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Receptor activator of NF-kB

Miller RE, Branstetter D, Armstrong A, Kennedy B, Jones J, Cowan L, Bussiere J, Dougall WC. Receptor activator of NF-kB hgand inhibition suppresses bone resorption and hypercalcemia but does not affect host immune responses to influenza infection. J Immunol 2007 179 266-274. [Pg.176]

Muroi, M. et al. (2002) Regions of the mouse CD14 molecule required for toll-like receptor 2-and 4-mediated activation of NF-kB. J. Biol. Chem. 277, 42372 12379. [Pg.1097]

Mn-SOD mediated by the following pathway interaction with membrane estrogen receptor, activation of MAPK, activation of NF-kB, and up-regulation of gene expression [Borras et ah, 2006 Vina et ah, 2008]. [Pg.244]

Serine proteases, released from immune cell granules, process cytokines and growth factors that control multiple cellular process [56], Proteinase 3, cathepsin G, and elastase all cleave membrane-bound TNF-o, IL-1, and IL-18, and activate epidermal growth factor receptor (EGFR) and toll-like receptor-4 (TLR-4). These actions inhibit growth and lead to apoptosis with transcriptional nuclear factor kB (NF-kB) inactivation. Bik suppresses release of TNF-o, IL-1, and IL-18 and prevents EGFR and TLR-4 activation. Activation of NF-kB is a mediator of cell proliferation, whereas inhibition of NF-/. B leads to apoptosis [82]. Overall, Bik inhibition of immune cell serine proteases increases cell proliferation and stability. [Pg.233]

SCs via activation of NF-kB. Although mechanisms behind p75-mecliated death of SCs are poorly understood, Yeiser et al. (2004) have shown that NGF signaling through the p75 receptor is deficient in TRAF-6 (-/-) mice and that NGF is unable to kill TRAF-6 (-/-) SCs. In addition, TGFp is also known to cause apoptosis of SCs via INK in culture (lessen and Mirsky, 2005). [Pg.85]

Figure 8.3. Various neurotoxins induce the expression of inducible nitric oxide synthase (iNOS) via the activation of NF-kB. Nitric oxide produced from iNOS then induces the activation of guanylate cyclase (GUCY) that catalyzes the production of cGMP. Inhibition of phosphodiesterase may also increase the level of cGMP. Cyclic GMP utilizes protein kinase G (PKG) to increase the expression of GFAP. IL-IR, IL-1 receptor TLR4, toll-like receptor4 GPCR, G protein-coupled receptor TLR3, toll-like receptor 3. Figure 8.3. Various neurotoxins induce the expression of inducible nitric oxide synthase (iNOS) via the activation of NF-kB. Nitric oxide produced from iNOS then induces the activation of guanylate cyclase (GUCY) that catalyzes the production of cGMP. Inhibition of phosphodiesterase may also increase the level of cGMP. Cyclic GMP utilizes protein kinase G (PKG) to increase the expression of GFAP. IL-IR, IL-1 receptor TLR4, toll-like receptor4 GPCR, G protein-coupled receptor TLR3, toll-like receptor 3.

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See also in sourсe #XX -- [ Pg.193 ]




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Active receptor

KB activities

Receptor activation

Receptor activator of NF-kB ligand

Receptor activity

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