ArticleJournal of virology1999
Characterization of an E1A-CBP interaction defines a novel transcriptional adapter motif (TRAM) in CBP/p300.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 80 citations in OpenAlex.
- How to Inhibit Nuclear Factor-Kappa B Signaling: Lessons from Poxviruses.Pathogens (Basel, Switzerland) · 2022Review
- Molecular mimicry of NF-κB by vaccinia virus protein enables selective inhibition of antiviral responses.Nature microbiology · 2022Article
- Beta-Genus Human Papillomavirus 8 E6 Destabilizes the Host Genome by Promoting p300 Degradation.Viruses · 2021Review
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- Epigenetics and the dynamics of chromatin during adenovirus infections.FEBS letters · 2019Review
- High-Risk Human Papillomaviral Oncogenes E6 and E7 Target Key Cellular Pathways to Achieve Oncogenesis.International journal of molecular sciences · 2018Review
- Competitive Inhibition of Lysine Acetyltransferase 2B by a Small Motif of the Adenoviral Oncoprotein E1A.The Journal of biological chemistry · 2016Article
- De-acetylation and degradation of HSPA5 is critical for E1A metastasis suppression in breast cancer cells.Oncotarget · 2014Article
- Transcriptional/epigenetic regulator CBP/p300 in tumorigenesis: structural and functional versatility in target recognition.Cellular and molecular life sciences : CMLS · 2013Review
- The HTLV-1-encoded protein HBZ directly inhibits the acetyl transferase activity of p300/CBP.Nucleic acids research · 2012Article
- Acetylation modulates cellular distribution and DNA sensing ability of interferon-inducible protein IFI16.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Article
- Article
- 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
- The adenoviral E1A protein displaces corepressors and relieves gene repression by unliganded thyroid hormone receptors in vivo.Cell research · 2009Article
- Viral manipulation of the host epigenome for oncogenic transformation.Nature reviews. Genetics · 2009Review
- Intrinsic structural disorder in adenovirus E1A: a viral molecular hub linking multiple diverse processes.Journal of virology · 2008Review
- MOZ-TIF2 repression of nuclear receptor-mediated transcription requires multiple domains in MOZ and in the CID domain of TIF2.Molecular cancer · 2007Article
- Negative regulation of transcription coactivator p300 by orphan receptor TR3.Nucleic acids research · 2007Article
- The E6 protein of the cutaneous human papillomavirus type 8 can stimulate the viral early and late promoters by distinct mechanisms.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The adenovirus E1A protein subverts cellular processes to induce mitotic activity in quiescent cells. Important targets of E1A include members of the transcriptional adapter family containing CBP/p300. Competition for CBP/p300 binding by various cellular transcription factors has been suggested as a means of integrating different signalling pathways and may also represent a potential mechanism by which E1A manipulates cell fate. Here we describe the characterization of the interaction between E1A and the C/H3 region of CBP. We define a novel conserved 12-residue transcriptional adapter motif (TRAM) within CBP/p300 that represents the binding site for both E1A and numerous cellular transcription factors. We also identify a sequence (FPESLIL) within adenovirus E1A that is required to bind the CBP TRAM. Furthermore, an E1A peptide containing the FPESLIL sequence is capable of preventing the interaction between CBP and TRAM-binding transcription factors, such as p53, E2F, and TFIIB, thus providing a molecular model for E1A action. As an in vivo demonstration of this model, we used a small region of CBP containing a functional TRAM that can bind to the p53 protein. The CBP TRAM binds p53 sequences targeted by the cellular regulator MDM2, and we demonstrate that an MDM2-p53 interaction can be disrupted by the CBP TRAM, leading to stabilization of cellular p53 levels and the activation of p53-dependent transcription. Transcriptional activation of p53 by the CBP TRAM is abolished by wild-type E1A but not by a CBP-binding-deficient E1A mutant.
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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.