Schlafen 14 (SLFN14) is a novel antiviral factor involved in the control of viral replication

Seong, Rak Kyun; Seo, Seong Wook; Kim, Ji Ae; Fletcher, Sarah J.; Morgan, Neil V.; Kumar, Mukesh; Choi, Young Ki; Shin, Ok Sarah

doi:10.1016/j.imbio.2017.07.002

Cited by 37 publications

(39 citation statements)

References 37 publications

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“…Several subgroup III SLFNs are suggested to restrict different viruses 21 , 23 . While hSLFN13 was reported to moderately inhibit influenza virus, it is intriguing as to whether SLFN13 also inhibits other types of viruses.…”

Section: Resultsmentioning

confidence: 99%

“…1a ). SLFNs were reported to be interferon (IFN)-inducible 18 – 21 , and their functions have been implicated in various biological processes including cell differentiation, tumour suppression, immune response regulation and the restriction of viruses 22 . Specifically, human SLFN11 has been reported to bind tRNAs and restrict HIV protein synthesis possibly by means of codon-bias discrimination 23 .…”

Section: Introductionmentioning

confidence: 99%

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Structure of Schlafen13 reveals a new class of tRNA/rRNA- targeting RNase engaged in translational control

Yang

Deng

Li³

et al. 2018

Nat Commun

101

163

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Cleavage of transfer (t)RNA and ribosomal (r)RNA are critical and conserved steps of translational control for cells to overcome varied environmental stresses. However, enzymes that are responsible for this event have not been fully identified in high eukaryotes. Here, we report a mammalian tRNA/rRNA-targeting endoribonuclease: SLFN13, a member of the Schlafen family. Structural study reveals a unique pseudo-dimeric U-pillow-shaped architecture of the SLFN13 N′-domain that may clamp base-paired RNAs. SLFN13 is able to digest tRNAs and rRNAs in vitro, and the endonucleolytic cleavage dissevers 11 nucleotides from the 3′-terminus of tRNA at the acceptor stem. The cytoplasmically localised SLFN13 inhibits protein synthesis in 293T cells. Moreover, SLFN13 restricts HIV replication in a nucleolytic activity-dependent manner. According to these observations, we term SLFN13 RNase S13. Our study provides insights into the modulation of translational machinery in high eukaryotes, and sheds light on the functional mechanisms of the Schlafen family.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Structure of Schlafen13 reveals a new class of tRNA/rRNA- targeting RNase engaged in translational control

Yang

Deng

Li³

et al. 2018

Nat Commun

101

163

View full text Add to dashboard Cite

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“…Lysates were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) on 10–12% acrylamide gels. Proteins were transferred to polyvinylidene difluoride (PVDF) membranes and blocked with 5% ( w / v ) skim milk in Tris-buffered saline (0.2 M Tris, 1.36 M NaCl) supplemented with 0.1% ( v / v ) Tween-20 (TBS-Tw) for 1 h at 25 °C as described previously [ 25 ]. This was followed by an overnight incubation with primary antibodies (Cell Signaling Technologies, Danvers, MA, USA) raised against phospho-AKT and total AKT at 4 °C.…”

Section: Methodsmentioning

confidence: 99%

Favipiravir and Ribavirin Inhibit Replication of Asian and African Strains of Zika Virus in Different Cell Models

Kim

Seong

Kumar

et al. 2018

Viruses

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Zika virus (ZIKV) has recently emerged as a new public health threat. ZIKV infections have caused a wide spectrum of neurological diseases, such as Guillain–Barré syndrome, myelitis, meningoencephalitis, and congenital microcephaly. No effective therapies currently exist for treating patients infected with ZIKV. Herein, we evaluated the anti-viral activity of favipiravir (T-705) and ribavirin against Asian and African strains of ZIKV using different cell models, including human neuronal progenitor cells (hNPCs), human dermal fibroblasts (HDFs), human lung adenocarcinoma cells (A549) and Vero cells. Cells were treated with favipiravir or ribavirin and effects on ZIKV replication were determined using quantitative real-time PCR and plaque assay. Our results demonstrate that favipiravir or ribavirin treatment significantly inhibited ZIKV replication in a dose-dependent manner. Moreover, favipiravir treatment of ZIKV-infected hNPCs led to reduced cell death, enhanced AKT pathway phosphorylation, and increased expression of anti-apoptotic factor B cell lymphoma 2. In conclusion, our results demonstrate conclusively that favipiravir inhibits ZIKV replication and prevents cell death, and can be a promising intervention for ZIKV-associated disease.

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“…Interestingly, SLFN 11 control of HIV-1 infection is independent of type I IFN signaling (119). IFNb induced SLFN14 exhibits antiviral activity in mouse macrophages, limiting infection with influenza virus or the DNA virus, varicella-zoster virus (120).…”

Section: Canonical and Non-canonical Ifn Signaling In Antiviral Respomentioning

confidence: 99%

Type I Interferon (IFN)-Regulated Activation of Canonical and Non-Canonical Signaling Pathways

et al. 2020

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For several decades there has been accumulating evidence implicating type I interferons (IFNs) as key elements of the immune response. Therapeutic approaches incorporating different recombinant type I IFN proteins have been successfully employed to treat a diverse group of diseases with significant and positive outcomes. The biological activities of type I IFNs are consequences of signaling events occurring in the cytoplasm and nucleus of cells. Biochemical events involving JAK/STAT proteins that control transcriptional activation of IFN-stimulated genes (ISGs) were the first to be identified and are referred to as “canonical” signaling. Subsequent identification of JAK/STAT-independent signaling pathways, critical for ISG transcription and/or mRNA translation, are denoted as “non-canonical” or “non-classical” pathways. In this review, we summarize these signaling cascades and discuss recent developments in the field, specifically as they relate to the biological and clinical implications of engagement of both canonical and non-canonical pathways.

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Schlafen 14 (SLFN14) is a novel antiviral factor involved in the control of viral replication

Cited by 37 publications

References 37 publications

Structure of Schlafen13 reveals a new class of tRNA/rRNA- targeting RNase engaged in translational control

Structure of Schlafen13 reveals a new class of tRNA/rRNA- targeting RNase engaged in translational control

Favipiravir and Ribavirin Inhibit Replication of Asian and African Strains of Zika Virus in Different Cell Models

Type I Interferon (IFN)-Regulated Activation of Canonical and Non-Canonical Signaling Pathways

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