ArticleJournal of cell science2011
PML isoforms I and II participate in PML-dependent restriction of HSV-1 replication.
Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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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Who cites it
72 citing papers in PubMed, 105 citations in OpenAlex.
- PXL: a nucleic acid-binding module of the promyelocytic leukemia protein.Nucleic acids research · 2026Article
- Time-resolved mapping in calves reveals bovine herpesvirus 1 shift from mucosal replication to trigeminal ganglion neuroinvasion with promyelocytic leukemia protein-centered host-virus antagonism.Microbiology spectrum · 2026Article
- PXL: a Nucleic Acid-Binding Module of Promyelocytic Leukemia Protein.bioRxiv : the preprint server for biology · 2026Article
- Daxx mediated histone H3.3 deposition on HSV-1 DNA restricts genome decompaction and the progression of immediate-early transcription.PLoS pathogens · 2025Article
- Conformational exchange at a CStructure (London, England : 1993) · 2023Article
- Interplay between PML NBs and HIRA for H3.3 dynamics following type I interferon stimulus.eLife · 2023Article
- Japanese encephalitis virus perturbs PML-nuclear bodies by engaging in interactions with distinct porcine PML isoforms.Frontiers in cellular and infection microbiology · 2023Article
- PML Alternative Splice Products Differentially Regulate HAdV Productive Infection.Microbiology spectrum · 2022Article
- A 77 Amino Acid Region in the N-Terminal Half of the HSV-1 E3 Ubiquitin Ligase ICP0 Contributes to Counteracting an Established Type 1 Interferon Response.Microbiology spectrum · 2022Article
- PML Body Component Sp100A Restricts Wild-Type Herpes Simplex Virus 1 Infection.Journal of virology · 2022Article
- Dual signaling via interferon and DNA damage response elicits entrapment by giant PML nuclear bodies.eLife · 2022Article
- New Evidence of the Importance of Weak Interactions in the Formation of PML-Bodies.International journal of molecular sciences · 2022Article
- Herpesvirus-mediated stabilization of ICP0 expression neutralizes restriction by TRIM23.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- PML-II regulates ERK and AKT signal activation and IFNα-induced cell death.Cell communication and signaling : CCS · 2021Article
- Host Innate Immune Response and Viral Immune Evasion During Alphaherpesvirus Infection.Current issues in molecular biology · 2021Review
- Crosstalk Between SUMO and Ubiquitin-Like Proteins: Implication for Antiviral Defense.Frontiers in cell and developmental biology · 2021Review
- Swine Promyelocytic Leukemia Isoform II Inhibits Pseudorabies Virus Infection by Suppressing Viral Gene Transcription in Promyelocytic Leukemia Nuclear Bodies.Journal of virology · 2020Article
- HSV-1 Hijacks the Host DNA Damage Response in Corneal Epithelial Cells through ICP4-Mediated Activation of ATM.Investigative ophthalmology & visual science · 2020Article
- The Fate of Speckled Protein 100 (Sp100) During Herpesviruses Infection.Frontiers in cellular and infection microbiology · 2020Review
- Autophagic degradation of PML promotes susceptibility to HSV-1 by stress-induced corticosterone.Theranostics · 2020Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Intrinsic antiviral resistance mediated by constitutively expressed cellular proteins is one arm of defence against virus infection. Promyelocytic leukaemia nuclear bodies (PML-NBs, also known as ND10) contribute to host restriction of herpes simplex virus type 1 (HSV-1) replication via mechanisms that are counteracted by viral regulatory protein ICP0. ND10 assembly is dependent on PML, which comprises several different isoforms, and depletion of all PML isoforms decreases cellular resistance to ICP0-null mutant HSV-1. We report that individual expression of PML isoforms I and II partially reverses the increase in ICP0-null mutant HSV-1 plaque formation that occurs in PML-depleted cells. This activity of PML isoform I is dependent on SUMO modification, its SUMO interaction motif (SIM), and each element of its TRIM domain. Detailed analysis revealed that the punctate foci formed by individual PML isoforms differ subtly from normal ND10 in terms of composition and/or Sp100 modification. Surprisingly, deletion of the SIM motif from PML isoform I resulted in increased colocalisation with other major ND10 components in cells lacking endogenous PML. Our observations suggest that complete functionality of PML is dependent on isoform-specific C-terminal sequences acting in concert.
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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 OpenQuestion graph.