ArticleJournal of virology2014
Human cytomegalovirus UL50 and UL53 recruit viral protein kinase UL97, not protein kinase C, for disruption of nuclear lamina and nuclear egress in infected cells.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 79 citations in OpenAlex.
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- Cytomegalovirus disrupts Lamin A/C to control microtubule-mediated nuclear movement and cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Primary envelopment of Kaposi's sarcoma-associated herpesvirus at the nucleoplasmic reticulum.Journal of virology · 2025Article
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- 'Getting Better'-Is It a Feasible Strategy of Broad Pan-Antiherpesviral Drug Targeting by Using the Nuclear Egress-Directed Mechanism?International journal of molecular sciences · 2024Review
- A small molecule exerts selective antiviral activity by targeting the human cytomegalovirus nuclear egress complex.PLoS pathogens · 2023Article
- Human herpesvirus 6A nuclear matrix protein U37 interacts with heat shock transcription factor 1 and activates the heat shock response.Journal of virology · 2023Article
- Molecular Characterization of UL50 (dUTPase) Gene of Bovine Herpes Virus 1.Animals : an open access journal from MDPI · 2023Article
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- UL34 Deletion Restricts Human Cytomegalovirus Capsid Formation and Maturation.International journal of molecular sciences · 2022Article
- The nuclear lamina binds the EBV genome during latency and regulates viral gene expression.PLoS pathogens · 2022Article
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- Nuclear Cytoskeleton in Virus Infection.International journal of molecular sciences · 2022Review
- The human cytomegalovirus decathlon: Ten critical replication events provide opportunities for restriction.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Herpesvirus nucleocapsids traverse the nuclear envelope into the cytoplasm in a process called nuclear egress that includes disruption of the nuclear lamina. In several herpesviruses, a key player in nuclear egress is a complex of two proteins, whose homologs in human cytomegalovirus (HCMV) are UL50 and UL53. However, their roles in nuclear egress during HCMV infection have not been shown. Based largely on transfection studies, UL50 and UL53 have been proposed to facilitate disruption of the nuclear lamina by recruiting cellular protein kinase C (PKC), as occurs with certain other herpesviruses, and/or the viral protein kinase UL97 to phosphorylate lamins. To investigate these issues during HCMV infection, we generated viral mutants null for UL50 or UL53. Correlative light electron microscopic analysis of null mutant-infected cells showed the presence of intranuclear nucleocapsids and the absence of cytoplasmic nucleocapsids. Confocal immunofluorescence microscopy revealed that UL50 and UL53 are required for disruption of the nuclear lamina. A subpopulation of UL97 colocalized with the nuclear rim, and this was dependent on UL50 and, to a lesser extent, UL53. However, PKC was not recruited to the nuclear rim, and its localization was not affected by the absence of UL50 or UL53. Immunoprecipitation from cells infected with HCMV expressing tagged UL53 detected UL97 but not PKC. In summary, HCMV UL50 and UL53 are required for nuclear egress and disruption of nuclear lamina during HCMV infection, and they recruit UL97, not PKC, for these processes. Thus, despite the strong conservation of herpesvirus nuclear egress complexes, a key function can differ among them.
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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.