Roles of GSK-3 and β-Catenin in Antiviral Innate Immune Sensing of Nucleic Acids

Marineau, Alexandre; Khan, Kashif Aziz; Servant, Marc J.

doi:10.3390/cells9040897

Cited by 21 publications

(18 citation statements)

References 152 publications

(163 reference statements)

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“…In addition to the ongoing characterisation of the direct involvement in the expression of ISGs, powerful in silico and sequencing approaches of recent years revealed a growing list of novel targets, including virus-inducible RNAs [ 107 , 239 ]. Moreover, some of the identified host modulators hint at regulation of IRF3 activity dependent on signalling of other pathways to enable the incorporation of further parameters into the type I IFN response [ 39 , 148 , 240 ]. To successfully harness this powerful system, an in-depth comprehension of all contributing factors will be necessary.…”

Section: To Be Continued—perspectivementioning

confidence: 99%

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

Schwanke

Stempel

Brinkmann

2020

Viruses

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The type I interferon (IFN) response is a principal component of our immune system that allows to counter a viral attack immediately upon viral entry into host cells. Upon engagement of aberrantly localised nucleic acids, germline-encoded pattern recognition receptors convey their find via a signalling cascade to prompt kinase-mediated activation of a specific set of five transcription factors. Within the nucleus, the coordinated interaction of these dimeric transcription factors with coactivators and the basal RNA transcription machinery is required to access the gene encoding the type I IFN IFNβ (IFNB1). Virus-induced release of IFNβ then induces the antiviral state of the system and mediates further mechanisms for defence. Due to its key role during the induction of the initial IFN response, the activity of the transcription factor interferon regulatory factor 3 (IRF3) is tightly regulated by the host and fiercely targeted by viral proteins at all conceivable levels. In this review, we will revisit the steps enabling the trans-activating potential of IRF3 after its activation and the subsequent assembly of the multi-protein complex at the IFNβ enhancer that controls gene expression. Further, we will inspect the regulatory mechanisms of these steps imposed by the host cell and present the manifold strategies viruses have evolved to intervene with IFNβ transcription downstream of IRF3 activation in order to secure establishment of a productive infection.

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Section: To Be Continued—perspectivementioning

confidence: 99%

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

Schwanke

Stempel

Brinkmann

2020

Viruses

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“…Moreover, PICART1 interacts with AKT/GSK3β/β-catenin signaling pathway ( 18 ). Notably, GSK-3 and β-catenin regulate the innate immune response against RNA and DNA viruses ( 19 ). Based on the importance of viral infections in the initiation of AIDP ( 20 ), the interplay between PICART1 and these two proteins might be implicated in the pathogenesis of this form of immune-related neuropathies.…”

Section: Discussionmentioning

confidence: 99%

A Diagnostic Panel for Acquired Immune-Mediated Polyneuropathies Based on the Expression of lncRNAs

et al. 2021

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Long non-coding RNAs (lncRNAs) have been shown to alter immune responses, thus contributing to the pathobiology of autoimmune conditions. We investigated the expression levels of ANRIL, PICART1, MALAT1, CCAT1, CCAT2, and CCHE1 lncRNAs in acute and chronic inflammatory demyelinating polyneuropathy (AIDP and CIDP). ANRIL, PICART1, MALAT1, CCAT1, CCAT2, and CCHE1 lncRNAs were significantly downregulated in individuals with both AIDP and CIDP compared with unaffected individuals. Gender-based comparisons also verified such downregulations in both male and female subjects compared with sex-matched unaffected controls for all lncRNAs. There was no significant difference in the expression of any of the lncRNAs between cases with AIDP and cases with CIDP. While the expression levels of ANRIL and PICART1 were significantly correlated in healthy subjects (r = 0.86, p = 8.5E-16), similar analysis in cases with AIDP and CIDP revealed no significant correlation. The most robust correlation among patients was detected between ANRIL and MALAT1 lncRNAs (r = 0.59, p = 3.52E-6). ANRIL, MALAT1, and PICART1 had the diagnostic power of 0.96, 0.94, and 0.92 in distinguishing between cases with CIDP and controls, respectively. A combination of all lncRNAs resulted in 0.95 diagnostic power with a sensitivity of 0.85 and specificity of 0.96 for this purpose. Diagnostic power values of these lncRNAs in differentiation between cases with AIDP and controls were 0.98, 0.95, and 0.93, respectively. The combinatorial diagnostic power reached 0.98 for differentiation between cases with AIDP and controls. The six-lncRNA panel could differentiate combined cases with AIDP and CIDP from controls with area under the curve (AUC), sensitivity, and specificity values of 0.97, 0.90, and 0.96, respectively. Collectively, the lncRNA panel is suggested as a sensitive and specific diagnostic panel for acquired immune-mediated polyneuropathies.

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“…This inhibition could not be overcome by increasing substrate concentration, implying that MARylation functions as an allosteric inhibitor of GSK3ß. ARTD10-modified GSK3β [ 87 , 149 ] has a regulatory role in type I IFN antiviral innate immune response, affecting the activation of IRF3 [ 150 ]. The nuclear transport protein RAN is also an ARTD10 substrate [ 87 ].…”

Section: Mono(adp-ribosyl) Transferases (Mart)mentioning

confidence: 99%

Mono(ADP-ribosyl)ation Enzymes and NAD+ Metabolism: A Focus on Diseases and Therapeutic Perspectives

Poltronieri

Celetti

Palazzo

2021

Cells

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Mono(ADP-ribose) transferases and mono(ADP-ribosyl)ating sirtuins use NAD+ to perform the mono(ADP-ribosyl)ation, a simple form of post-translational modification of proteins and, in some cases, of nucleic acids. The availability of NAD+ is a limiting step and an essential requisite for NAD+ consuming enzymes. The synthesis and degradation of NAD+, as well as the transport of its key intermediates among cell compartments, play a vital role in the maintenance of optimal NAD+ levels, which are essential for the regulation of NAD+-utilizing enzymes. In this review, we provide an overview of the current knowledge of NAD+ metabolism, highlighting the functional liaison with mono(ADP-ribosyl)ating enzymes, such as the well-known ARTD10 (also named PARP10), SIRT6, and SIRT7. To this aim, we discuss the link of these enzymes with NAD+ metabolism and chronic diseases, such as cancer, degenerative disorders and aging.

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Roles of GSK-3 and β-Catenin in Antiviral Innate Immune Sensing of Nucleic Acids

Cited by 21 publications

References 152 publications

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

A Diagnostic Panel for Acquired Immune-Mediated Polyneuropathies Based on the Expression of lncRNAs

Mono(ADP-ribosyl)ation Enzymes and NAD+ Metabolism: A Focus on Diseases and Therapeutic Perspectives

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