ArticleProceedings of the National Academy of Sciences of the United States of America2023
The human adenovirus E1B-55K oncoprotein coordinates cell transformation through regulation of DNA-bound host transcription factors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- The adenovirus oncoprotein E1B-55K reshapes epigenetic histone modifications in primary human cells.mBio · 2026Article
- Adenovirus E1B-55K regulates p53-dependent and -independent gene expression during infection.PLoS pathogens · 2025Article
- Establishment of a novel cell line for producing replication-competent adenovirus-free adenoviruses.BMC biotechnology · 2024Article
- Cellular SUMO-specific proteases regulate HAdV-C5 E1B-55K SUMOylation and virus-induced cell transformation.Frontiers in cellular and infection microbiology · 2024Article
- Identification of Adenovirus E1B-55K Interaction Partners through a Common Binding Motif.Viruses · 2023Article
- 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
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The multifunctional adenovirus E1B-55K oncoprotein can induce cell transformation in conjunction with adenovirus E1A gene products. Previous data from transient expression studies and in vitro experiments suggest that these growth-promoting activities correlate with E1B-55K-mediated transcriptional repression of p53-targeted genes. Here, we analyzed genome-wide occupancies and transcriptional consequences of species C5 and A12 E1B-55Ks in transformed mammalian cells by combinatory ChIP and RNA-seq analyses. E1B-55K-mediated repression correlates with tethering of the viral oncoprotein to p53-dependent promoters via DNA-bound p53. Moreover, we found that E1B-55K also interacts with and represses transcription of numerous p53-independent genes through interactions with transcription factors that play central roles in cancer and stress signaling. Our results demonstrate that E1B-55K oncoproteins function as promiscuous transcriptional repressors of both p53-dependent and -independent genes and further support the model that manipulation of cellular transcription is central to adenovirus-induced cell transformation and oncogenesis.
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