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Sensitized tumor necrosis factor

Jung EM, Lim JH, Lee TJ, Park JW, Choi KS, Kwon TK. 2005. Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through reactive oxygen species-mediated upregulation of death receptor 5 (DR5). [Pg.390]

B21. Bertini, R., Bianchi, M., and Ghezzi, P Adrenalectomy sensitizes mice to the lethal effects of interleukin 1 and tumor necrosis factor. J. Exp. Med 167,1708-1712 (1988). [Pg.109]

Kull Jr., F.C., Jacobs, S., and Cuatrecasas, P. (1985) Cellular receptor for 1251-labeled tumor necrosis factor Specific binding, affinity labeling, and relationship to sensitivity. Proc. Natl. Acad. Sci. USA 82, 5756-5760. [Pg.1085]

Early research showed that Pb exposure could increase sensitivity to bacterially-derived endotoxins [63] as well as increase production of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-a) by macrophages [64-67], Studies in several species indicate that Pb boosts production of TNF-a both immediately following adult exposure and in later life following gestational exposure. Flohe and coworkers [67] reported that Pb-induced elevation in TNF-a production is sensitive to both protein kinase C signaling as well as protein production. Not only can the production of TNF-a be elevated following exposure to Pb, but also the expression of the receptor for TNF-a (TNF-R) is elevated [68], Therefore, the combined effect of elevated cytokine production by macrophages as well as increased receptor expression would be expected to contribute to problematic inflammatory responses. [Pg.213]

Dentener, M.A.et al., Role of tumor necrosis factor in the enhanced sensitivity of mice to endotoxin after exposure to lead, Immunopharmacol. Immunotoxicol. 11, 321, 1989. [Pg.222]

Buonamici M, Young GA, Khazan N. (1982). EEG power spectra in the rat. Effects of acute delta 9-THC administration on EEG and EEG power spectra in the rat. Neuropharmacology. 21(8) 825-29. Cabral GA, Toney DM, Fischer-Stenger K, Harrison MP, Marciano-Cabral F. (1995). Anandamide inhibits macrophage-mediated killing of tumor necrosis factor-sensitive cells. Life Sci. 56(23-24) 2065-72. [Pg.556]

Andiieu, N., Salvayre, R., and Levade, T., 1996, Comparative study ofthe metabohc pools of sphingomyelin and phosphatidylchohne sensitive to tumor necrosis factor. Eur. J. Biochem. 236 738-745. [Pg.279]

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. [Pg.467]

Fulda S, Debatin KM. 2004. Sensitization for tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by the chemopreventive agent resveratrol. Cancer Res. 64 337-346. [Pg.323]

Hudziak, R. M., Lewis, G. D., Winger, M., Fendly, B. M., Shepard, H. M., and Ullrich, A., 1989. pl85 HER2 monoclonal antibody has antiproliferative effects in vitro and sensitizes human breast tumor cells to tumor necrosis factor. Mol. Cell Biol. 9 1165-1172. [Pg.322]

Sanna PP, Weiss F, Samson ME, Bloom FE, Pich EM. Rapid induction of tumor necrosis factor alpha in the cerebrospinal fluid after intracerebroventricular injection of lipopolysaccharide revealed by a sensitive capture immuno-PCR assay. Proc Natl Acad Sci USA 1995 92(l) 272-275. [Pg.287]

Saito K, Kobayashi D, Sasaki M, Araake H, Kida T, Yagihashi A, Yajima T, Kameshima H, Watanabe N. Detection of human serum tumor necrosis factor-alpha in healthy donors, using a highly sensitive immuno-PCR assay. Clin Chem 1999 45(5) 665-669. [Pg.287]

Komatsu M, Kobayashi D, Saito K, Furuya D, Yagihashi A, Araake H, Tsuji N, Sakamaki S, Niitsu Y, Watanabe N. Tumor necrosis factor-alpha in serum of patients with inflammatory bowel disease as measured by a highly sensitive immuno-PCR. Clin Chem 2001 47(7) 1297-1301. [Pg.288]

Souza, S. C., Yamamoto, M. T., Franciosa, M. D., Lien, P., and Greenberg A. S. (1998). BRL 49653 Blocks the Lipolytic Actions of Tumor Necrosis Factor-a A Potential New Insulin Sensitizing Mechanism for Thiazolidinediones. Diabetes AH, 691-695. [Pg.209]

E., Reed, J. C. (2006) Identification of small molecules that sensitize resistant tumor cells to tumor necrosis factor-family death receptors. Cancer Research, 66, 2367—2375. [Pg.540]

Vercammen D, et al. Inhibition of caspases increases the sensitivity of L929 cells to necrosis mediated by tumor necrosis factor. J. Exp. Med. 1998 187 1477-1485. [Pg.183]


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See also in sourсe #XX -- [ Pg.794 ]




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