The DOI matches its Crossref record; 119 of the 119 references it cites were found in a registry or an index.
All TRAFs are not created equal: common and distinct molecular mechanisms of TRAF-mediated signal transduction
Abstract
The tumor necrosis factor (TNF) receptor associated factors (TRAFs) have emerged as the major signal transducers for the TNF receptor superfamily and the interleukin-1 receptor/Toll-like receptor (IL-1R/TLR) superfamily. TRAFs collectively play important functions in both adaptive and innate immunity. Recent functional and structural studies have revealed the individuality of each of the mammalian TRAFs and advanced our understanding of the underlying molecular mechanisms. Here, we examine this functional divergence among TRAFs from a perspective of both upstream and downstream TRAF signal transduction pathways and of signaling-dependent regulation of TRAF trafficking. We raise additional questions and propose hypotheses regarding the molecular basis of TRAF signaling specificity.
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Cited by
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Metadata
- Authors
- Chung, J. Y., Park, Y. C., Ye, H., & Wu, H.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2002-02-15
- Volume
- 115
- Issue
- 4
- Pages
- 679-688
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W1504914687
- Cited by
- 613
- References
- 119
- FWCI
- 14.93
- Type
- journal article
- Language
- en
- Open access
- closed
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- Chung, J. Y., Park, Y. C., Ye, H., & Wu, H. (2002). All TRAFs are not created equal: common and distinct molecular mechanisms of TRAF-mediated signal transduction. Journal of Cell Science. https://doi.org/10.1242/jcs.115.4.679
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
