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Roles of tumor necrosis factor receptor associated factor 3 (TRAF3) and TRAF5 in immune cell functions
Open accessAbstract
Summary: A large and diverse group of receptors utilizes the family of cytoplasmic signaling proteins known as tumor necrosis factor receptor (TNFR)‐associated factors (TRAFs). In recent years, there has been a resurgence of interest and exploration of the roles played by TRAF3 and TRAF5 in cellular regulation, particularly in cells of the immune system, the cell types of focus in this review. This work has revealed that TRAF3 and TRAF5 can play diverse roles for different receptors even in the same cell type, as well as distinct roles in different cell types. Evidence indicates that TRAF3 and TRAF5 play important roles beyond the TNFR‐superfamily (SF) and viral mimics of its members, mediating certain innate immune receptor and cytokine receptor signals, and most recently, signals delivered by the T‐cell receptor (TCR) signaling complex. Additionally, much research has demonstrated the importance of TRAF3‐mediated cellular regulation via its cytoplasmic interactions with additional signaling proteins. In particular, we discuss below evidence for the participation by TRAF3 in a number of the regulatory post‐translational modifications involving ubiquitin that are important in various signaling pathways.
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“TRAF3 (FC = −1.12, p = 0.03) is a TNF-receptor-associated factor which is critical for NF-kappaB activation and cell death pathways [60].”
From Early onset senescence and cognitive impairment in a murine model of repeated mTBI (2021) · cites this paper as [60]
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Metadata
- Authors
- Hildebrand, J. M., Yi, Z., Buchta, C. M., Poovassery, J., Stunz, L. L., & Bishop, G. A.
- Affiliations
- University of Iowa (US)
- Corresponding author
- Bishop, Gail A.
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2011-10-21
- Volume
- 244
- Issue
- 1
- Pages
- 55-74
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- PMC
- PMC3202299
- OpenAlex
- W1583006772
- Cited by
- 110
- References
- 187
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 6 · 2023: 10 · 2022: 7 · 2021: 6 · 2020: 4 · 2019: 7 · 2018: 10 · 2017: 8 · 2016: 13 · 2015: 9 · 2014: 8 · 2013: 11 · 2012: 4
- FWCI
- 0.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Immunological Reviews (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (CA 099997, R01CA099997)
- National Institute of Allergy and Infectious Diseases (AI 49993, R01AI049993, R56AI049993, R56AI028847, R01AI028847, AI28847, T32AI007485)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Keywords
- TRAF3, TRAF5, TRAF, immune cell signaling, TNF receptor superfamily, innate immune receptors, cytokine receptor signaling, T cell receptor signaling, ubiquitination, post-translational modification
- MeSH terms
- Animals, B-Lymphocytes, Cell Survival, Humans, Immunity, Innate, Protein Binding, Protein Processing, Post-Translational, T-Lymphocytes, Tumor Necrosis Factor-alpha, Signal Transduction, Gene Expression, NF-kappa B, Receptors, Tumor Necrosis Factor, Mice, Knockout, Myeloid Cells, Ubiquitin, TNF Receptor-Associated Factor 3, TNF Receptor-Associated Factor 5, Mice
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