ArticleJournal of virology2012
Herpes simplex virus requires poly(ADP-ribose) polymerase activity for efficient replication and induces extracellular signal-related kinase-dependent phosphorylation and ICP0-dependent nuclear localization of tankyrase 1.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- NADThe Journal of general virology · 2026Review
- Tankyrases and Their Binding Proteins: Origins of Their Roles in Diverse Cellular Pathways.Cells · 2026Review
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Tankyrases positively regulate influenza A virus replication via type I interferon response.Journal of virology · 2025Article
- Review
- Understanding Tankyrase Inhibitors and Their Role in the Management of Different Cancer.Current cancer drug targets · 2025Review
- Three-Dimensional Chromatin Structure of the EBV Genome: A Crucial Factor in Viral Infection.Viruses · 2023Review
- Axin1: A novel scaffold protein joins the antiviral network of interferon.Molecular microbiology · 2022Article
- ADP-Ribosylation Post-Translational Modification: An Overview with a Focus on RNA Biology and New Pharmacological Perspectives.Biomolecules · 2022Review
- NAD+-consuming enzymes in immune defense against viral infection.The Biochemical journal · 2021Review
- Interplay between ADP-ribosyltransferases and essential cell signaling pathways controls cellular responses.Cell discovery · 2021Review
- Tankyrase inhibitors hinderParasitology · 2021Article
- Review
- Tankyrases as modulators of pro-tumoral functions: molecular insights and therapeutic opportunities.Journal of experimental & clinical cancer research : CR · 2021Review
- The Antiviral Activities of Poly-ADP-Ribose Polymerases.Viruses · 2021Review
- MicroRNA-206 inhibits influenza A virus replication by targeting tankyrase 2.Cellular microbiology · 2021Article
- Elucidating the tunability of binding behavior for the MERS-CoV macro domain with NAD metabolites.Communications biology · 2021Article
- NADFrontiers in molecular biosciences · 2021Review
- Viral macrodomains: a structural and evolutionary assessment of the pharmacological potential.Open biology · 2020Article
- The impact of PARPs and ADP-ribosylation on inflammation and host-pathogen interactions.Genes & development · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tankyrase 1 is a poly(ADP-ribose) polymerase (PARP) which localizes to multiple subcellular sites, including telomeres and mitotic centrosomes. Poly(ADP-ribosyl)ation of the nuclear mitotic apparatus (NuMA) protein by tankyrase 1 during mitosis is essential for sister telomere resolution and mitotic spindle pole formation. In interphase cells, tankyrase 1 resides in the cytoplasm, and its role therein is not well understood. In this study, we found that herpes simplex virus (HSV) infection induced extensive modification of tankyrase 1 but not tankyrase 2. This modification was dependent on extracellular signal-regulated kinase (ERK) activity triggered by HSV infection. Following HSV-1 infection, tankyrase 1 was recruited to the nucleus. In the early phase of infection, tankyrase 1 colocalized with ICP0 and thereafter localized within the HSV replication compartment, which was blocked in cells infected with the HSV-1 ICP0-null mutant R7910. In the absence of infection, ICP0 interacted with tankyrase 1 and efficiently promoted its nuclear localization. HSV did not replicate efficiently in cells depleted of both tankyrases 1 and 2. Moreover, XAV939, an inhibitor of tankyrase PARP activity, decreased viral titers to 2 to 5% of control values. We concluded that HSV targets tankyrase 1 in an ICP0- and ERK-dependent manner to facilitate its replication.
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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.