ArticlePLoS pathogens2023
Kaposi's sarcoma-associated herpesvirus (KSHV) utilizes the NDP52/CALCOCO2 selective autophagy receptor to disassemble processing bodies.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 16 citations in OpenAlex.
- Herpesviruses and autophagy: An intracellular conflict.Virulence · 2026Review
- Single-cell and spatial transcriptomics reveal mTOR-driven cellular fate of spindle cells and immune evasion in classic Kaposi's sarcoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Role of soluble human leukocyte antigen-G in virus-associated cancers: A focused minireview.World journal of virology · 2026Review
- Bacteria use P-body condensates to attenuate host translation during infection.Science advances · 2026Article
- Multi-omics data mining combined with experimental validation reveals ferroptosis- and autophagy-associated hub genes as diagnostic candidates and immune modulators in atherosclerosis.Animal models and experimental medicine · 2026Article
- Evolution of a truncated nucleocapsid protein enhances SARS-CoV-2 fitness by suppressing antiviral responses.PLoS biology · 2026Article
- Major histocompatibility complex class I chain-related A and B molecules and their potential role in virus-associated cancers.World journal of virology · 2026Review
- The anti-viral protein Shiftless blocks p-body formation during KSHV infection.The Journal of general virology · 2026Article
- Inflammasomes and autophagy in cancer: unlocking targeted therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- A Guideline Strategy for Identifying a Viral Gene/Protein Evading Antiviral Innate Immunity.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- Machine-learning-based prediction of a diagnostic model using autophagy-related genes based on RNA sequencing for patients with papillary thyroid carcinoma.Open medicine (Warsaw, Poland) · 2024Article
- Shiftless Restricts Viral Gene Expression and Influences RNA Granule Formation during Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Journal of virology · 2022Article
- Human coronaviruses disassemble processing bodies.PLoS pathogens · 2022Article
- A Panel of Kaposi's Sarcoma-Associated Herpesvirus Mutants in the Polycistronic Kaposin Locus for Precise Analysis of Individual Protein Products.Journal of virology · 2022Article
- Viral Manipulation of a Mechanoresponsive Signaling Axis Disassembles Processing Bodies.Molecular and cellular biology · 2021Article
- Stress granule and P-body clearance: Seeking coherence in acts of disappearance.Seminars in cell & developmental biologyReview
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) causes the inflammatory and angiogenic endothelial cell neoplasm, Kaposi's sarcoma (KS). We previously demonstrated that the KSHV Kaposin B (KapB) protein promotes inflammation via the disassembly of cytoplasmic ribonucleoprotein granules called processing bodies (PBs). PBs modify gene expression by silencing or degrading labile messenger RNAs (mRNAs), including many transcripts that encode inflammatory or angiogenic proteins associated with KS disease. Although our work implicated PB disassembly as one of the causes of inflammation during KSHV infection, the precise mechanism used by KapB to elicit PB disassembly was unclear. Here we reveal a new connection between the degradative process of autophagy and PB disassembly. We show that both latent KSHV infection and KapB expression enhanced autophagic flux via phosphorylation of the autophagy regulatory protein, Beclin. KapB was necessary for this effect, as infection with a recombinant virus that does not express the KapB protein did not induce Beclin phosphorylation or autophagic flux. Moreover, we showed that PB disassembly mediated by KSHV or KapB, depended on autophagy genes and the selective autophagy receptor NDP52/CALCOCO2 and that the PB scaffolding protein, Pat1b, co-immunoprecipitated with NDP52. These studies reveal a new role for autophagy and the selective autophagy receptor NDP52 in promoting PB turnover and the concomitant synthesis of inflammatory molecules during KSHV infection.
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