A20 (tnfaip3) is a negative feedback regulator of RIG-I-Mediated IFN induction in teleost

Mérour, Emilie; Jami, Raphaël; Lamoureux, Annie; Bernard, Julie; Brémont, Michel; Biacchesi, Stéphane

doi:10.1016/j.fsi.2018.10.082

Cited by 18 publications

(7 citation statements)

References 36 publications

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“…These genes are known as a virus-induced host factors that control the recruitment of Tcells and correlates to chronic virus infections ). In addition, the tumor necrosis factor, alpha-induced protein 3 (TNFAIP3), is a central regulator of immunopathology and associated with the maintenance of immune homeostasis and severe viral infections (Mérour et al 2019;.…”

Section: Given the Important Association Between Heparin-binding Go Amentioning

confidence: 99%

The transcriptomic profiling of COVID-19 compared to SARS, MERS, Ebola, and H1N1

Alsamman

Zayed

2020

Preprint

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COVID-19 pandemic is a global crisis that threatens our way of life. As of April 29, 2020, COVID-19 has claimed more than 200,000 lives, with a global mortality rate of~7% and recovery rate of~30%. Understanding the interaction of cellular targets to the SARS-CoV2 infection is crucial for therapeutic development. Therefore, the aim of this study was to perform a comparative analysis of transcriptomic signatures of infection of COVID-19 compared to different respiratory viruses (Ebola, H1N1, MERS-CoV, and SARS-CoV), to determine unique anti-COVID1-19 gene signature. We identified for the first time molecular pathways for Heparin-binding, RAGE, miRNA, and PLA2 inhibitors, to be associated with SARS-CoV2 infection. The NRCAM and SAA2 that are involved in severe inflammatory response, and FGF1 and FOXO1genes, which are associated with immune regulation, were found to be associated with a cellular gene response to COVID-19 infection. Moreover, several cytokines, most significantly the IL-8, IL-6, demonstrated key associations with COVID-19 infection. Interestingly, the only response gene that was shared between the five viral infections was SERPINB1. The PPI study sheds light on genes with high interaction activity that COVID-19 shares with other viral infections. The findings showed that the genetic pathways associated with Rheumatoid arthritis, AGE-RAGE signaling system, Malaria, Hepatitis B, and Influenza A were of high significance. We found that the virogenomic transcriptome of infection, gene modulation of host antiviral responses, and GO terms of both COVID-19 and Ebola are more similar compared to SARS, H1N1, and MERS. This work compares the virogenomic signatures of highly pathogenic viruses and provides valid targets for potential therapy against COVID-19.

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Section: Given the Important Association Between Heparin-binding Go Amentioning

confidence: 99%

The transcriptomic profiling of COVID-19 compared to SARS, MERS, Ebola, and H1N1

Alsamman

Zayed

2020

Preprint

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“…ZNRF4 [195] ITCH [336] (indirectly) A20 [187] OTULIN [185] CYLD [190] MYSM1 [193] LUBAC (E3 ligase) OTULIN [188,189,191] TBK1 DTX4 [113][114][115] TRAIP [116] TRIM27 [118] SOCS3 [337] TRIM11 [338] RNF144B [339] ASB8 [340] CYLD [67] USP38 [117] USP2b [341] A20 [110,342] TAK1 USP18 [343] TAB2/3 TRIM30α [344] NEMO TRIM29 [244] TRAF7 [345] TRIM40 [346] TRAF4 [347] CYLD [218,220,223] A20 [210,348] USP18 [343] USP7 [349] UCHL1 [326] OTULIN [191] [8] SOCS1 [9] SOCS3 [9] NDRG1 [391] TRIM35+PIN1 [290] Unknown [288,299]…”

Section: Discussionmentioning

confidence: 99%

Negative Regulation of the Innate Immune Response through Proteasomal Degradation and Deubiquitination

Budroni

Versteeg

2021

Viruses

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The rapid and dynamic activation of the innate immune system is achieved through complex signaling networks regulated by post-translational modifications modulating the subcellular localization, activity, and abundance of signaling molecules. Many constitutively expressed signaling molecules are present in the cell in inactive forms, and become functionally activated once they are modified with ubiquitin, and, in turn, inactivated by removal of the same post-translational mark. Moreover, upon infection resolution a rapid remodeling of the proteome needs to occur, ensuring the removal of induced response proteins to prevent hyperactivation. This review discusses the current knowledge on the negative regulation of innate immune signaling pathways by deubiquitinating enzymes, and through degradative ubiquitination. It focusses on spatiotemporal regulation of deubiquitinase and E3 ligase activities, mechanisms for re-establishing proteostasis, and degradation through immune-specific feedback mechanisms vs. general protein quality control pathways.

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“…As previously published ( 48 ), the expression of a constitutively active form of RIG-I (RIG-I Nter; in which the C-terminal repressor domain maintaining the protein in an inactive state is deleted) significantly activates the IFN1 promoter of EPC cells. As a control, the co-expression RIG-I Nter with A20, a negative feedback regulator of the RLR signaling ( 89 ), drastically reduced the induction. In contrast, co-expression of PP1A with RIG-I Nter significantly increase IFN1 promoter activation, indicating that fish PP1A share a common function with its mammalian orthologs by enhancing RIG-I activity.…”

Section: Regulation By Kinases and Phosphatasesmentioning

confidence: 99%

“…Several DUBs of ovarian tumor proteases (OTUs) and ubiquitin-specific proteases (USPs) families, have been described as important regulators of RLR pathway. Among them, mammalian and fish A20 has been shown to be a strong inhibitor of the RLR signaling ( Figures 1C, D ) ( 89 – 91 ). In addition, the function of OTUB1, OTUD1, YOD1, and USP22 fish orthologs was investigated ( Table 1 ).…”

Section: Regulation By Ubiquitin Ligases and Deubiquitinasesmentioning

confidence: 99%

Deciphering the Fine-Tuning of the Retinoic Acid-Inducible Gene-I Pathway in Teleost Fish and Beyond

et al. 2021

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Interferons are the first lines of defense against viral pathogen invasion during the early stages of infection. Their synthesis is tightly regulated to prevent excessive immune responses and possible deleterious effects on the host organism itself. The RIG-I-like receptor signaling cascade is one of the major pathways leading to the production of interferons. This pathway amplifies danger signals and mounts an appropriate innate response but also needs to be finely regulated to allow a rapid return to immune homeostasis. Recent advances have characterized different cellular factors involved in the control of the RIG-I pathway. This has been most extensively studied in mammalian species; however, some inconsistencies remain to be resolved. The IFN system is remarkably well conserved in vertebrates and teleost fish possess all functional orthologs of mammalian RIG-I-like receptors as well as most downstream signaling molecules. Orthologs of almost all mammalian regulatory components described to date exist in teleost fish, such as the widely used zebrafish, making fish attractive and powerful models to study in detail the regulation and evolution of the RIG-I pathway.

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A20 (tnfaip3) is a negative feedback regulator of RIG-I-Mediated IFN induction in teleost

Cited by 18 publications

References 36 publications

The transcriptomic profiling of COVID-19 compared to SARS, MERS, Ebola, and H1N1

The transcriptomic profiling of COVID-19 compared to SARS, MERS, Ebola, and H1N1

Negative Regulation of the Innate Immune Response through Proteasomal Degradation and Deubiquitination

Deciphering the Fine-Tuning of the Retinoic Acid-Inducible Gene-I Pathway in Teleost Fish and Beyond

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