ArticleOncogene2008
Adenovirus type 5 early region 1B 55-kDa oncoprotein can promote cell transformation by a mechanism independent from blocking p53-activated transcription.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Metaproteomic profiling reveals viral proteins and associated host proteomic alterations in glioblastoma.Scientific reports · 2026Article
- Differential oligomerization regulates PHF13 chromatin affinity and function.Nucleic acids research · 2025Article
- Adenovirus E1B-55K controls SUMO-dependent degradation of antiviral cellular restriction factors.Journal of virology · 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
- Article
- Human Kinase/Phosphatase-Wide RNAi Screening Identified Checkpoint Kinase 2 as a Cellular Factor Facilitating Japanese Encephalitis Virus Infection.Frontiers in cellular and infection microbiology · 2018Article
- Sp100A is a tumor suppressor that activates p53-dependent transcription and counteracts E1A/E1B-55K-mediated transformation.Oncogene · 2016Article
- PML isoforms IV and V contribute to adenovirus-mediated oncogenic transformation by functionally inhibiting the tumor-suppressor p53.Oncogene · 2016Article
- Adenovirus replaces mitotic checkpoint controls.Journal of virology · 2015Article
- E1B and E4 oncoproteins of adenovirus antagonize the effect of apoptosis inducing factor.Virology · 2014Article
- High-affinity Rb binding, p53 inhibition, subcellular localization, and transformation by wild-type or tumor-derived shortened Merkel cell polyomavirus large T antigens.Journal of virology · 2014Article
- Aggresome formation by the adenoviral protein E1B55K is not conserved among adenovirus species and is not required for efficient degradation of nuclear substrates.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
- Cross-talk between phosphorylation and SUMOylation regulates transforming activities of an adenoviral oncoprotein.Oncogene · 2013Article
- Article
- 2-aminopurine enhances the oncolytic activity of an E1b-deleted adenovirus in hepatocellular carcinoma cells.PloS one · 2013Article
- Adenovirus type 5 early region 1B 55K oncoprotein-dependent degradation of cellular factor Daxx is required for efficient transformation of primary rodent cells.Journal of virology · 2011Article
- SUMO modification of E1B-55K oncoprotein regulates isoform-specific binding to the tumour suppressor protein PML.Oncogene · 2010Article
- A proteomic approach to identify candidate substrates of human adenovirus E4orf6-E1B55K and other viral cullin-based E3 ubiquitin ligases.Journal of virology · 2009Article
- Viral manipulation of DNA repair and cell cycle checkpoints.DNA repair · 2009Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of p53-activated transcription is an integral part of the mechanism by which early region 1B 55K oncoprotein (E1B-55K) from adenovirus type 5 (Ad5) contributes to complete cell transformation in combination with Ad E1A. In addition, more recent data suggest that the mode of action of the Ad protein during transformation may involve additional functions and other protein interactions. In the present study, we performed a comprehensive mutational analysis to assign further transforming functions of Ad5 E1B-55K to distinct domains within the viral polypeptide. Results from these studies show that the functions required for transformation are encoded within several patches of the 55K primary sequence, including several clustered cysteine and histidine residues, some of which match the consensus for zinc fingers. In addition, two amino-acid substitutions (C454S/C456S) created a 55K mutant protein, which had substantially reduced transforming activity. Interestingly, the same mutations neither affected binding to p53 nor inhibition of p53-mediated transactivation. Therefore, an activity necessary for efficient transformation of primary rat cells can be separated from functions required for inhibition of p53-stimulated transcription. Our data indicate that this activity is linked to the ability of the Ad5 protein to bind to components of the Mre11/Rad50/NBS1 DNA double-strand break repair complex, and/or its ability to assemble multiprotein aggregates in the cytoplasm and nucleus of transformed rat cells. These results introduce a new function for Ad5 E1B-55K and suggest that the viral protein contributes to cell transformation through p53 transcription-dependent and -independent pathways.
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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.