TRIM13 Is a Negative Regulator of MDA5-Mediated Type I Interferon Production

Narayan, Kavitha; Waggoner, Lisa; Pham, Serena; Hendricks, Gabriel; Waggoner, Stephen N.; Conlon, Joseph E.; Wang, Jennifer; Fitzgerald, Katherine A.; Kang, Joonsoo

doi:10.1128/jvi.02593-13

Cited by 82 publications

(77 citation statements)

References 46 publications

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“…MDA5 was reported to be negatively regulated by another E3 ubiquitin ligase, TRIM13 [83]. This study showed that overexpression of TRIM13 inhibited MDA5-mediated signaling.…”

Section: The Role Of Ubiquitin In Rlr Signal Transductionmentioning

confidence: 96%

“…This study showed that overexpression of TRIM13 inhibited MDA5-mediated signaling. Furthermore, infection with encephalomyocarditis virus (EMCV) induced significantly higher type-I IFN levels in trim13 −/− mice than in WT mice [83]. In support of this, trim13 −/− mice had an increased resistance to EMCV infection than their WT littermates.…”

Section: The Role Of Ubiquitin In Rlr Signal Transductionmentioning

confidence: 99%

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Ubiquitination in the antiviral immune response

2015

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Ubiquitination has long been known to regulate fundamental cellular processes through the induction of proteasomal degradation of target proteins. More recently, ‘atypical’ nondegradative types of polyubiquitin chains have been appreciated as important regulatory moieties by modulating the activity or subcellular localization of key signaling proteins. Intriguingly, many of these non-degradative types of ubiquitination regulate the innate sensing pathways initiated by pattern recognition receptors (PRRs), ultimately coordinating an effective antiviral immune response. Here we discuss recent advances in understanding the functional roles of degradative and atypical types of ubiquitination in innate immunity to viral infections, with a specific focus on the signaling pathways triggered by RIG-I-like receptors, Toll-like receptors, and the intracellular viral DNA sensor cGAS.

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“…MDA5 was reported to be negatively regulated by another E3 ubiquitin ligase, TRIM13 [83]. This study showed that overexpression of TRIM13 inhibited MDA5-mediated signaling.…”

Section: The Role Of Ubiquitin In Rlr Signal Transductionmentioning

confidence: 96%

Section: The Role Of Ubiquitin In Rlr Signal Transductionmentioning

confidence: 99%

Ubiquitination in the antiviral immune response

2015

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“…1). Interestingly, many ubiquitin related proteins are induced by IFN to enhance (TRIM25) or to block (TRIM13 or 21) the IFN response (Zhang et al, 2013a; Narayan et al, 2014). Similarly, many viruses express ubiquitin ligases or DUBs to alter ubiquitin regulation and favor replication (Kwon and Ahn, 2013) or express proteins that block the action of several ubiquitin enzymes that lead to the activation of the IFN pathway (Rajsbaum et al, 2012).…”

Section: Protein-modulated Control Of the Antiviral Responsementioning

confidence: 99%

Long noncoding RNAs in viral infections

2016

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Viral infections induce strong modifications in the cell transcriptome. Among the RNAs whose expression is altered by infection are long noncoding RNAs (lncRNAs). LncRNAs are transcripts with potential to function as RNA molecules. Infected cells may express viral lncRNAs, cellular lncRNAs and chimeric lncRNAs formed by viral and cellular sequences. Some viruses express viral lncRNAs whose function is essential for viral viability. They are transcribed by polymerase II or III and some of them can be processed by unique maturation steps performed by host cell machineries. Some viral lncRNAs control transcription, stability or translation of cellular and viral genes. Surprisingly, similar functions can be exerted by cellular lncRNAs induced by infection. Expression of cellular lncRNAs may be altered in response to viral replication or viral protein expression. However, many cellular lncRNAs respond to the antiviral pathways induced by infection. In fact, many lncRNAs function as positive or negative regulators of the innate antiviral response. Our current knowledge about the identity and function of lncRNAs in infected cells is very limited. However, research into this field has already helped in the identification of novel cellular pathways and may help in the development of therapeutic tools for the treatment of viral infections, autoimmune diseases, neurological disorders and cancer.

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“…For example, TRIM5a was documented to have a restrictive ability against HIV-1 and other retroviruses [3,4]. TRIM13 has recently been reported to be a negative regulator of MDA5-mediated type I interferon production [5]. TRIM38 enabled to mediate lysosome-dependent degradation of TAB2/3 to inhibit the NF-κB signaling pathway [6].…”

Section: Introductionmentioning

confidence: 99%

Molecular Characterization, Tissue Distribution and Expression, and Potential Antiviral Effects of TRIM32 in the Common Carp (Cyprinus carpio)

Wang

et al. 2016

IJMS

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Tripartite motif-containing protein 32 (TRIM32) belongs to the tripartite motif (TRIM) family, which consists of a large number of proteins containing a RING (Really Interesting New Gene) domain, one or two B-box domains, and coiled coil motif followed by different C-terminal domains. The TRIM family is known to be implicated in multiple cellular functions, including antiviral activity. However, it is presently unknown whether TRIM32 of common carp (Cyprinus carpio) has the antiviral effect. In this study, the sequence, expression, and antiviral function of TRIM32 homolog from common carp were analyzed. The full-length coding sequence region of trim32 was cloned from common carp. The results showed that the expression of TRIM32 (mRNA) was highest in the brain, remained stably expressed during embryonic development, and significantly increased following spring viraemia of carp virus (SVCV) infection. Transient overexpression of TRIM32 in affected Epithelioma papulosum cyprinid cells led to significant decrease of SVCV production as compared to the control group. These results suggested a potentially important role of common carp TRIM32 in enhancing host immune response during SVCV infection both in vivo and in vitro.

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TRIM13 Is a Negative Regulator of MDA5-Mediated Type I Interferon Production

Abstract: Retinoic acid-inducible gene I (RIG-I

Cited by 82 publications

References 46 publications

Ubiquitination in the antiviral immune response

Ubiquitination in the antiviral immune response

Long noncoding RNAs in viral infections

Molecular Characterization, Tissue Distribution and Expression, and Potential Antiviral Effects of TRIM32 in the Common Carp (Cyprinus carpio)

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