ArticleMolecular and cellular biology1999
Corepressor required for adenovirus E1B 55,000-molecular-weight protein repression of basal transcription.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- Adenovirus E1B-55K regulates p53-dependent and -independent gene expression during infection.PLoS pathogens · 2025Article
- Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.Tumour virus research · 2025Review
- 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
- ATO (Arsenic Trioxide) Effects on Promyelocytic Leukemia Nuclear Bodies Reveals Antiviral Intervention Capacity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Normal human cell proteins that interact with the adenovirus type 5 E1B 55kDa protein.Virology · 2017Article
- 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
- Cross-talk between phosphorylation and SUMOylation regulates transforming activities of an adenoviral oncoprotein.Oncogene · 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
- 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
- Inhibition of p53 by adenovirus type 12 E1B-55K deregulates cell cycle control and sensitizes tumor cells to genotoxic agents.Journal of virology · 2011Article
- Adenovirus E1B 55-kilodalton protein is a p53-SUMO1 E3 ligase that represses p53 and stimulates its nuclear export through interactions with promyelocytic leukemia nuclear bodies.Journal of virology · 2010Article
- SUMO modification of E1B-55K oncoprotein regulates isoform-specific binding to the tumour suppressor protein PML.Oncogene · 2010Article
- 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
- Adenovirus type 5 early region 1B 156R protein promotes cell transformation independently of repression of p53-stimulated transcription.Journal of virology · 2007Article
- Adenovirus type 5 exerts genome-wide control over cellular programs governing proliferation, quiescence, and survival.Genome biology · 2007Article
- Recent lessons in gene expression, cell cycle control, and cell biology from adenovirus.Oncogene · 2005Review
- Viruses - seeking and destroying the tumor program.Oncogene · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Adenovirus E1B 55,000-molecular-weight protein (55K) binds to host cell p53, stabilizing it, greatly increasing its affinity for its cognate DNA-binding site, and converting it from a regulated activator to a constitutive repressor. Here we analyzed the mechanism of repression by the p53-E1B 55K complex. E1B 55K repression requires that 55K be tethered to the promoter by binding directly to DNA-bound p53. Transcription from an assembled, p53-activated preinitiation complex was not repressed by the subsequent addition of E1B 55K, suggesting that either sites of 55K interaction with p53 or targets of 55K in the preinitiation complex are blocked. Specific E1B 55K repression was observed in reactions lacking TFIIA and with recombinant TATA-binding protein in place of TFIID, conditions under which p53 does not activate transcription. Thus, E1B 55K does not simply inhibit a p53-specific activation mechanism but rather blocks basal transcription. As a consequence, E1B 55K may repress transcription from any promoter with an associated p53-binding site, no matter what other activators associate with the promoter. E1B 55K did not repress basal transcription in reactions with recombinant and highly purified general transcription factors and RNA polymerase II but rather required a corepressor that copurifies with the polymerase.
Indexed as
Identifiers
What OpenQuestion holds
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.