C5a des Arg increases its chemoattractant activity more than 10-fold, and its dependency upon cochemotaxin is decreased. [Pg.81]

Complement A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed components of complement and are designated by the symbols... [Pg.63]

Soliris is a protein-based drug that specifically blocks cleavage of the C5 component of the complement system, thereby preventing the final stages of complement activation. [Pg.263]

The synthetic polymeric components as well as their combinations with proteins such as human serum albumin (HSA), bovine serum albumin (BSA), human serum albumin/a-interferon mixtures (HSA-IFNa) and myoglobin (MYO) did not give any negative response to in vitro and in vivo biocompatibility tests, such as platelet aggregation, complement activation, acute toxicity, and acute thromboembolic potential. [Pg.70]

Murthy, K. H., et al. (2001). Crystal structure of a complement control protein that regulates both pathways of complement activation and binds heparan sulfate proteoglycans. Cell 104,301-311. [Pg.126]

About 20 different proteins are included in the complement system Proteins C1-C9, factors B and D, and a series of regulatory proteins. All these proteins are made in the liver, and they circulate freely in the blood and extracellular fluid. Activation of the complement system involves a cascade of proteolytic reactions. In addition to forming membrane attack complexes, the proteolytic fragments released during the activation process promote dilation of blood vessels and the accumulation of phagocytes at the site of infection. [Pg.841]


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See also in sourсe #XX -- [ Pg.97 ]




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