ArticleOncogene2005
Blockage of CRM1-dependent nuclear export of the adenovirus type 5 early region 1B 55-kDa protein augments oncogenic transformation of primary rat cells.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Viral Subversion of the Chromosome Region Maintenance 1 Export Pathway and Its Consequences for the Cell Host.Viruses · 2023Review
- 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
- Conserved E1B-55K SUMOylation in Different Human Adenovirus Species Is a Potent Regulator of Intracellular Localization.Journal of virology · 2022Article
- E1B-55K-Mediated Regulation of RNF4 SUMO-Targeted Ubiquitin Ligase Promotes Human Adenovirus Gene Expression.Journal of virology · 2018Article
- Normal human cell proteins that interact with the adenovirus type 5 E1B 55kDa protein.Virology · 2017Article
- Efficient Transformation of Primary Human Mesenchymal Stromal Cells by Adenovirus Early Region 1 Oncogenes.Journal of virology · 2017Article
- Sp100A is a tumor suppressor that activates p53-dependent transcription and counteracts E1A/E1B-55K-mediated transformation.Oncogene · 2016Article
- KAP1 Is a Host Restriction Factor That Promotes Human Adenovirus E1B-55K SUMO Modification.Journal of virology · 2016Article
- PML isoforms IV and V contribute to adenovirus-mediated oncogenic transformation by functionally inhibiting the tumor-suppressor p53.Oncogene · 2016Article
- Impact of the adenoviral E4 Orf3 protein on the activity and posttranslational modification of p53.Journal of virology · 2015Article
- Sp100 isoform-specific regulation of human adenovirus 5 gene expression.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
- The adenoviral oncogene E1A-13S interacts with a specific isoform of the tumor suppressor PML to enhance viral transcription.Journal of virology · 2013Article
- Timely synthesis of the adenovirus type 5 E1B 55-kilodalton protein is required for efficient genome replication in normal human cells.Journal of virology · 2012Article
- Human pathogens and the host cell SUMOylation system.Journal of virology · 2012Review
- The human adenovirus type 5 E1B 55 kDa protein obstructs inhibition of viral replication by type I interferon in normal human cells.PLoS pathogens · 2012Article
- 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
- Role of the RNA recognition motif of the E1B 55 kDa protein in the adenovirus type 5 infectious cycle.Virology · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 55-kDa gene product from subgroup C adenovirus type 5 (Ad5) early region 1 (E1B-55kDa) plays a central role in the oncogenic transformation of primary rodent cells primarily by inactivating transcriptional and presumably other functional properties of the tumor suppressor protein p53. We have previously shown that Ad5 E1B-55kDa possesses a leucine-rich nuclear export signal (NES), which confers rapid nucleocytoplasmic shuttling via the CRM1-dependent export pathway. In this study we report that an export-deficient mutant of the viral protein (E1B-NES) substantially enhances focus formation of primary baby rat kidney cells in combination with Ad E1A. Transformed rat cells stably expressing the E1B-NES protein exhibited increased tumorigenicity and accelerated tumor growth in nude mice compared to transformants containing the wild-type E1B product. This 'gain of function' correlated with enhanced inhibition of p53 transactivation in transient reporter assays and the accumulation of the mutant protein and p53 in several dot-like subnuclear aggregates. Interestingly, these structures also contained a large fraction of cellular promyelocytic leukemia protein (PML), a known regulator of p53. These data indicate that E1B-NES promotes oncogenic transformation by combinatorial mechanisms that involve modulation of p53 in the context of PML nuclear bodies. In sum, these results extend our previous observation that inhibition of PML activities by E1B-55kDa is required for efficient focus formation and provide further support for the view that blocking p53 transcriptional functions is the principal mechanism by which the Ad protein contributes to complete cell transformation in conjunction with Ad E1A.
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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.