Tumor necrosis factor signaling

By Harald Wajant, K. Pfizenmaier, Peter Scheurich. Cell Death and Differentiation, 2003

2,531 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c9f5ab56531e2ebf4d043d687996785c4d0202cc

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Citations in the corpus

Information transduction capacity of noisy biochemical signaling networks (2011, neutral): “S4), respectively (29).”
Mixed lineage kinase domain-like is a key receptor interacting protein 3 downstream component of TNF-induced necrosis (2012, background): “TRADD (TNF-R1–associated death domain protein) is the first protein to interact with the receptor through its death domain and recruits other effector proteins, such as RIP1 (receptor interacting protein) and TRAF2 (TNFR-associated factor 2) to form the TNF-R1 signaling complex leading to the activa”
Regulation of reactive oxygen species generation in cell signaling (2011, background): “(Locksley et al., 2001; Wajant et al., 2003).”
Life and death by death receptors (2009, background): “Tumor necrosis factor- (TNF- ) plays a key role in inflammation and immunity, as well as in proliferation and differentiation of many different target cells (128).”
Evidence for a cytokine model of cognitive function. (2009, background): “Often referred to as TNF-R1 and TNF-R2 respectively, these two distinct receptors have been shown to elicit different molecular and cellular responses (Baud and Karin, 2001; Chen and Goeddel, 2002; MacEwan, 2002a,b; Wajant et al., 2003).”
Reactive oxygen species in tumor progression. (2005, background): “1888 regulation of NF-κB has been extensively studied during the last decade mostly by analyzing cytokine-mediated activation mechanisms (165-167).”
Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF (2015, background): “Similarly, the canonical NF𝜅B pathway is predominantly activated by various proinflammatory cytokines such as TNF and IL-1 [109, 110] and, at least in immune cells, also by ROS [110].”
Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, neutral): “In early studies, their contribution to hepatotoxicity was assessed by treating acetaminophenintoxicated mice with gadolinium chloride (GdCl3), a compound that inhibits phagocytic activity and generation of ROS in macrophages (Lee et al. 2004), and depletes macrophages in the periportal zone of the ”
Mathematical model of NF- κB regulatory module (2004, background): “There are several proteins, like Caspase-8, GSK-3, FADD, FLIP, MEKK3, T2K, involved in TNF-NF-kB signaling, the knockout of which leads to the embryonic lethality (Wajant et al., 2003 and references therein).”
Mechanisms of Liver Injury. I. TNF-α-induced liver injury: role of IKK, JNK, and ROS pathways (2006, background): “If antiapoptotic signals such as TRAF2 and NF- B are blocked, TNF-induced caspase-8 activation leads to the activation of proapototic members of the Bcl-2 homology (BH)3 domain proteins, mitochondrial depolarization, cytochrome c release, and the activation of executioner caspases (4, 43).”
Glyoxalase and Methylglyoxal as Biomarkers for Plant Stress Tolerance (2014, background): “TNF induces two signaling pathways, one leading to gene activation and is mediated by NF-kappaB, and the other leads to cell death by apoptosis or necrosis (Wajant et al., 2003).”
Tumor Necrosis Factor Alpha: A Link between Neuroinflammation and Excitotoxicity (2014, neutral): “With the exception of the SMase pathways, the above signal transduction pathways can also be induced through TNFR2 signaling because TRAF2 (along with TRAF1) can directly associate to the intracellular domain of the TNFR2 receptor (reviewed by [32, 33]).”