ArticleJournal of virology2013
Inactivation of retinoblastoma protein does not overcome the requirement for human cytomegalovirus UL97 in lamina disruption and nuclear egress.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- 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
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- The nuclear lamina binds the EBV genome during latency and regulates viral gene expression.PLoS pathogens · 2022Article
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- Antiviral Drugs Against Herpesviruses.Advances in experimental medicine and biology · 2021Article
- A Role for Myosin Va in Human Cytomegalovirus Nuclear Egress.Journal of virology · 2018Article
- Human Cytomegalovirus nuclear egress and secondary envelopment are negatively affected in the absence of cellular p53.Virology · 2016Article
- Article
- Article
- Discovery of a Coregulatory Interaction between Kaposi's Sarcoma-Associated Herpesvirus ORF45 and the Viral Protein Kinase ORF36.Journal of virology · 2016Article
- Preparation of the Human Cytomegalovirus Nuclear Egress Complex and Associated Proteins.Methods in enzymology · 2016Article
- Antagonistic Relationship between Human Cytomegalovirus pUL27 and pUL97 Activities during Infection.Journal of virology · 2015Article
- Human cytomegalovirus pUL97 kinase induces global changes in the infected cell phosphoproteome.Proteomics · 2015Article
- Human cytomegalovirus UL97 phosphorylates the viral nuclear egress complex.Journal of virology · 2015Article
- Comparison of effects of inhibitors of viral and cellular protein kinases on human cytomegalovirus disruption of nuclear lamina and nuclear egress.Journal of virology · 2014Article
- Article
- An epistatic relationship between the viral protein kinase UL97 and the UL133-UL138 latency locus during the human cytomegalovirus lytic cycle.Journal of virology · 2014Article
- 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.Journal of virology · 2014Article
- The ULb' region of the human cytomegalovirus genome confers an increased requirement for the viral protein kinase UL97.Journal of virology · 2013Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Human cytomegalovirus (HCMV) encodes one conventional protein kinase, UL97. During infection, UL97 phosphorylates the retinoblastoma tumor suppressor protein (pRb) on sites ordinarily phosphorylated by cyclin-dependent kinases (CDK), inactivating the ability of pRb to repress host genes required for cell cycle progression to S phase. UL97 is important for viral DNA synthesis in quiescent cells, but this function can be replaced by human papillomavirus type 16 E7, which targets pRb for degradation. However, viruses in which E7 replaces UL97 are still defective for virus production. UL97 is also required for efficient nuclear egress of viral nucleocapsids, which is associated with disruption of the nuclear lamina during infection, and phosphorylation of lamin A/C on serine 22, which antagonizes lamin polymerization. We investigated whether inactivation of pRb might overcome the requirement of UL97 for these roles, as pRb inactivation induces CDK1, and CDK1 phosphorylates lamin A/C on serine 22. We found that lamin A/C serine 22 phosphorylation during HCMV infection correlated with expression of UL97 and was considerably delayed in UL97-null mutants, even when E7 was expressed. E7 failed to restore gaps in the nuclear lamina seen in wild-type but not UL97-null virus infections. In electron microscopy analyses, a UL97-null virus expressing E7 was as impaired as a UL97-null mutant in cytoplasmic accumulation of viral nucleocapsids. Our results demonstrate that pRb inactivation is insufficient to restore efficient viral nuclear egress of HCMV in the absence of UL97 and instead argue further for a direct role of UL97 in this stage of the infectious cycle.
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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.