Tumor necrosis factor receptor modulation

Suda T, Takahashi N, Udagawa N, Jimi E, Gillespie MT, Martin TJ (1999) Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families. Endocr Rev 20 345-357... 

In addition to these downstream enzymatic effectors, IFs interact with receptors in the death pathway. K8 and K18 interact directly with the cytoplasmic domain of tumor necrosis factor receptor 2 (TNFR2) and attenuate TNF-induced, Jun NH(2)-terminal kinase (JNK) signaling, NFkB activation, and cell death (Gaulin et al, 2000). Modulation of cell... 

The stress or growth pathways modulated by vanadium involve specialized effectors and often can be activated by excess ROS. Cytokines, small proteins that effect communication between cells or cell behavior, can be involved in the cellular stress response. Tumor necrosis factor a (TNFa) is a cytokine stress signal that binds to a membrane receptor (tumor necrosis factor receptor, or TNFR). This interaction stimulates kinase activity that leads to cell injury and inflammation and also to the activation of caspases, a family of cysteine-dependent aspartate-directed proteases that are involved in apoptosis. The mitogen-activated protein (MAP) kinase cascade regulates both mitosis and apoptosis signaling pathways. 

Lee, N.K. and Lee, S.Y. (2002) Modulation of life and death by the tumor necrosis factor receptor-associated factors (TRAFs). J. Biochem. Mol. Biol. 35,61-66. 

Tannenbaum, C. S., Major, J. A., and Hamilton, T. A. (1993). IFN-y and lipopolysaccharide differentially modulate expression of tumor necrosis factor receptor mRNA in murine peritoneal macrophages. /. Immunol. 151, 6833-6839. 

Liu IS, lohn GR, Sikora A, Lee SC, Brosnan CF (2000) Modulation of interleukin-1 beta and tumor necrosis factor alpha signaling by P2 purinergic receptors in human fetal astrocytes. 1 Neurosci 20 5292-5299... 

There is some evidence that adenosine also participates in modulating peripheral somatosensory function through A3 receptors on immune cells. A predominant response to the activation of A3 receptors is degranulation of mast cells causing the release of multiple proinflammatory mediators (IL-6/IL-10/IL-12). Further involvement of A3 receptors in pain and inflammation may be a result of adenosine-mediated inhibition of the release of tumor necrosis factor a (TNF-a), a proinflammatory cytokine produced by monocytes and macrophages. 

Henkler, F., Baumann, B., Fotin-Mleczek, M., Weingartner, M., Schwenzer, R., Peters, N., Graness, A., et al., Caspase-mediated cleavage converts the tumor necrosis factor (TNF) receptor-associated factor (TRAF)-l from a selective modulator of TNF receptor signaling to a general inhibitor of NF-kappaB activation. J Biol Chem 278 (2003) 29216-29230. 

The neurotrophin receptor p75 was first identified as a nerve growth factor (NGF)-binding protein and was subsequently shown to interact with each of the other neurotrophic factors, BDNF, neurotrophin-3, and neurotrophin-4/-5. It also modulates the activity of several members of the tropomyosin-related receptor tyrosine kinase family (Trk) (reviewed in Chao, 2003). p75, a member of the tumor necrosis factor superfamily, is a type I transmembrane protein with four cysteine-rich domains in its extracellular region and a Death domain in its cytoplasmic protein (Fig. 11). 

D. M. Rose, B. W. Winston, E. D. Chan, D. W. H. Riches, and P. M. Henson, Interferon-y and Transforming Growth Factor-P Modulate the Activation of Mitogen-Activated Protein Kinases and Tumor Necrosis Factor-a Production Induced by Fcg-Receptor Stimulation in Murine Macrophages, Biochemical Biophysical Research Communication, 238 (1997) 256-260. 

Endotoxin pyrogen induces fever by an indirect process. On entry into the circulatory system, endotoxin is bound to LPS-binding protein (LPB) that transports it to receptor cells in the reticuloendothelial system. The main target cells are circulating mononuclear cells, which produce proinflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-a (TNFot). These cytokines are involved in acute and chronic inflammation, induce fever, and modulate the host s response to bacterial infection. ° ... 

Medvedev AE, Espevik T, Ranges G, Sundan A. Distinct roles of the two tumor necrosis factor (TNF) receptors in modulating TNF and lymphotoxin a effects. J Biol Chem 1996 271 9778-84. 

Ferran C, Dy M, Sheehan K, Schreiber R, Grau G, Bluestone J, Bach JF, Chatenoud L. Cascade modulation by anti-tumor necrosis factor monoclonal antibody of interferon-y, interleukin 3 and interleukin 6 release after triggering of the CD3/T cell receptor activation pathway. Eur J Immunol 1991 21(10) 2349-2353. 

B46. Bird, T. A., and Saklatvala, J. Down-modulation of epidermal growth factor receptor affinity in fibroblasts treted with interleukin-1 or tumor necrosis factor is associated with phosphorylation at a site other than threonine 654. J. Biol. Chem. 265, 235-240 (1990). 

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