Reactome: A Curated Pathway Database
Results 1 to 10 of 16
Pathways (4) Reactions (5) Proteins (1) Others (6)
Protein: UniProt:P01375 TNF (Homo sapiens)
Last changed: 2015-03-12 14:00:50

Pathway: Signal Transduction (Homo sapiens)
Signal transduction is a process in which extracellular signals elicit changes in cell state and activity. Transmembrane receptors sense changes in the cellular environment by binding ligands, such as hormones and growth factors, or reacting to other types of stimuli, such as light. Stimulation of transmembrane receptors leads to their conformational change which propagates the signal to the intracellu
Last changed: 2015-03-06 23:15:47

Pathway: Death Receptor Signalling (Homo sapiens)
The death receptors, all cell-surface receptors, begin the process of caspase activation. The common feature of these type 1 transmembrane proteins is the "death-domain" a conserved cytoplasmic motif found on all of the three receptors (FAS/CD95, TNF-receptor, and TRAIL-receptor) that binds the Fas-associated protein with death domain (FADD). Ligand binding to death receptors (DR) results in receptor o
Last changed: 2015-03-06 10:40:16

Pathway: TNF signaling (Homo sapiens)
The inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) is expressed in immune and nonimmune cell types including macrophages, T cells, mast cells, granulocytes, natural killer (NK) cells, fibroblasts, neurons, keratinocytes and smooth muscle cells as a response to tissue injury or upon immune responses to pathogenic stimuli (Köck A. et al. 1990; Dubravec DB et al. 1990; Walsh LJ et al. 1991
Last changed: 2015-03-06 10:40:16

Pathway: TNFR1-mediated proapoptotic signaling (Homo sapiens)
Activation of tumor necrosis factor receptor 1 (TNFR1) can trigger multiple signal transduction pathways to induce cell survival or cell death (Ward C et al. 1999; Micheau O and Tschopp J 2003; Widera D et al. 2006). While pro-survival signaling is initiated and regulated via the activated TNFR1 receptor complex at the cell membrane, cell death signals are induced upon the release of TRADD:TRAF2:RIP1 c
Last changed: 2015-03-06 10:40:16

Reaction: TRADD:TRAF2:RIP1 complex dissociates from the TNF-alpha:TNF-R1 complex. (Homo sapiens)
Once formed the TRADD:TRAF2:RIP1 complex may dissociate from the TNF:TNF-R1 platform and become cytosolic. With the recruitment of FADD the cell is pushed along the apoptotic pathway
Last changed: 2015-03-06 10:40:16

Reaction: Membrane-anchored TNF-alpha binds TNFR1 (Homo sapiens)
The inflammatory cytokine tumor necrosis factor (TNF) alpha exerts its biological activity through the membrane bound (tmTNF-alpha) or soluble (sTNF-alpha) forms. Both sTNF-alpha and tmTNF-alpha ligands interact with either TNFR1 (p55, CD120a) or TNFR2 (p75, CD120b) on a variety of immune and nonimmune cell types. Transmembrane TNF-alpha functions as a bipolar molecule that can transmit signals both
Last changed: 2015-03-06 10:40:16

Reaction: TNF-alpha is cleaved by ADAM17 (TACE) (Homo sapiens)
TNF-alpha is initially synthesized as a 26kDa transmembrane precursor (pro-TNF-alpha), which is processed by proteolytic cleavage known as ectodomain shedding (Tang P et al. 1996). TNF-alpha-converting enzyme (TACE or ADAM17) mediates the cleavage of TNF-alpha generating the soluble 17kDa mature form (Robertshaw HJ & Brennan FM 2005). Inhibition of TACE activity resulted in an accumulation of unprocess
Last changed: 2015-03-06 10:40:16

Reaction: Soluble TNF-alpha binds TNFR1 (Homo sapiens)
The soluble form of TNF-alpha is cleaved from membrane-anchored TNF-alpha followed by binding to TNF receptors (TNFR1 and -R2). BAG4, also known as silencer of death domain (SODD), belongs to the BAG family of anti-apoptotic proteins. Mammalian BAG4 was found to associate with TNF receptor 1 (TNFR1) preventing receptor signaling in the absence of ligand (Jiang Y et al. 1999; Miki K and Eddy EM 2002).
Last changed: 2015-03-06 10:40:16

Reaction: TNF:TNF-R1 binds TRADD, TRAF2 and RIP (Homo sapiens)
Once the TNF-aplha:TNF-R1:TRADD complex is formed the two TNF-alpha mediated pathways are possible. The variable is the recruitment of FADD to the larger TNF-aplha:TNF-R1 platform via the interaction of the Death Domains. The steps leading to the Jun, NF kappaB, or apoptotic pathways are rife with opportunities for modulation
Last changed: 2015-03-06 10:40:16

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