Role of TRAF1 in Regulating Inflammation and Cell Survival
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".
Deadline for manuscript submissions: 30 June 2024 | Viewed by 471
Special Issue Editor
Interests: novel regulators of inflammation; innate immunity; inflammatory response; TRAF1; individual Type I interferons; bacterial and viral responses
Special Issue Information
Dear Colleagues,
Tumor Necrosis Factor Receptor-Associated Factor 1 (TRAF1) is a pivotal molecule in many immune and non-immune cellular processes. Acting as an essential adapter protein, TRAF1 plays a central role in recruiting key components of inflammatory signalling pathways (e.g., Toll-like receptors, Nod-like receptors, and RIG-I-like receptors), TNFRs responsible for signalling survival (e.g., CD40 and 4-1BB), inflammasomes, and apoptosis signal-regulating kinase 1 (ASK1), a mitogen-activated protein kinase involved in stress response, apoptosis, inflammation, and cell differentiation. The multi-faceted role of TRAF1 in controlling inflammation and cell survival stems from its ability to activate or inhibit these signalling pathways and downstream transcription factors. Importantly, TRAF1 has been associated with several human diseases, including inflammation-driven diseases (e.g., rheumatoid arthritis, gout, and sepsis), ischemia of the heart and brain, and liver fibrosis. TRAF1 is also linked to blood cancers, including chronic lymphocytic leukemia (CLL), lymphomas, and multiple myeloma. Consequently, further research is required to explore the potential for targeting TRAF1 in complex inflammatory diseases and cancers involving multiple signalling pathways.
This Special Issue compiles the latest research findings on TRAF1's role in regulating inflammatory responses and cellular survival.
Dr. Ali Abdul-Sater
Guest Editor
Manuscript Submission Information
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Keywords
- TRAF1
- inflammation
- inflammasome
- TNFRs
- apoptosis
- cellular survival
