ArticleJournal of virology2008
pRB-E2F1 complexes are resistant to adenovirus E1A-mediated disruption.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- The R2TP complex stabilises E7 to drive human papillomavirus-mediated pathogenesis in cellular models of cervical cancer.Virology journal · 2026Article
- Targeting Cell Cycle Facilitates E1A-Independent Adenoviral Replication.Journal of virology · 2023Article
- RB1 loss triggers dependence on ESRRG in retinoblastoma.Science advances · 2022Article
- The retinoblastoma tumor suppressor promotes efficient human cytomegalovirus lytic replication.Journal of virology · 2015Article
- Review
- A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene-targeted mice.Molecular and cellular biology · 2014Article
- Molecular mechanisms underlying RB protein function.Nature reviews. Molecular cell biology · 2013Review
- E2F1 mediated apoptosis induced by the DNA damage response is blocked by EBV nuclear antigen 3C in lymphoblastoid cells.PLoS pathogens · 2012Article
- Opposing oncogenic activities of small DNA tumor virus transforming proteins.Trends in microbiology · 2011Review
- An overlapping kinase and phosphatase docking site regulates activity of the retinoblastoma protein.Nature structural & molecular biology · 2010Article
- A cancer derived mutation in the retinoblastoma gene with a distinct defect for LXCXE dependent interactions.Cancer cell international · 2010Article
- Cellular mechanisms of tumour suppression by the retinoblastoma gene.Nature reviews. Cancer · 2008Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruption of pRB-E2F interactions by E1A is a key event in the adenoviral life cycle that drives expression of early viral transcription and induces cell cycle progression. This function of E1A is complicated by E2F1, an E2F family member that controls multiple processes besides proliferation, including apoptosis and DNA repair. Recently, a second interaction site in pRB that only contacts E2F1 has been discovered, allowing pRB to control proliferation separately from other E2F1-dependent activities. Based on this new insight into pRB-E2F1 regulation, we investigated how E1A affects control of E2F1 by pRB. Our data reveal that pRB-E2F1 interactions are resistant to E1A-mediated disruption. Using mutant forms of pRB that selectively force E2F1 to bind through only one of the two binding sites on pRB, we determined that E1A is unable to disrupt E2F1's unique interaction with pRB. Furthermore, analysis of pRB-E2F complexes during adenoviral infection reveals the selective maintenance of pRB-E2F1 interactions despite the presence of E1A. Our experiments also demonstrate that E2F1 functions to maintain cell viability in response to E1A expression. This suggests that adenovirus E1A's seemingly complex mechanism of disrupting pRB-E2F interactions provides selectivity in promoting viral transcription and cell cycle advancement, while maintaining cell viability.
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Registered trials
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.