ArticleVirology2010
Significance of host cell kinases in herpes simplex virus type 1 egress and lamin-associated protein disassembly from the nuclear lamina.
Article in Virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
The trial behind it
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
51 citing papers in PubMed, 83 citations in OpenAlex.
- Herpesviruses show consistency in their nuclear egress-associated induction of lamina-depleted areas as measured in an autofluorescent reporter cell model.Virology journal · 2026Article
- Nucleus softens during herpesvirus infection.PLoS pathogens · 2026Article
- HSV-1 US3: A Master Mimic Hijacking Host Kinase Networks for Viral Dominance.Journal of medical virology · 2025Review
- ER protein CLCC1 promotes nuclear envelope fusion in herpesviral and host processes.Nature communications · 2025Article
- Primary envelopment of Kaposi's sarcoma-associated herpesvirus at the nucleoplasmic reticulum.Journal of virology · 2025Article
- Nuclear warfare: pathogen manipulation of the nuclear pore complex and nuclear functions.mBio · 2025Review
- HSV-1 exploits host heterochromatin for nuclear egress.The Journal of cell biology · 2023Article
- Inhibitors of One or More Cellular Aurora Kinases Impair the Replication of Herpes Simplex Virus 1 and Other DNA and RNA Viruses with Diverse Genomes and Life Cycles.Microbiology spectrum · 2023Article
- Redundant and Specific Roles of A-Type Lamins and Lamin B Receptor in Herpes Simplex Virus 1 Infection.Journal of virology · 2022Article
- Putative targeting by BX795 causes decrease in protein kinase C protein levels and inhibition of HSV1 infection.Antiviral research · 2022Article
- Recent progress in the mechanistic understanding of NET formation in neutrophils.The FEBS journal · 2022Review
- Role of the Orphan Transporter SLC35E1 in the Nuclear Egress of Herpes Simplex Virus 1.Journal of virology · 2022Article
- Article
- Nuclear Cytoskeleton in Virus Infection.International journal of molecular sciences · 2022Review
- Junin Virus Activates p38 MAPK and HSP27 Upon Entry.Frontiers in cellular and infection microbiology · 2022Article
- Cell Culture Evolution of a Herpes Simplex Virus 1 (HSV-1)/Varicella-Zoster Virus (VZV) UL34/ORF24 Chimeric Virus Reveals Novel Functions for HSV Genes in Capsid Nuclear Egress.Journal of virology · 2021Article
- Herpes Simplex Virus 1 UL34 Mutants That Affect Membrane Budding Regulation and Nuclear Lamina Disruption.Journal of virology · 2021Article
- Promising role of defensins peptides as therapeutics to combat against viral infection.Microbial pathogenesis · 2021Review
- Mechanism of Nuclear Lamina Disruption and the Role of pUS3 in HSV-1 Nuclear Egress.Journal of virology · 2021Article
- Viral use and subversion of membrane organization and trafficking.Journal of cell science · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The nuclear lamina is thought to be a steric barrier to the herpesvirus capsid. Disruption of the lamina accompanied by phosphorylation of lamina proteins is a conserved feature of herpesvirus infection. In HSV-1-infected cells, protein kinase C (PKC) alpha and delta isoforms are recruited to the nuclear membrane and PKC delta has been implicated in phosphorylation of emerin and lamin B. We tested two critical hypotheses about the mechanism and significance of lamina disruption. First, we show that chemical inhibition of all PKC isoforms reduced viral growth five-fold and inhibited capsid egress from the nucleus. However, specific inhibition of either conventional PKCs or PKC delta does not inhibit viral growth. Second, we show hyperphosphorylation of emerin by viral and cellular kinases is required for its disassociation from the lamina. These data support hypothesis that phosphorylation of lamina components mediates lamina disruption during HSV nuclear egress.
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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.