Protein tumour necrosis factor

Receptor for hyaluronic acld-medlated motility Hepatocyte-bindmg protein lntracellular hyaluronic acld-binding protein Tumour necrosis factor - stimulating gene 6... 

Hyperphosphorylation of ERAK-1 by itself and ERAK-4 causes ERAK-1 to dissociate from the membrane-bound complex. Tumour necrosis factor (TNF) receptor-associated factor-6 ( TRAF-6), a cytoplasmic protein, is activated by ERAK-1 and with TAB-2, another cytoplasmic protein, activates transforming growth factor-P (TFG-P)-activating kinase (TAK-1). During this process both TRAF-6 and TAK-1 become ubiquitinated. TAK-1 then promotes activation of the IkB kinases, or the IKK family, EKKa and EKK 3 (found in a complex with NFicB-essential modulator [NEMO]), which phosphorylate the IkB family, notably IkB-u. IkB-u is an inhibitor of NFkB as it sequesters NFkB in an... 

IkB inhibitory protein kappa B lCAM-1 intercellular adhesion molecule 1 lL-1 interleukin-1 LDL low density lipoprotein MAPKs mitogen activated protein kinases MCP-1 macrophage chemotactic protein 1 M-CSF macrophage colony stimulating factor mmLDL minimally modified LDL NAC A-acetylcysteine NF-kB nuclear factor-kappa B oxLDL oxidised LDL PKC protein kinase C PMA phobol myristate acetate ROS reactive oxygen species TNF-a tumour necrosis factor alpha AM-1 vascular cell adhesion molecule 1... 

A number of diflFerent animal models of uveitis have been developed) including that induced by organ-specific ocular antigens such as retinal S-antigen, rhodopsin and lens protein (Wacker et al., 1977 Rao et al., 1979). Other models are based on the injection of proteins foreign to the host, such as intravitreal injections of albumin or 7-globulin (Zimmerman and Silverstein, 1959 Kaplan etal., 1979). More recently, a third group of models has been developed based on the injection of inflammatory mediators such as interleukins-1 and 2, and tumour necrosis factor (Bhattacherjee and Henderson, 1987 ... 

K16. Kragsbjerg, P Holmberg, H and Vikerfors, T., Serum concentration of interleukin-6, tumour necrosis factor-a, and C-reactive protein in patients undergoing major operations. Eur. J. Surg. 161, 17-22 (1995). 

Chevalier S et al. Proteomic analysis of differential protein expression in primary hepatocytes induced by EGF, tumour necrosis factor alpha or the peroxisome pro-liferator nafenopin. Eur J Biochem 2000 267 4624-4634. 

While the majority of attention has focused on peptides contained within the nervous system, two other important methods for delivering peptides to the vicinity of the mast cell have been established (1) peptides produced and secreted by other cells of inflammation that may affect mast-cell function and (2) the local generation of mast-cell-active peptides by secreted enzymes acting on circulating protein precursors. Examples of the former include several, as yet ill-defined, peptide factors and cationic proteins from other immunocompetent cells [66-69], defined lymphokines such as the interleukin-1 [70] and interleukin-3 [71], and tumour necrosis factor [70], Examples of the latter include bradykinin [72] and a recently identified peptide produced by the action of acid proteinases on albumin [73, 74]. 

Tumour necrosis factor is so named because it can result in necrosis of tumour cells in vivo and in vitro. However, diis is not a physiological action attempts to use TNF for cancer treatment were abandoned since it is toxic. It was originally termed cachectin, since it causes cachexia, i.e. wasting of body protein, which is a better term since it indicates its physiological role, but tumour necrosis factor is the name that persists. 

Increased plasma concentrations of glucocorticoids and proinflammatory cytokines (tumour necrosis factor and some interleukins) produced by both tumour cells and macrophages within the tumour stimulate hpolysis and protein degradation. This is accompanied by low levels of insuhn which also encourage hpolysis and proteolysis. 

Exposure of the SECs to pathogens or cytokines produced by other cells during stress induces activation of the SECs and subsequent production of cytokines, eicosanoids, and/or adhesion molecules. For instance, after activation with EPS, a main component of the walls of gramnegative bacteria and a major inducer of inflammation and non-specific immune functions [20], SECs produce a number of pro- and anti-inflammatory cytokines. Pro-inflammatory cytokines shown to be produced were tumour necrosis factor alpha (TNFa) [26] interleukin-1 alpha/beta(IL-lo/p) [27] the major inducer of acute phase proteins interleukin-6 (IL-6) [28] and the neutrophil chemo-attractant interleukin-8 (IL-8) [29]. Anti-inflammatory cytokines shown to be produced were interleukin-10 (IL-10) [27] and hepatocyte growth factor (HGF) [30]. 

Yarim GF, Karahan S, Nisbet C (2007) Elevated plasma levels of interleukin 1 beta, tumour necrosis factor alpha and monocyte chemotac-tic protein 1 are associated with pregnancy toxaemia in ewes. Vet Res Commun 31 565-573... 

Etanercept. Soluble tumour necrosis factor receptor, TNF receptor fusion protein, TNFR-Fc, TNR 001, Enbrel. Drugs R D, 1999.1(1) 75-7. 

Recent evidence suggests that atherosclerosis is a chronic inflammatory process. The recruitment of mononuclear leukocytes and formation of intimal macrophage-rich lesions at specific sites of the arterial tree are key events in atherogenesis. Alterations of chemotactic and adhesive properties of the endothelium play an important role in this process [82]. Quercetin has been reported to inhibit the expression in glomerular cells of monocyte chemoattractant protein-1 (MCP-1) [83] a potent chemoattractant for circulating monocytes. Red wine reduced MCP-1 mRNA and protein expression in abdominal aorta of cholesterol fed rabbits after balloon injury and this effect was associated with a reduced neointimal hyperplasia [84]. The antioxidant-mediated inhibition of nuclear factor k B (NFkB) and the subsequent non selective reduction of cytokine transcription have been suggested to be responsible for these effects [83]. Additionally, quercetin downregulated both phorbol 12-myristate 13-acetate (PMA)- and tumour necrosis factor-a (TNFa)-induced intercellular adhesion molecule-1 (ICAM-1) expression in human endothelial cells [86]. 

T. Knittel, L. Muller, B. Saile, and G. Ramadori, Effect of tumour necrosis factor-alpha on proliferation, activation and protein synthesis of rat hepatic stellate cells, J. Hepatol. 27 1067-1080 (1997). 

PI. Paajanen, H., Laato, M., Jaakkola, M., Pulkki, K., Ninikoski, J., and Nordback, I., Serum tumour necrosis factor compared with C-reactive protein in the early assessment of severity of acute pancreatitis. Br. J. Surg. 82,271—273 (1995). 

Caspases are involved in intracellular proteolytic protease activation cascades leading to apoptosis that are initiated by ligands such as tumour necrosis factor (TNF) and Fas ligand. These proteins bind to PM receptors with cytosolic death domains that activate the cas-pase cascades leading to cell death. Caspases are cysteine proteases that cleave peptide bonds on the carboxyl side of aspartate (hence c-asp-ases). 

---