ArticleProceedings of the National Academy of Sciences of the United States of America2009
Structural basis for subversion of cellular control mechanisms by the adenoviral E1A oncoprotein.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 133 citations in OpenAlex.
- Review
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- Identification of a novel, pathogenicFrontiers in genetics · 2025Article
- The effect of phosphorylation efficiency on the oncogenic properties of the protein E7 from high-risk HPV.Virus research · 2024Article
- Expanding the Landscape of Amyloid Sequences with CARs-DB: A Database of Polar Amyloidogenic Peptides from Disordered Proteins.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Adenovirus E1A binding to DCAF10 targets proteasomal degradation of RUVBL1/2 AAA+ ATPases required for quaternary assembly of multiprotein machines, innate immunity, and responses to metabolic stress.Journal of virology · 2023Article
- TAZ2 truncation confers overactivation of p300 and cellular vulnerability to HDAC inhibition.Nature communications · 2023Article
- Epigenetic mechanisms to propagate histone acetylation by p300/CBP.Nature communications · 2023Article
- Vital for Viruses: Intrinsically Disordered Proteins.Journal of molecular biology · 2023Review
- Structural insights into p300 regulation and acetylation-dependent genome organisation.Nature communications · 2022Article
- Recognizing the Binding Pattern and Dissociation Pathways of the p300 Taz2-p53 TAD2 Complex.JACS Au · 2022Article
- Conformational buffering underlies functional selection in intrinsically disordered protein regions.Nature structural & molecular biology · 2022Article
- Insights into a Cancer-Target Demethylase: Substrate Prediction through Systematic Specificity Analysis for KDM3A.Biomolecules · 2022Article
- Disruption of NBS1/MRN Complex Formation by E4orf3 Supports NF-κB That Licenses E1B55K-Deleted Adenovirus-Infected Cells to Accumulate DNA>4n.Microbiology spectrum · 2022Article
- Transactivation domain of Adenovirus Early Region 1A (E1A): Investigating folding dynamics and aggregation.Current research in structural biology · 2022Article
- Characterization of the High-Affinity Fuzzy Complex between the Disordered Domain of the E7 Oncoprotein from High-Risk HPV and the TAZ2 Domain of CBP.Biochemistry · 2021Article
- Synergies of Single Molecule Fluorescence and NMR for the Study of Intrinsically Disordered Proteins.Biomolecules · 2021Review
- NMR illuminates intrinsic disorder.Current opinion in structural biology · 2021Review
- Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The adenovirus early region 1A (E1A) oncoprotein mediates cell transformation by deregulating host cellular processes and activating viral gene expression by recruitment of cellular proteins that include cyclic-AMP response element binding (CREB) binding protein (CBP)/p300 and the retinoblastoma protein (pRb). While E1A is capable of independent interaction with CBP/p300 or pRb, simultaneous binding of both proteins is required for maximal biological activity. To obtain insights into the mechanism by which E1A hijacks the cellular transcription machinery by competing with essential transcription factors for binding to CBP/p300, we have determined the structure of the complex between the transcriptional adaptor zinc finger-2 (TAZ2) domain of CBP and the conserved region-1 (CR1) domain of E1A. The E1A CR1 domain is unstructured in the free state and upon binding folds into a local helical structure mediated by an extensive network of intermolecular hydrophobic contacts. By NMR titrations, we show that E1A efficiently competes with the N-terminal transactivation domain of p53 for binding to TAZ2 and that pRb interacts with E1A at 2 independent sites located in CR1 and CR2. We show that pRb and the CBP TAZ2 domain can bind simultaneously to the CR1 site of E1A to form a ternary complex and propose a structural model for the pRb:E1A:CBP complex on the basis of published x-ray data for homologous binary complexes. These observations reveal the molecular basis by which E1A inhibits p53-mediated transcriptional activation and provide a rationale for the efficiency of cellular transformation by the adenoviral E1A oncoprotein.
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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.