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More to life than NF-κB in TNFR1 signaling

(2016) TRENDS IN IMMUNOLOGY. 37(8). p.535-545
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Abstract
TNF is a master proinflammatory cytokine whose pathogenic role in inflammatory disorders has long been attributed to induction of proinflammatory mediators. TNF also activates cell survival and death pathways, and recent studies demonstrated that TNF also causes inflammation by inducing cell death. The default response of most cells to TNF is survival and NF-kappa B-mediated upregulation of prosurvival molecules is a well-documented protective mechanism downstream of TNFR1. Recent studies revealed the existence of an NF-kappa B independent cell death checkpoint that restricts cell demise by inactivating RIPK1. Disruption of this checkpoint leads to RIPK1 kinase-dependent death and causes inflammation in vivo. These revelations bring complexity to the control of TNF-induced cell death, and suggest clinical benefit of RIPK1 inhibitors in TNF-driven human inflammatory disorders.
Keywords
RECEPTOR INTERACTING PROTEIN, CELL-DEATH, LINEAR UBIQUITIN, DEUBIQUITINATING ENZYME, POLYUBIQUITIN CHAINS, PROGRAMMED NECROSIS, INDUCED APOPTOSIS, LUBAC DEFICIENCY, KINASE-ACTIVITY, IAP PROTEINS

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Citation

Please use this url to cite or link to this publication:

Chicago
Ting, Adrian T, and Mathieu Bertrand. 2016. “More to Life Than NF-κB in TNFR1 Signaling.” Trends in Immunology 37 (8): 535–545.
APA
Ting, A. T., & Bertrand, M. (2016). More to life than NF-κB in TNFR1 signaling. TRENDS IN IMMUNOLOGY, 37(8), 535–545.
Vancouver
1.
Ting AT, Bertrand M. More to life than NF-κB in TNFR1 signaling. TRENDS IN IMMUNOLOGY. 2016;37(8):535–45.
MLA
Ting, Adrian T, and Mathieu Bertrand. “More to Life Than NF-κB in TNFR1 Signaling.” TRENDS IN IMMUNOLOGY 37.8 (2016): 535–545. Print.
@article{8522590,
  abstract     = {TNF is a master proinflammatory cytokine whose pathogenic role in inflammatory disorders has long been attributed to induction of proinflammatory mediators. TNF also activates cell survival and death pathways, and recent studies demonstrated that TNF also causes inflammation by inducing cell death. The default response of most cells to TNF is survival and NF-kappa B-mediated upregulation of prosurvival molecules is a well-documented protective mechanism downstream of TNFR1. Recent studies revealed the existence of an NF-kappa B independent cell death checkpoint that restricts cell demise by inactivating RIPK1. Disruption of this checkpoint leads to RIPK1 kinase-dependent death and causes inflammation in vivo. These revelations bring complexity to the control of TNF-induced cell death, and suggest clinical benefit of RIPK1 inhibitors in TNF-driven human inflammatory disorders.},
  author       = {Ting, Adrian T and Bertrand, Mathieu},
  issn         = {1471-4906},
  journal      = {TRENDS IN IMMUNOLOGY},
  keywords     = {RECEPTOR INTERACTING PROTEIN,CELL-DEATH,LINEAR UBIQUITIN,DEUBIQUITINATING ENZYME,POLYUBIQUITIN CHAINS,PROGRAMMED NECROSIS,INDUCED APOPTOSIS,LUBAC DEFICIENCY,KINASE-ACTIVITY,IAP PROTEINS},
  language     = {eng},
  number       = {8},
  pages        = {535--545},
  title        = {More to life than NF-κB in TNFR1 signaling},
  url          = {http://dx.doi.org/10.1016/j.it.2016.06.002},
  volume       = {37},
  year         = {2016},
}

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