ArticleOncogene2011
Infection with E1B-mutant adenovirus stabilizes p53 but blocks p53 acetylation and activity through E1A.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 19 citations in OpenAlex.
- The multilayered control of acetylation during adenovirus-based immunotherapy of cancer.Molecular therapy. Oncology · 2025Review
- Histone deacetylase-2 controls IL-1β production through the regulation of NLRP3 expression and activation in tuberculosis infection.iScience · 2022Article
- Histone modifiers at the crossroads of oncolytic and oncogenic viruses.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
- Lysine-specific post-translational modifications of proteins in the life cycle of viruses.Cell cycle (Georgetown, Tex.) · 2019Review
- Methods for characterizing protein acetylation during viral infection.Methods in enzymology · 2019Article
- Orchestration of protein acetylation as a toggle for cellular defense and virus replication.Nature communications · 2018Article
- The effects of AICAR and rapamycin on mitochondrial function in immortalized mitochondrial DNA mutator murine embryonic fibroblasts.Biology open · 2018Article
- Adenovirus-based strategies enhance antitumor capability through p53-mediated downregulation of MGMT in uveal melanoma.Cancer biology & therapy · 2017Article
- A p53-independent apoptotic mechanism of adenoviral mutant E1A was involved in its selective antitumor activity for human cancer.Oncotarget · 2016Article
- Impact of the adenoviral E4 Orf3 protein on the activity and posttranslational modification of p53.Journal of virology · 2015Article
- Article
- Acetylation is indispensable for p53 antiviral activity.Cell cycle (Georgetown, Tex.) · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wild-type adenovirus type 5 eliminates p53 through the E1B-55kDa and E4-34kDa gene products. Deletion or mutation of E1B-55kDa has long been thought to confer p53-selective replication of oncolytic viruses. We show here that infection with E1B-defective adenovirus mutants induces massive accumulation of p53, without obvious defects in p53 localization, phosphorylation, conformation and oligomerization. Nonetheless, p53 completely failed to induce its target genes in this scenario, for example, p21/CDKN1A, Mdm2 and PUMA. Two regions of the E1A gene products independently contributed to the suppression of p21 transcription. Depending on the E1A conserved region 3, E1B-defective adenovirus impaired the ability of the transcription factor Sp1 to bind the p21 promoter. Moreover, the amino terminal region of E1A, binding the acetyl transferases p300 and CREB-binding protein, blocked p53 K382 acetylation in infected cells. Mutating either of these E1A regions, in addition to E1B, partially restored p21 mRNA levels. Our findings argue that adenovirus attenuates p53-mediated p21 induction, through at least two E1B-independent mechanisms. Other virus species and cancer cells may employ analogous strategies to impair p53 activity.
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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.