ArticleOncogene2008
The transcription-repression domain of the adenovirus E1A oncoprotein targets p300 at the promoter.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 19 citations in OpenAlex.
- Dynamic Phosphorylation of G9a Regulates its Repressive Activity on Chromatin Accessibility and Mitotic Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
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- The adenoviral E1A N-terminal domain represses MYC transcription in human cancer cells by targeting both p300 and TRRAP and inhibiting MYC promoter acetylation of H3K18 and H4K16.Genes & cancer · 2016Article
- Intrinsically disordered proteins in cellular signalling and regulation.Nature reviews. Molecular cell biology · 2015Review
- The adenovirus E1A oncoprotein N-terminal transcriptional repression domain enhances p300 autoacetylation and inhibits histone H3 Lys18 acetylation.Genes & cancer · 2015Article
- Article
- Distribution and dynamics of transcription-associated proteins during parvovirus infection.Journal of virology · 2012Article
- The adenovirus E1A N-terminal repression domain represses transcription from a chromatin template in vitro.Virology · 2012Article
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- Transcriptional tools: Small molecules for modulating CBP KIX-dependent transcriptional activators.Biopolymers · 2011Article
- Structural basis for subversion of cellular control mechanisms by the adenoviral E1A oncoprotein.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Viral manipulation of the host epigenome for oncogenic transformation.Nature reviews. Genetics · 2009Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Extensive mutational/functional analysis of the transcription-repression domain encoded in the N-terminal 80 amino acids of the adenovirus E1A 243R oncoprotein suggests a model for the molecular mechanism of E1A repression: E1A accesses transcriptional co-activators such as p300 on specific promoters and then interacts with TBP to disrupt the TBP-TATA complex. In support of this model, as reported here, a basal core promoter activated by tethering p300 is repressible by E1A at the promoter level as shown by chromatin immunoprecipitation (ChIP) analysis. Sequestration of p300 by E1A does not play a significant role, as indicated by dose-response measurements. Furthermore, when the core promoter is transcriptionally activated by tethering activation domains of several transcription factors that can recruit p300 (p65, MyoD, cMyb and TFE3), transcription is repressible by E1A. However, when the core promoter is activated by factors not known to recruit p300 (USF1 and USF2), transcription is resistant to E1A repression. Finally, tethering p300 to the non-repressible adenovirus major late promoter (MLP) renders it repressible by E1A. ChIP analysis shows that E1A occupies the repressed MLP. These findings provide support for the hypothesis that p300 can serve as a scaffold for the E1A repression domain to access specific cellular gene promoters involved in growth regulation.
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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.