ArticleFrontiers in microbiology2019
BICP0 Negatively Regulates TRAF6-Mediated NF-κB and Interferon Activation by Promoting K48-Linked Polyubiquitination of TRAF6.
Article in Frontiers in microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Astragaloside IV relieves passive heymann nephritis and podocyte injury by suppressing the TRAF6/NF-κb axis.Renal failure · 2024Article
- Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.Molecular cancer · 2024Review
- The roles of E3 ubiquitin ligases in cancer progression and targeted therapy.Clinical and translational medicine · 2023Review
- ASB17 Facilitates the Burst of LPS-Induced Inflammation Through Maintaining TRAF6 Stability.Frontiers in cellular and infection microbiology · 2022Article
- SARS-CoV-2 3C-like protease antagonizes interferon-beta production by facilitating the degradation of IRF3.Cytokine · 2021Article
- TRAF6 Phosphorylation Prevents Its Autophagic Degradation and Re-Shapes LPS-Triggered Signaling Networks.Cancers · 2021Article
- Ubiquitination modification: critical regulation of IRF family stability and activity.Science China. Life sciences · 2021Review
- Structural and Functional Diversity among Five RING Finger Proteins from Carassius Auratus Herpesvirus (CaHV).Viruses · 2021Article
- Apoptosis and Cell Proliferation Markers in Inflammatory-Fibroproliferative Diseases of the Vessel Wall (Review).Sovremennye tekhnologii v meditsine · 2021Review
- TRAF6 Regulates the Immunosuppressive Effects of Myeloid-Derived Suppressor Cells in Tumor-Bearing Host.Frontiers in immunology · 2021Article
- The Functional Deubiquitinating Enzymes in Control of Innate Antiviral Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
The infected cell protein 0 (BICP0) is an immediate early protein encoded by BHV-1, and its RING finger domain, which endows BICP0 with intrinsic E3 ubiquitin ligase activity, is common in all ICP0 proteins. Tumor necrosis factor receptor-associated factor 6 (TRAF6) is one of the TRAF family members and is ubiquitously expressed in mammalian tissues. TRAF6 forms the MyD88-TRAF6-IRF7 complex and activates interferon induction in the TLR (Toll-like receptors) and the RLR (RIG-I-like receptor) pathway. Previous studies showed that BICP0 reduced IFN-β promoter activity by interacting with IRF7. In this study, we found that BICP0 promoted the K48-ubiquitination and degradation of TRAF6 through the ubiquitin proteasome system. The interaction between BICP0 and TRAF6 is a prerequisite for ubiquitination modification, and the 346-PAERQY-351 of BICP0 is indispensable. The motif mutation experiments showed that the tyrosine 351 of BICP0 is the key amino acid involved. Further studies demonstrated that BICP0 suppressed the NF-κB pathway via the interference of TRAF6. Moreover, degradation of TRAF6 protein influenced the K63-linked ubiquitination of IRF7 and activation of interferon promoter. Collectively, these findings indicate that the BICP0 protein suppresses the inflammation signaling and IFN production by K48-linked polyubiquitination of TRAF6 and may further clarify the immune evasion function of BICP0.
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