ArticleProceedings of the National Academy of Sciences of the United States of America2014
Human cytomegalovirus pUL37x1-induced calcium flux activates PKCα, inducing altered cell shape and accumulation of cytoplasmic vesicles.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Review
- Rab10-associated tubulation as an early marker for biogenesis of the assembly compartment in cytomegalovirus-infected cells.Frontiers in cell and developmental biology · 2024Article
- Cytomegaloviruses reorganize endomembrane system to intersect endosomal and amphisome-like egress pathway.Frontiers in cell and developmental biology · 2023Article
- Restructured membrane contacts rewire organelles for human cytomegalovirus infection.Nature communications · 2022Article
- Endoplasmic reticulum & mitochondrial calcium homeostasis: The interplay with viruses.Mitochondrion · 2021Article
- TRANSPIRE: A Computational Pipeline to Elucidate Intracellular Protein Movements from Spatial Proteomics Data Sets.Journal of the American Society for Mass Spectrometry · 2020Article
- Human Cytomegalovirus Alters Host Cell Mitochondrial Function during Acute Infection.Journal of virology · 2020Article
- Systems Virology and Human Cytomegalovirus: Using High Throughput Approaches to Identify Novel Host-Virus Interactions During Lytic Infection.Frontiers in cellular and infection microbiology · 2020Review
- Tuning the Orchestra: HCMV vs. Innate Immunity.Frontiers in microbiology · 2020Review
- Human Cytomegalovirus pUL37x1 Is Important for Remodeling of Host Lipid Metabolism.Journal of virology · 2019Article
- Rho-Associated Coiled-Coil Kinase 1 Translocates to the Nucleus and Inhibits Human Cytomegalovirus Propagation.Journal of virology · 2019Article
- P2Y2 purinergic receptor modulates virus yield, calcium homeostasis, and cell motility in human cytomegalovirus-infected cells.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Human cytomegalovirus US21 protein is a viroporin that modulates calcium homeostasis and protects cells against apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- High-Throughput Small Interfering RNA Screening Identifies Phosphatidylinositol 3-Kinase Class II Alpha as Important for Production of Human Cytomegalovirus Virions.Journal of virology · 2016Article
- Article
- Trehalose, an mTOR-Independent Inducer of Autophagy, Inhibits Human Cytomegalovirus Infection in Multiple Cell Types.Journal of virology · 2016Article
- Pathophysiological Consequences of Calcium-Conducting Viroporins.Annual review of virology · 2015Review
- RhoB is a component of the human cytomegalovirus assembly complex and is required for efficient viral production.Cell cycle (Georgetown, Tex.) · 2015Article
- Cyclophilin A as a target in the treatment of cytomegalovirus infections.Antiviral chemistry & chemotherapyReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The human cytomegalovirus immediate-early protein pUL37x1 induces the release of Ca(2+) stores from the endoplasmic reticulum into the cytosol. This release causes reorganization of the cellular actin cytoskeleton with concomitant cell rounding. Here we demonstrate that pUL37x1 activates Ca(2+)-dependent protein kinase Cα (PKCα). Both PKCα and Rho-associated protein kinases are required for actin reorganization and cell rounding; however, only PKCα is required for the efficient production of virus progeny, arguing that HCMV depends on the kinase for a second function. PKCα activation is also needed for the production of large (1-5 μm) cytoplasmic vesicles late after infection. The production of these vesicles is blocked by inhibition of fatty acid or phosphatidylinositol-3-phosphate biosynthesis, and the failure to produce vesicles is correlated with substantially reduced production of enveloped virus capsids. These results connect earlier work identifying a requirement for lipid synthesis with specific morphological changes, and support the argument that the PKCα-induced large vesicles are either required for the efficient production of mature virus particles or serve as a marker for the process.
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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.