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TNF receptor associated factors in cytokine signaling
H Wajant1, M Grell, P Scheurich
1Institute of Cell Biology and Immunology, University of Stuttgart, Germany. harald.wajant@po.uni-stuttgart.de
Abstract:
Just four years ago the first two members of a new family of molecules involved in signal transduction by members of the TNF receptor superfamily were described and designated TNF Receptor Associated Factors (TRAFs). In the meantime six human and murine TRAFs as well as a TRAF protein from C. elegans have been molecularly cloned. From our current point of view, TRAF proteins appear to represent multifunctional signal adaptors, tightly embedded in a network of signals culminating in the activation of kinase cascades that finally lead to the activation of c-Jun N-terminal kinase. p38 mitogen activated protein kinase, and the transcription factor NF-kappaB, thereby also affecting the balance between survival and cell death. Some of the activities of the individual TRAF family members may be redundant although transgenic knockout animal models have already shown that crucial signaling pathways for single TRAF molecules in vivo can be defined.
Insights
TNF Receptor Associated Factors (TRAFs) are crucial signal adaptors in cell signaling pathways. Research shows TRAFs activate kinase cascades, influencing cell survival and death, with specific roles identified in knockout models.
Area of Science:
- Molecular biology
- Cell signaling
- Immunology
Background:
- TNF Receptor Associated Factors (TRAFs) are newly identified molecules central to signal transduction.
- Six human and murine TRAFs, plus a C. elegans TRAF, have been cloned.
- TRAFs act as multifunctional adaptors in complex signaling networks.
Purpose of the Study:
- To elucidate the role of TRAF proteins in cellular signal transduction.
- To investigate the signaling pathways regulated by TRAFs.
- To understand the impact of TRAFs on cell survival and death.
Main Methods:
- Molecular cloning of TRAF proteins.
- Analysis of signaling cascades involving TRAFs.
- Generation and study of transgenic knockout animal models.
Main Results:
- TRAF proteins are integral to pathways activating c-Jun N-terminal kinase, p38 MAPK, and NF-kappaB.
- These pathways regulate critical cellular processes, including survival and apoptosis.
- Transgenic models demonstrate essential in vivo roles for individual TRAF molecules.
Conclusions:
- TRAFs are multifunctional adaptors critical for TNF receptor superfamily signaling.
- TRAF-mediated signaling impacts key cellular functions like survival and death.
- Further research can define specific roles of individual TRAFs in vivo.