ArticleJournal of virology2009
The adenoviral E1B 55-kilodalton protein controls expression of immune response genes but not p53-dependent transcription.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 33 citations in OpenAlex.
- Integration of a multimeric STAT consensus site into the adenoviral genome to interfere with IFN signaling represents a novel concept to improve oncolytic virotherapy.Journal of virology · 2026Article
- Adenovirus E1B-55K regulates p53-dependent and -independent gene expression during infection.PLoS pathogens · 2025Article
- Going viral: targeting glioblastoma using oncolytic viruses.Immunotherapy advances · 2025Review
- Adenovirus E1B-55K interferes with cellular IκB kinase complex subunit proteins.Frontiers in immunology · 2025Article
- YB-1-based oncolytic virotherapy in combination with CD47 blockade enhances phagocytosis of pediatric sarcoma cells.Frontiers in oncology · 2024Article
- The human adenovirus E1B-55K oncoprotein coordinates cell transformation through regulation of DNA-bound host transcription factors.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Ixovex-1, a novel oncolytic E1B-mutated adenovirus.Cancer gene therapy · 2022Article
- 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
- E4orf1 SuppressesVaccines · 2022Article
- The immunological impact of adenovirus early genes on vaccine-induced responses in mice and nonhuman primates.Journal of virology · 2021Article
- The human adenovirus type 5 E1B 55kDa protein interacts with RNA promoting timely DNA replication and viral late mRNA metabolism.PloS one · 2019Article
- Normal human cell proteins that interact with the adenovirus type 5 E1B 55kDa protein.Virology · 2017Article
- Long story short: p53 mediates innate immunity.Biochimica et biophysica acta · 2016Review
- Article
- Impact of the adenoviral E4 Orf3 protein on the activity and posttranslational modification of p53.Journal of virology · 2015Article
- Unabated adenovirus replication following activation of the cGAS/STING-dependent antiviral response in human cells.Journal of virology · 2014Article
- Extensive post-translational modification of active and inactivated forms of endogenous p53.Molecular & cellular proteomics : MCP · 2014Article
- The human adenovirus 5 L4 promoter is activated by cellular stress response protein p53.Journal of virology · 2013Article
- The p53 protein does not facilitate adenovirus type 5 replication in normal human cells.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The human adenovirus type 5 (Ad5) E1B 55-kDa protein modulates several cellular processes, including activation of the tumor suppressor p53. Binding of the E1B protein to the activation domain of p53 inhibits p53-dependent transcription. This activity has been correlated with the transforming activity of the E1B protein, but its contribution to viral replication is not well understood. To address this issue, we used microarray hybridization methods to examine cellular gene expression in normal human fibroblasts (HFFs) infected by Ad5, the E1B 55-kDa-protein-null mutant Hr6, or a mutant carrying substitutions that impair repression of p53-dependent transcription. Comparison of the changes in cellular gene expression observed in these and our previous experiments (D. L. Miller et al., Genome Biol. 8:R58, 2007) by significance analysis of microarrays indicated excellent reproducibility. Furthermore, we again observed that Ad5 infection led to efficient reversal of the p53-dependent transcriptional program. As this same response was also induced in cells infected by the two mutants, we conclude that the E1B 55-kDa protein is not necessary to block activation of p53 in Ad5-infected cells. However, groups of cellular genes that were altered in expression specifically in the absence of the E1B protein were identified by consensus k-means clustering of the hybridization data. Statistical analysis of the enrichment of genes associated with specific functions in these clusters established that the E1B 55-kDa protein is necessary for repression of genes encoding proteins that mediate antiviral and immune defenses.
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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.