ArticleOncogene2007
Polyomavirus small T antigen transactivates genes by its ability to provoke the synthesis and the stabilization of MYC.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- EZH2-Myc Hallmark in Oncovirus/Cytomegalovirus Infections and Cytomegalovirus' Resemblance to Oncoviruses.Cells · 2024Review
- Sustained AMPK Activation and Proline Metabolism Play Critical Roles in the Survival of Matrix-Deprived Transformed Cells.Frontiers in cell and developmental biology · 2021Article
- Human Polyomaviruses: The Battle of Large and Small Tumor Antigens.Virology : research and treatment · 2017Review
- Comparisons between murine polyomavirus and Simian virus 40 show significant differences in small T antigen function.Journal of virology · 2011Article
- Simian virus 40 small T antigen activates AMPK and triggers autophagy to protect cancer cells from nutrient deprivation.Journal of virology · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA tumor viruses are capable of driving quiescent cells into the cell cycle. In case of polyomaviridae, two viral proteins, the large and the small (ST) T antigens are responsible for this outcome. ST interacts with the protein phosphatase PP2A and with chaperons of the dnaK type and leads to the transactivation of several genes, which play a role in S-phase induction. One of these is the transcription factor myelocytomatosis (MYC), which by itself is an important regulator of growth. Microarray analysis has revealed several ST-induced genes, which are also targets of MYC; hence, ST may induce these genes via MYC. Experiments shown here are in line with this assumption. MYC-regulated genes are induced by ST at later times than MYC and a MYC responsive promoter is stimulated by ST. Regulation of MYC occurs through signal transduction pathways, which are co-ordinated by PP2A suggesting that they may be targets of ST. Here, we show that this is the case as important kinases involved in these pathways appear in the active phosphorylated form in the presence of ST. Inhibition of these kinases interferes with MYC induction and inhibition of MYC activity blocks ST-mediated transactivation.
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Registered trials
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