ArticleJournal of virology2007
A new crucial protein interaction element that targets the adenovirus E4-ORF1 oncoprotein to membrane vesicles.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- The human adenovirus PI3K-Akt activator E4orf1 is targeted by the tumor suppressor p53.Journal of virology · 2024Article
- E4orf1 SuppressesVaccines · 2022Article
- Intracellular trafficking of adeno-associated virus (AAV) vectors: challenges and future directions.Gene therapy · 2021Review
- Review
- Viral PDZ Binding Motifs Influence Cell Behavior Through the Interaction with Cellular Proteins Containing PDZ Domains.Methods in molecular biology (Clifton, N.J.) · 2021Review
- Characterization of the adipogenic protein E4orf1 from adenovirus 36 through an in silico approach.Journal of molecular modeling · 2020Article
- Review
- Molecular Evolution of Human Adenovirus (HAdV) Species C.Scientific reports · 2019Article
- Tissue-specific endothelial cells: a promising approach for augmentation of soft tissue repair in orthopedics.Annals of the New York Academy of Sciences · 2017Review
- Hepatic Expression of Adenovirus 36 E4ORF1 Improves Glycemic Control and Promotes Glucose Metabolism Through AKT Activation.Diabetes · 2017Article
- Herpesviruses dUTPases: A New Family of Pathogen-Associated Molecular Pattern (PAMP) Proteins with Implications for Human Disease.Pathogens (Basel, Switzerland) · 2016Review
- Adenovirus Protein E4-ORF1 Activation of PI3 Kinase Reveals Differential Regulation of Downstream Effector Pathways in Adipocytes.Cell reports · 2016Article
- Targeted Gene Resequencing (Astrochip) to Explore the Tripartite Synapse in Autism-Epilepsy Phenotype with Macrocephaly.Neuromolecular medicine · 2016Article
- Viral Interactions with PDZ Domain-Containing Proteins-An Oncogenic Trait?Pathogens (Basel, Switzerland) · 2016Review
- Adenovirus E4-ORF1 Dysregulates Epidermal Growth Factor and Insulin/Insulin-Like Growth Factor Receptors To Mediate Constitutive Myc Expression.Journal of virology · 2015Article
- Hijacking Dlg1 for oncogenic phosphatidylinositol 3-kinase activation in human epithelial cells is a conserved mechanism of human adenovirus E4-ORF1 proteins.Journal of virology · 2014Article
- The human adenovirus E4-ORF1 protein subverts discs large 1 to mediate membrane recruitment and dysregulation of phosphatidylinositol 3-kinase.PLoS pathogens · 2014Article
- Adenovirus E4ORF1-induced MYC activation promotes host cell anabolic glucose metabolism and virus replication.Cell metabolism · 2014Article
- Metabolism goes viral.Cell metabolism · 2014Article
- Human herpesviruses-encoded dUTPases: a family of proteins that modulate dendritic cell function and innate immunity.Frontiers in microbiology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Human adenovirus type 9 exclusively elicits mammary tumors in experimental animals, and the primary oncogenic determinant of this virus is the E4-ORF1 oncogene, as opposed to the well-known E1A and E1B oncogenes. The tumorigenic potential of E4-ORF1, as well as its ability to oncogenically stimulate phosphatidylinositol 3-kinase (PI3K), depends on a carboxyl-terminal PDZ domain-binding motif (PBM) that mediates interactions with several different membrane-associated cellular PDZ proteins, including MUPP1, PATJ, MAGI-1, ZO-2, and Dlg1. Nevertheless, because certain E4-ORF1 mutations that alter neither the sequence nor the function of the PBM abolish E4-ORF1-induced PI3K activation and cellular transformation, we reasoned that E4-ORF1 must possess an additional crucial protein element. In the present study, we identified seven E4-ORF1 amino acid residues that define this new element, designated domain 2, and showed that it mediates binding to a 70-kDa cellular phosphoprotein. We also discovered that domain 2 or the PBM independently promotes E4-ORF1 localization to cytoplasmic membrane vesicles and that this activity of domain 2 depends on E4-ORF1 trimerization. Consistent with the latter observation, molecular-modeling analyses predicted that E4-ORF1 trimerization brings together six out of seven domain 2 residues at each of the three subunit interfaces. These findings importantly demonstrate that PI3K activation and cellular transformation induced by E4-ORF1 require two separate protein interaction elements, domain 2 and the PBM, each of which targets E4-ORF1 to vesicle membranes in cells.
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