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Biomolecules
Special Issues
Role of TRAF1 in Regulating Inflammation and Cell Survival
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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: 28 February 2025 | Viewed by 1694

Special Issue Editor

Dr. Ali Abdul-Sater

E-Mail Website
Guest Editor
Muscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, ON M3J 1P3, Canada
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

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • TRAF1
  • inflammation
  • inflammasome
  • TNFRs
  • apoptosis
  • cellular survival

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Published Papers (2 papers)

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Review

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9 pages, 1418 KiB  
Review
TRAF1 from a Structural Perspective
by Hyunseok Jang, Subin Kim, Do Yeon Kim, Ju Hee Han and Hyun Ho Park
Biomolecules 2024, 14(5), 510; https://doi.org/10.3390/biom14050510 - 23 Apr 2024
Viewed by 944
Abstract
Tumor necrosis factor receptor-associated factor (TRAF) proteins play pivotal roles in a multitude of cellular signaling pathways, encompassing immune response, cell fate determination, development, and thrombosis. Their involvement in these processes hinges largely on their ability to interact directly with diverse receptors via [...] Read more.
Tumor necrosis factor receptor-associated factor (TRAF) proteins play pivotal roles in a multitude of cellular signaling pathways, encompassing immune response, cell fate determination, development, and thrombosis. Their involvement in these processes hinges largely on their ability to interact directly with diverse receptors via the TRAF domain. Given the limited binding interface, understanding how specific TRAF domains engage with various receptors and how structurally similar binding interfaces of TRAF family members adapt their distinct binding partners has been the subject of extensive structural investigations over several decades. This review presents an in-depth exploration of the current insights into the structural and molecular diversity exhibited by the TRAF domain and TRAF-binding motifs across a range of receptors, with a specific focus on TRAF1. Full article
(This article belongs to the Special Issue Role of TRAF1 in Regulating Inflammation and Cell Survival)
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7 pages, 2549 KiB  
Brief Report
TRAF1 Deficiency in Macrophages Drives Exacerbated Joint Inflammation in Rheumatoid Arthritis
by Ali Mirzaesmaeili and Ali A. Abdul-Sater
Biomolecules 2024, 14(7), 864; https://doi.org/10.3390/biom14070864 - 19 Jul 2024
Cited by 1 | Viewed by 490
Abstract
The tumor necrosis factor receptor-associated factor 1 (TRAF1) plays a key role in promoting lymphocyte survival, proliferation, and cytokine production. Recent evidence showed that TRAF1 plays opposing roles in monocytes and macrophages where it controls NF-κB activation and limits pro-inflammatory cytokine production as [...] Read more.
The tumor necrosis factor receptor-associated factor 1 (TRAF1) plays a key role in promoting lymphocyte survival, proliferation, and cytokine production. Recent evidence showed that TRAF1 plays opposing roles in monocytes and macrophages where it controls NF-κB activation and limits pro-inflammatory cytokine production as well as inflammasome-dependent IL-1β secretion. Importantly, TRAF1 polymorphisms have been strongly linked to an increased risk of rheumatoid arthritis (RA). However, whether and how TRAF1 contributes to RA pathogenesis is not fully understood. Moreover, investigating the role of TRAF1 in driving RA pathogenesis is complicated by its multifaceted and opposing roles in various immune cells. In this study, we subjected wildtype (WT) mice to the collagen antibody-induced arthritis (CAIA) model of RA and injected them intra-articularly with WT- or TRAF1-deficient macrophages. We show that mice injected with TRAF1-deficient macrophages exhibited significantly exacerbated joint inflammation, immune cell infiltration, and tissue damage compared to mice injected with WT macrophages. This study may lay the groundwork for novel therapies for RA that target TRAF1 in macrophages. Full article
(This article belongs to the Special Issue Role of TRAF1 in Regulating Inflammation and Cell Survival)
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