ArticleJournal of virology2022
PML Body Component Sp100A Restricts Wild-Type Herpes Simplex Virus 1 Infection.
Article in Journal of virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- Epigenetic regulation of transgenes.Journal of biotechnology · 2026Review
- SUMOylation and ubiquitination reciprocally regulate SMCHD1 antiviral activity against herpes simplex virus 1.PLoS pathogens · 2026Article
- An SP110-SP100 axis is a critical regulator of promyelocytic leukaemia body dynamics and mitotic fidelity.Nature cell biology · 2026Article
- Nuclear translocation of Sp100A suppresses multiple DNA viruses and limits HSV-1 lytic replication in vivo.Virologica Sinica · 2026Article
- Interactions between extracellular vesicles and viruses: lessons learned across species and kingdoms.FEMS microbiology reviews · 2026Review
- Mendelian randomization study implicates inflammaging biomarkers in retinal vasculature, cardiovascular diseases, and longevity.Science advances · 2025Article
- Inflammatory, transcriptomic, and cell fate responses underlying the mammalian transmission of avian influenza viruses.Journal of virology · 2025Article
- Review
- HSV-1 virions and related particles: biogenesis and implications in the infection.Journal of virology · 2025Review
- Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity.Frontiers in microbiology · 2025Review
- The Nucleolus and Its Interactions with Viral Proteins Required for Successful Infection.Cells · 2024Review
- Comparative proteomic analysis of PK-15 cells infected with wild-type strain and its EP0 gene-deleted mutant strain of pseudorabies virus.Journal of veterinary science · 2024Article
- A CRISPR-based rapid DNA repositioning strategy and the early intranuclear life of HSV-1.eLife · 2023Article
- African Swine Fever Virus Host-Pathogen Interactions.Sub-cellular biochemistry · 2023Article
- HSV-1 selectively packs the transcription factor Oct-1 into EVs to facilitate its infection.Frontiers in microbiology · 2023Article
- PML Body Component Sp100A Is a Cytosolic Responder to IFN and Activator of Antiviral ISGs.mBio · 2022Article
- Antimicrobial peptides: Defending the mucosal epithelial barrier.Frontiers in oral health · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sp100 (speckled protein 100 kDa) is a constituent component of nuclear structure PML (promyelocytic leukemia) bodies, playing important roles in mediating intrinsic and innate immunity. The Sp100 gene encodes four isoforms with distinct roles in the transcriptional regulation of both cellular and viral genes. Since Sp100 is a primary intranuclear target of infected-cell protein 0 (ICP0), an immediate early E3 ligase encoded by herpes simplex virus 1 (HSV-1), previous investigations attempting to analyze the functions of individual Sp100 variants during HSV-1 infection mostly avoided using a wild-type virus. Therefore, the role of Sp100 under natural infection by HSV-1 remains to be clarified. Here, we reappraised the antiviral capacity of four Sp100 isoforms during infection by a nonmutated HSV-1, examined the molecular behavior of the Sp100 protein in detail, and revealed the following intriguing observations. First, Sp100 isoform A (Sp100A) inhibited wild-type HSV-1 propagation in HEp-2, Sp100
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Registered trials
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 Socratic graph.