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Cartilage binding

Regulates specific immunity and bone turnover binds to RANK receptor stimulates naive T cell proliferation promotes survival of RANK -t-T cells regulates T cell-dependent immune response binds to OPG inhibits osteoclastogenesis and leads to excess accumulation of bone and cartilage Binds to RANKL... [Pg.1209]

Recombinant human DL-1 receptor antagonist (Anakinra, Kineret ) blocks the biological activity of interleukin-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. Thereby it reduces the pro-inflammatory activities of IL-1 including cartilage destiuction and bone resorption. Side effects include an increased risk of infections and neutropenia. [Pg.412]

Chondronectin May play role in binding type II collagen to surface of cartilage. [Pg.551]

Renkema, G.H., Boot, R.G., Au, F.L., Donker-Koopman, W.E., Strijland, A., Muijsers, A.O., Hrebicek, M. and Aerts, J.M. (1998) Chitotriosidase, a chitinase, and the 39-kDa human cartilage glycoprotein, a chitin-binding lectin, are homologues of family 18 glycosyl hydrolases secreted by human macrophages. European Journal of Biochemistry 251, 504-509. [Pg.217]

GH primarily displays an anabolic activity. It partially stimulates the growth of bone, muscle and cartilage cells directly. Binding of GH to its hepatic receptor results in the synthesis and release of... [Pg.308]

GH primarily displays an anabolic activity. It partially stimulates the growth of bone, muscle and cartilage cells directly. Binding of GH to its hepatic receptor results in the synthesis and release of insulin-like growth factor (IGF-1), which mediates most of GH s growth-promoting activity on, for example, bone and skeletal muscle (Chapter 7). The major effeets mediated by hGH are summarized in Table 8.6. [Pg.327]

TNF-a and IL-1 are current targets of antiinflammatory drug therapy. A homotrimer of 17-kDa protein subunits whose effects include the activation of neutrophils and eosinophils, induction of COX-2, induction of proinflammatory cytokines (e.g., IL-1, IL-6), enhancement of endothelial layer permeabihty, induction of adhesion molecules by endothelial cells and leukocytes, stimulation of fibroblast proliferation, degradation of cartilage, and stimulation of bone reabsorption. Two receptors mediate these effects a 55-kDa receptor (p55) and a 75-kDa receptor (p75). Each of these receptors is found in both cell surface and soluble forms. The binding of two or three cell surface receptors to TNF-a initiates an inflammatory response. Soluble p55 also acts as a signaling receptor for inflammatory responses, whereas soluble p75 acts as an antagonist. [Pg.426]

Pharmacokinetics Sequestered into bone and cartilage. Protein binding 14%-17%. Primarily excreted unchanged in urine. Removed by hemodialysis. Half-life 3.3-6.8 hr (increased in impaired renal function). [Pg.539]

V. Vilim and J. Krajickova, Proteoglycans of human articular cartilage. Identification of several populations of large and small proteoglycans and of hyaluronic acid-binding proteins in successive cartilage extracts. Biochem. J., 273 (1991) 579-585. [Pg.261]


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See also in sourсe #XX -- [ Pg.131 ]




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Cartilage

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