ArticlePLoS pathogens2019
Kaposi's sarcoma-associated herpesvirus ORF57 protein protects viral transcripts from specific nuclear RNA decay pathways by preventing hMTR4 recruitment.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- ORF57/MTA in KSHV Biology and Pathogenesis: Update From 2015.Journal of medical virology · 2026Review
- Review
- Exploration of RNA-binding proteins identified RPS27 as a potential regulator associated with Kaposi's sarcoma development.BMC cancer · 2025Article
- Review
- Article
- Nuclear mRNA decay: regulatory networks that control gene expression.Nature reviews. Genetics · 2024Review
- KSHV promotes oncogenic FOS to inhibit nuclease AEN and transactivate RGS2 for AKT phosphorylation.bioRxiv : the preprint server for biology · 2024Article
- Functional analysis of 3'-UTR hairpins supports a two-tiered model for posttranscriptional regulation ofRNA (New York, N.Y.) · 2023Article
- PABPN1 prevents the nuclear export of an unspliced RNA with a constitutive transport element and controls human gene expression via intron retention.RNA (New York, N.Y.) · 2023Article
- The PNUTS-PP1 complex acts as an intrinsic barrier to herpesvirus KSHV gene expression and replication.Nature communications · 2022Article
- Shiftless Restricts Viral Gene Expression and Influences RNA Granule Formation during Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Journal of virology · 2022Article
- Dysregulation of the miR-30c/DLL4 axis by circHIPK3 is essential for KSHV lytic replication.EMBO reports · 2022Article
- The Expression and Nuclear Retention Element of Polyadenylated Nuclear RNA Is Not Required for Productive Lytic Replication of Kaposi's Sarcoma-Associated Herpesvirus.Journal of virology · 2021Article
- SAM homeostasis is regulated by CFIeLife · 2021Article
- NCBP3: A Multifaceted Adaptive Regulator of Gene Expression.Trends in biochemical sciences · 2021Review
- Review
- Kaposi's Sarcoma-Associated Herpesvirus Fine-Tunes the Temporal Expression of Late Genes by Manipulating a Host RNA Quality Control Pathway.Journal of virology · 2020Article
- Regulation of long non-coding RNAs and genome dynamics by the RNA surveillance machinery.Nature reviews. Molecular cell biology · 2020Review
- CRISPR/Cas9-Mediated Knockout andJournal of virology · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Nuclear RNAs are subject to a number of RNA decay pathways that serve quality control and regulatory functions. As a result, any virus that expresses its genes in the nucleus must have evolved mechanisms that avoid these pathways, but the how viruses evade nuclear RNA decay remains largely unknown. The multifunctional Kaposi's sarcoma-associated herpesvirus (KSHV) ORF57 (Mta) protein is required for the nuclear stability of viral transcripts. In the absence of ORF57, we show that viral transcripts are subject to degradation by two specific nuclear RNA decay pathways, PABPN1 and PAPα/γ-mediated RNA decay (PPD) in which decay factors are recruited through poly(A) tails, and an ARS2-mediated RNA decay pathway dependent on the 5' RNA cap. In transcription pulse chase assays, ORF57 appears to act primarily by inhibiting the ARS2-mediated RNA decay pathway. In the context of viral infection in cultured cells, inactivation of both decay pathways by RNAi is necessary for the restoration of ORF57-dependent viral genes produced from an ORF57-null bacmid. Mechanistically, we demonstrate that ORF57 protects viral transcripts by preventing the recruitment of the exosome co-factor hMTR4. In addition, our data suggest that ORF57 recruitment of ALYREF inhibits hMTR4 association with some viral RNAs, whereas other KSHV transcripts are stabilized by ORF57 in an ALYREF-independent fashion. In conclusion, our studies show that KSHV RNAs are subject to nuclear degradation by two specific host pathways, PPD and ARS2-mediated decay, and ORF57 protects viral transcripts from decay by inhibiting hMTR4 recruitment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.