Recent advances in tumor necrosis factor and CD40 signaling
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Cited by (77)
An immunohistochemical study of increased tumor necrosis factor-α in the skin of patients with amyotrophic lateral sclerosis
2013, Journal of Clinical NeuroscienceCitation Excerpt :The lack of bedsore formation even in the terminal stages in patients with ALS is considered characteristic.6 Tumor necrosis factor-α (TNF-α) is a major inflammatory cytokine that elicits a wide range of biological responses, including neuronal apoptosis.7 TNF-α mediates its biological effects through activation of two distinct receptors, TNF-R1 and R2.8
Molecular identification and expression analysis of a novel tumor necrosis factor receptor from the black rockfish, Sebastes schlegelii
2011, Developmental and Comparative ImmunologyCitation Excerpt :Tumor necrosis factor (TNF), a protein initially characterized by its ability to cause hemorrhagic necrosis in certain transplanted tumors (Carswell et al., 1975), is now understood to be a multifunctional cytokine (Beutler and Cerami, 1988; Old, 1988). Members of the TNF and TNF receptor (TNFR) superfamilies play crucial roles in both innate and adaptive immunity, regulating cell proliferation, differentiation, survival, and death; cytokine production; lymphocyte costimulation; and isotype switching (Almitage, 1994; Tewari and Dixit, 1996). Members of the TNF and TNFR superfamilies can be distinguished on the basis of their function and expression patterns, despite a partial overlap (Collette et al., 2003).
Gelsolin, but not its cleavage, is required for TNF-induced ROS generation and apoptosis in MCF-7 cells
2009, Biochemical and Biophysical Research CommunicationsCitation Excerpt :TNF-α can induce apoptotic or necrotic cell death in vitro, depending on the nature of the cell line used [1,2].
Molecular cloning and preliminary expression analysis of banded dogfish (Triakis scyllia) TNF decoy receptor 3 (TNFRSF6B)
2008, Fish and Shellfish ImmunologyPhosphorylation of Tumor Necrosis Factor Receptor 1 (p55) Protects Macrophages from Silica-induced Apoptosis
2004, Journal of Biological ChemistryCitation Excerpt :To determine whether or not silica induced changes in TNF receptor-associated proteins in the macrophage cell lines, we studied the protein expression for the p55 TNF receptor-associated death domain (TRADD), and the p75 TNF receptor factor-associated (TRAF1 and TRAF2) proteins, by immunoblotting (Fig. 1D). TRADD is the p55 receptor death domain-associated protein and is involved in TNFα-mediated apoptosis and NF-κB activation (33, 34). TRAF1 and TRAF2 contribute in a direct manner to NF-κB and AP-1 activation (8, 35, 36).
Identification of a ligand for glucocorticoid-induced tumor necrosis factor receptor constitutively expressed in dendritic cells
2003, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Taken together, these data suggest that TNFRL derived from EOMA is a GITRL whose presence has long been suspected. A salient feature of signaling through TNFR is induction of NF-κB activation [3,13]. It has been shown that overexpression of GITR activates NF-κB and the association of the intracellular domain of GITR with an adaptor protein called Siva induces apoptosis [14].