ArticleProceedings of the National Academy of Sciences of the United States of America2004
Herpes simplex virus protein kinase US3 activates and functionally overlaps protein kinase A to block apoptosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
96 citing papers in PubMed, 153 citations in OpenAlex.
- Identification of UL3.5 as a novel substrate of DPV US3 kinase whose phosphorylation at Ser64/Ser84 enhances protein stability and promotes viral release, and cell-to-cell spread.Poultry science · 2026Article
- HSV-1 US3: A Master Mimic Hijacking Host Kinase Networks for Viral Dominance.Journal of medical virology · 2025Review
- Impact of the changes in substrate specificity of herpes simplex virus 1 protein kinase Us3 on viral infectionJournal of virology · 2025Article
- Unveiling the Involvement of Herpes Simplex Virus-1 in Alzheimer's Disease: Possible Mechanisms and Therapeutic Implications.Molecular neurobiology · 2025Review
- Marek's disease virus protein kinase US3 inhibits DNA-sensing antiviral innate immunity via abrogating activation of NF-κB.Microbiology spectrum · 2025Article
- Impaired endocytosis and accumulation in early endosomal compartments defines herpes simplex virus-mediated disruption of the nonclassical MHC class I-related molecule MR1.The Journal of biological chemistry · 2024Article
- Viral Infections, Are They a Trigger and Risk Factor of Alzheimer's Disease?Pathogens (Basel, Switzerland) · 2024Review
- Review
- Mechanistic insights into the role of herpes simplex virus 1 in Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- Article
- New Insights into the Molecular Interplay between Human Herpesviruses and Alzheimer's Disease-A Narrative Review.Brain sciences · 2022Review
- Duck plague virus US3 protein kinase phosphorylates UL47 and regulates the subcellular localization of UL47.Frontiers in microbiology · 2022Article
- Disrupting Neurons and Glial Cells Oneness in the Brain-The Possible Causal Role of Herpes Simplex Virus Type 1 (HSV-1) in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Review
- Review
- pUL21 regulation of pUs3 kinase activity influences the nature of nuclear envelope deformation by the HSV-2 nuclear egress complex.PLoS pathogens · 2021Article
- pUL21 is a viral phosphatase adaptor that promotes herpes simplex virus replication and spread.PLoS pathogens · 2021Article
- Mechanism of Nuclear Lamina Disruption and the Role of pUS3 in HSV-1 Nuclear Egress.Journal of virology · 2021Article
- Marek's disease virus US3 protein kinase phosphorylates chicken HDAC 1 and 2 and regulates viral replication and pathogenesis.PLoS pathogens · 2021Article
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
36 more citing papers are in PubMed but not listed here.
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
Herpes simplex virus 1 encodes at least four genes whose functions include blocking apoptosis induced by exogenous agents (e.g., sorbitol, Fas ligand, and BAD protein) or replication-incompetent mutants (e.g., the d120 mutant lacking both copies of the alpha 4 gene). U(S)3, one of these four genes, encodes a serine-threonine kinase that has been demonstrated to block apoptosis induced by proapoptotic cellular proteins or by the d120 mutant. The amino acid context of serine-threonine phosphorylated by U(S)3 is similar to that of the cAMP-dependent protein kinase PKA. We report that (i) the pattern of proteins phosphorylated by U(S)3 in transduced cells or in cells infected with WT virus overlaps that of phosphoproteins targeted by PKA, (ii) activation of PKA blocks apoptosis induced by d120 mutant or by BAD protein independently of U(S)3, (iii) U(S)3 protein kinase phosphorylates peptides containing the serine or threonine targeted by PKA including that present in the regulatory type II alpha subunit of PKA, and (iv) in WT virus-infected cells the regulatory type II alpha subunit is phosphorylated in a U(S)3-dependent manner. We conclude that a major determinant of the antiapoptotic activity of the U(S)3 protein kinase is the phosphorylation of PKA substrates by either or both enzymes.
Indexed as
Identifiers
What OpenQuestion holds
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.