ReviewBiochimica et biophysica acta2016
TRAF3 signaling: Competitive binding and evolvability of adaptive viral molecular mimicry.
Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed.
- Human papillomavirus and the landscape of secondary genetic alterations in oral cancers.Genome research · 2019Trial
- Pioneer in Molecular Biology: Conformational Ensembles in Molecular Recognition, Allostery, and Cell Function.Journal of molecular biology · 2025Review
- Bioinformatics analysis and validation of novel biomarkers and competitive endogenous RNA networks involved in pyroptosis in diabetic nephropathy.Scientific reports · 2025Article
- Review
- The Interaction of OTUB1 and TRAF3 Mediates NLRP3 Inflammasome Activity to Regulate TGF-β1-induced BEAS-2B Cell Injury.Applied biochemistry and biotechnology · 2023Article
- Article
- Delineating functional mechanisms of the p53/p63/p73 family of transcription factors through identification of protein-protein interactions using interface mimicry.Molecular carcinogenesis · 2022Article
- Review
- Thrombocytopenia in COVID‑19 and vaccine‑induced thrombotic thrombocytopenia.International journal of molecular medicine · 2022Article
- TRAF3 Positively Regulates Host Innate Immune Resistance to Influenza A Virus Infection.Frontiers in cellular and infection microbiology · 2022Article
- NF-κB over-activation portends improved outcomes in HPV-associated head and neck cancer.Oncotarget · 2022Article
- Article
- TRAF Regulation of IL-17 Cytokine Signaling.Frontiers in immunology · 2019Review
- Oncoviruses Can Drive Cancer by Rewiring Signaling Pathways Through Interface Mimicry.Frontiers in oncology · 2019Article
- TRAF3 enhances STING-mediated antiviral signaling during the innate immune activation of black carp.Developmental and comparative immunology · 2018Article
- Dysregulated TRAF3 and BCL2 Expression Promotes Multiple Classes of Mature Non-hodgkin B Cell Lymphoma in Mice.Frontiers in immunology · 2018Article
- Structural host-microbiota interaction networks.PLoS computational biology · 2017Review
- Article
- Surveilling the Potential for Precision Medicine-driven PD-1/PD-L1-targeted Therapy in HNSCC.Journal of Cancer · 2017Review
- Intracellular and intercellular signaling networks in cancer initiation, development and precision anti-cancer therapy: RAS acts as contextual signaling hub.Seminars in cell & developmental biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundThe tumor necrosis factor receptor (TNFR) associated factor 3 (TRAF3) is a key node in innate and adaptive immune signaling pathways. TRAF3 negatively regulates the activation of the canonical and non-canonical NF-κB pathways and is one of the key proteins in antiviral immunity. SCOPE OF REVIEW: Here we provide a structural overview of TRAF3 signaling in terms of its competitive binding and consequences to the cellular network. For completion, we also include molecular mimicry of TRAF3 physiological partners by some viral proteins. MAJOR
conclusionsBy out-competing host partners, viral proteins aim to subvert TRAF3 antiviral action. Mechanistically, dynamic, competitive binding by the organism's own proteins and same-site adaptive pathogen mimicry follow the same conformational selection principles. GENERAL SIGNIFICANCE: Our premise is that irrespective of the eliciting event - physiological or acquired pathogenic trait - pathway activation (or suppression) may embrace similar conformational principles. However, even though here we largely focus on competitive binding at a shared site, similar to physiological signaling other pathogen subversion mechanisms can also be at play. This article is part of a Special Issue entitled "System Genetics" Guest Editor: Dr. Yudong Cai and Dr. Tao Huang.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.