ArticleJournal of virology2004
E1B-55-kilodalton protein is not required to block p53-induced transcription during adenovirus infection.
Article in Journal of virology, 2004. 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, 41 citations in OpenAlex.
- 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
- Combining Oncolytic Virotherapy with p53 Tumor Suppressor Gene Therapy.Molecular therapy oncolytics · 2017Review
- 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
- 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
- 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 repression domain of the E1B 55-kilodalton protein participates in countering interferon-induced inhibition of adenovirus replication.Journal of virology · 2013Article
- Molecular basis for viral selective replication in cancer cells: activation of CDK2 by adenovirus-induced cyclin E.PloS one · 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
- 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
- Inhibition of p53 by adenovirus type 12 E1B-55K deregulates cell cycle control and sensitizes tumor cells to genotoxic agents.Journal of virology · 2011Article
- Infection with E1B-mutant adenovirus stabilizes p53 but blocks p53 acetylation and activity through E1A.Oncogene · 2011Article
- Targeting of p53-transcriptional dysfunction by conditionally replicating adenovirus is not limited by p53-homologues.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
- alpha-Tocopheryl succinate and derivatives mediate the transcriptional repression of androgen receptor in prostate cancer cells by targeting the PP2A-JNK-Sp1-signaling axis.Carcinogenesis · 2009Article
- Adenovirus E1B 55-kilodalton protein: multiple roles in viral infection and cell transformation.Journal of virology · 2009Review
- The adenoviral E1B 55-kilodalton protein controls expression of immune response genes but not p53-dependent transcription.Journal of virology · 2009Article
- Article
- Adenovirus E1B55K region is required to enhance cyclin E expression for efficient viral DNA replication.Journal of virology · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adenovirus E1B-55-kDa protein binds and inactivates the tumor suppressor protein p53. However, the role of this interaction during infection is still poorly understood and was therefore examined here. Infection with a virus carrying the E1B-55-kDa mutation R239A, preventing the interaction with p53, led to the accumulation of p53. However, p53 target genes were not activated in the infected cells, although p53 phosphorylation did occur and the p53 antagonists Mdm2 and deltaNp73 did not accumulate. Deletion of E4orf6, alone or in combination with E1B-55-kDa, did not allow the induction of p53-responsive genes either. In transient reporter assays, the viral E1A-13S protein antagonized p53 activity; mutational analysis suggested that this depends partially on p300 binding, but it depends even more strongly on the interaction of E1A with the p400/TRRAP protein complex. However, viruses expressing E1A mutants lacking these binding activities, in combination with E1B-55-kDa R239A, still abolished p53 activity. In contrast, when the mutation of E1B-55-kDa at R239A was combined with a deletion of the apoptosis inhibitor E1B-19-kDa, infected cells showed more extensive apoptosis than after infection with single mutants, suggesting that accumulated p53, albeit transcriptionally inactive, might nonetheless enhance apoptosis. Despite extensive apoptosis of the infected cells, the deletion of E1B-19-kDa, in combination with the E1B-55-kDa mutation or in the presence of the constitutively active p53 mutant p53mt24-28, reduced virus replication less than fivefold. In conclusion, adenovirus does not need direct binding of E1B-55-kDa to inactivate p53, and forced p53 activity with consecutive apoptosis does not severely impair virus replication.
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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.