Journal
CELLULAR SIGNALLING
Volume 24, Issue 6, Pages 1297-1305Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2012.02.006
Keywords
TNF receptors; Death receptors; TRAF2; Apoptosis; NF-kappa B
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Funding
- Spanish Ministry of Science and Technology (MICINN) [SAF2009-07227]
- Plan Regional de Ciencia y Tecnologia del Principado de Asturias (PCTI) [IB09-066]
- Pal
- Obra Social Cajastur
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Tumor necrosis factor (TNF) is a key mediator in the inflammatory response which is implicated in the onset of a number of diseases. Research on TNF led to the characterization of the largest family of cytokines known until now, the TNF superfamily, which exert their biological effects through the interaction with transmembrane receptors of the TNFR superfamily. TNF itself exerts its biological effects interacting with two different receptors: TNFR1 and TNFR2. TNFR1 presents a death domain on its intracellular region. In contrast to TNFR1, TNFR2 does riot have a death domain. Activation of TNFR1 implies the consecutive formation of two different TNF receptor signalling complexes. Complex I controls the expression of antiapoptotic proteins that prevent the triggering of cell death processes, whereas Complex II triggers cell death processes. TNFR2 only signals for antiapoptotic reactions. However, recent evidence indicates that INFR2 also signals to induce TRAF2 degradation. TRAF2 is a key mediator in signal transduction of both TNFR1 and TNFR2. Thus, this novel signalling pathway has two important implications: on one hand, it represents an auto regulatory loop for INFR2; on the other hand, when this signal is triggered TNFR1 activity is modified so that antiapoptotic pathways are inhibited and apoptotic reactions are enhanced. (c) 2012 Elsevier Inc. All rights reserved.
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