ArticleJournal of virology2006
Adenovirus E1B 55-kilodalton protein is required for both regulation of mRNA export and efficient entry into the late phase of infection in normal human fibroblasts.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Viral interference of nucleocytoplasmic transport.The Journal of biological chemistry · 2025Review
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- Understanding the performance of HIV-1 viral vector vaccines: adenovirus and poxvirus case studies.Frontiers in immunology · 2025Review
- Novel viral splicing events and open reading frames revealed by long-read direct RNA sequencing of adenovirus transcripts.PLoS pathogens · 2022Article
- E1B-55K Is a Phosphorylation-Dependent Transcriptional and Posttranscriptional Regulator of Viral Gene Expression in Human Adenovirus C5 Infection.Journal of virology · 2022Article
- Article
- Recent Advances in Novel Antiviral Therapies against Human Adenovirus.Microorganisms · 2020Review
- The human adenovirus type 5 E1B 55kDa protein interacts with RNA promoting timely DNA replication and viral late mRNA metabolism.PloS one · 2019Article
- Multiple nuclear-replicating viruses require the stress-induced protein ZC3H11A for efficient growth.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Normal human cell proteins that interact with the adenovirus type 5 E1B 55kDa protein.Virology · 2017Article
- Article
- Automatic detection and measurement of viral replication compartments by ellipse adjustment.Scientific reports · 2016Article
- An Adenovirus DNA Replication Factor, but Not Incoming Genome Complexes, Targets PML Nuclear Bodies.Journal of virology · 2016Article
- Morphological, Biochemical, and Functional Study of Viral Replication Compartments Isolated from Adenovirus-Infected Cells.Journal of virology · 2016Article
- Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells.Journal of visualized experiments : JoVE · 2015Article
- Oncolytic Replication of E1b-Deleted Adenoviruses.Viruses · 2015Review
- Impact of the adenoviral E4 Orf3 protein on the activity and posttranslational modification of p53.Journal of virology · 2015Article
- Evaluation of apoptogenic adenovirus type 5 oncolytic vectors in a Syrian hamster head and neck cancer model.Cancer gene therapy · 2014Article
- The p53 protein does not facilitate adenovirus type 5 replication in normal human cells.Journal of virology · 2013Article
- The repression domain of the E1B 55-kilodalton protein participates in countering interferon-induced inhibition of adenovirus replication.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human adenovirus type 5 (Ad5) E1B 55-kDa protein is required for selective nuclear export of viral late mRNAs from the nucleus and concomitant inhibition of export of cellular mRNAs in HeLa cells and some other human cell lines, but its contributions(s) to replication in normal human cells is not well understood. We have therefore examined the phenotypes exhibited by viruses carrying mutations in the E1B 55-kDa protein coding sequence in normal human fibroblast (HFFs). Ad5 replicated significantly more slowly in HFFs than it does in tumor cells, a difference that is the result of delayed entry into the late phase of infection. The A143 mutation, which specifically impaired export of viral late mRNAs from the nucleus in infected HeLa cells (R. A. Gonzalez and S. J. Flint, J. Virol. 76:4507-4519, 2002), induced a more severe defect in viral mRNA export in HFFs. This observation indicates that the E1B 55-kDa protein regulates mRNA export during the late phase of infection of normal human cells. Other mutants exhibited phenotypes not observed in HeLa cells. In HFFs infected by the null mutant Hr6, synthesis of viral late mRNAs and proteins was severely impaired. Such defects in late gene expression were the result of inefficient progression into the late phase of infection, for viral DNA synthesis was 10-fold less efficient in Hr6-infected HFFs than in cells infected by Ad5. Similar, but less severe, defects in viral DNA synthesis were induced by the insertion mutation H224, which has been reported to inhibit binding of the E1B 55-kDa protein to p53 (C. C. Kao, P. R. Yew, and A. J. Berk, Virology 179:806-814, 1990).
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