TRAF Family Member-associated NF-κB Activator (TANK) Inhibits Genotoxic Nuclear Factor κB Activation by Facilitating Deubiquitinase USP10-dependent Deubiquitination of TRAF6 Ligase

Wang, Wei; Huang, Xuan; Xiao, Hong; Fu, Mingui; Xue, Aimin; Wu, Zhao-Hui

doi:10.1074/jbc.m115.643767

Cited by 87 publications

(73 citation statements)

References 47 publications

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“…8D and F). These results are consistent with previous findings (40,41,52). These findings, to a certain extent, probably can answer why different degrees of inflammation were observed in SVV-infected animals.…”

Section: Discussionsupporting

confidence: 83%

“…TANK also suppressed TRAF6-mediated NF-B activation by downregulating TRAF6 ubiquitination (41,50,51). In this study, we found that wild-type 3C pro promoted TRAF6-mediated NF-B activation even when TANK was overexpressed.…”

Section: Discussionmentioning

confidence: 50%

“…It has been reported that TANK associates with the monocyte chemoattractant proteininduced protein 1 (MCPIP1)-ubiquitin-specific peptidase 10 (USP10) complex to decrease TRAF6 ubiquitination, resulting in the inhibition of TRAF6-mediated NF-B signaling (41). In this study, we investigated the effect of the cleavage of TANK by SVV 3C pro on its suppression in TRAF6-mediated NF-B activation.…”

Section: Resultsmentioning

confidence: 99%

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Seneca Valley Virus Suppresses Host Type I Interferon Production by Targeting Adaptor Proteins MAVS, TRIF, and TANK for Cleavage

Qian

Fan

Liu

et al. 2017

J Virol

107

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Seneca Valley virus (SVV) is an oncolytic RNA virus belonging to the Picornaviridae family. Its nucleotide sequence is highly similar to those of members of the Cardiovirus genus. SVV is also a neuroendocrine cancer-selective oncolytic picornavirus that can be used for anticancer therapy. However, the interaction between SVV and its host is yet to be fully characterized. In this study, SVV inhibited antiviral type I interferon (IFN) responses by targeting different host adaptors, including mitochondrial antiviral signaling (MAVS), Toll/interleukin 1 (IL-1) receptor domain-containing adaptor inducing IFN-␤ (TRIF), and TRAF family member-associated NF-B activator (TANK), via viral 3C protease (3C pro ). SVV 3C pro mediated the cleavage of MAVS, TRIF, and TANK at specific sites, which required its protease activity. The cleaved MAVS, TRIF, and TANK lost the ability to regulate pattern recognition receptor (PRR)-mediated IFN production. The cleavage of TANK also facilitated TRAF6-induced NF-B activation. SVV was also found to be sensitive to IFN-␤. Therefore, SVV suppressed antiviral IFN production to escape host antiviral innate immune responses by cleaving host adaptor molecules. IMPORTANCE Host cells have developed various defenses against microbial pathogen infection. The production of IFN is the first line of defense against microbial infection. However, viruses have evolved many strategies to disrupt this host defense. SVV, a member of the Picornavirus genus, is an oncolytic virus that shows potential functions in anticancer therapy. It has been demonstrated that IFN can be used in anticancer therapy for certain tumors. However, the relationship between oncolytic virus and innate immune response in anticancer therapy is still not well known. In this study, we showed that SVV has evolved as an effective mechanism to inhibit host type I IFN production by using its 3C pro to cleave the molecules MAVS, TRIF, and TANK directly. These molecules are crucial for the Toll-like receptor 3 (TLR3)-mediated and retinoic acid-inducible gene I (RIG-I)-like receptor (RLR)-mediated signaling pathway. We also found that SVV is sensitive to IFN-␤. These findings increase our understanding of the interaction between SVV and host innate immunity.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 50%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Seneca Valley Virus Suppresses Host Type I Interferon Production by Targeting Adaptor Proteins MAVS, TRIF, and TANK for Cleavage

Qian

Fan

Liu

et al. 2017

J Virol

107

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“…As discussed above, MCPIP1 acts as an RNase to promote the degradation of a subset of mRNAs encoding pro-inflammatory cytokines, including IL-1β, IL-6 and IL-12p40, by directly targeting their 3′ UTRs 11,43 . In addition, several studies suggest that MCPIP1 may act as an adaptor molecule that recruits other proteins, such as TANK and USP10, to form a complex that inhibits NF-βB and the mitogen-activated protein kinase JNK by promoting the deubiquitylation of TNF-receptor-associated factor 3 (TRAF3) and TRAF6 (REFS 44–46). …”

Section: Regulation Of Immune Cell Activationmentioning

confidence: 99%

RNA-binding proteins in immune regulation: a focus on CCCH zinc finger proteins

2016

Self Cite

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Nearly 60 CCCH zinc finger proteins have been identified in humans and mice. These proteins are involved in the regulation of multiple steps of RNA metabolism, including mRNA splicing, polyadenylation, transportation, translation and decay. Several CCCH zinc finger proteins, such as tristetraprolin (TTP), roquin 1 and MCPIP1 (also known as regnase 1), are crucial for many aspects of immune regulation by targeting mRNAs for degradation and modulation of signalling pathways. In this Review, we focus on the emerging roles of CCCH zinc finger proteins in the regulation of immune responses through their effects on cytokine production, immune cell activation and immune homeostasis.

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“…Wang et al . proposed that TANK acts as a negative regulator of the NF‐κB pathway by inducing TRAF6 deubiquitination.…”

Section: Rna‐virus Proteases Interfering With the Host Innate Immune mentioning

confidence: 99%

RNA‐virus proteases counteracting host innate immunity

Lei

Hilgenfeld

2017

FEBS Letters

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Virus invasion triggers host immune responses, in particular, innate immune responses. Pathogen‐associated molecular patterns of viruses (such as dsRNA, ssRNA, or viral proteins) released during virus replication are detected by the corresponding pattern‐recognition receptors of the host, and innate immune responses are induced. Through production of type‐I and type‐III interferons as well as various other cytokines, the host innate immune system forms the frontline to protect host cells and inhibit virus infection. Not surprisingly, viruses have evolved diverse strategies to counter this antiviral system. In this review, we discuss the multiple strategies used by proteases of positive‐sense single‐stranded RNA viruses of the families Picornaviridae, Coronaviridae, and Flaviviridae, when counteracting host innate immune responses.

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TRAF Family Member-associated NF-κB Activator (TANK) Inhibits Genotoxic Nuclear Factor κB Activation by Facilitating Deubiquitinase USP10-dependent Deubiquitination of TRAF6 Ligase

Cited by 87 publications

References 47 publications

Seneca Valley Virus Suppresses Host Type I Interferon Production by Targeting Adaptor Proteins MAVS, TRIF, and TANK for Cleavage

Seneca Valley Virus Suppresses Host Type I Interferon Production by Targeting Adaptor Proteins MAVS, TRIF, and TANK for Cleavage

RNA-binding proteins in immune regulation: a focus on CCCH zinc finger proteins

RNA‐virus proteases counteracting host innate immunity

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