ArticleThe Journal of clinical investigation2011
Human Merkel cell polyomavirus small T antigen is an oncoprotein targeting the 4E-BP1 translation regulator.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 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.
The trial behind it
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
214 citing papers in PubMed, 372 citations in OpenAlex.
- Merkel Cell Polyomavirus and DNA Damage Response.International journal of molecular sciences · 2026Review
- An immunocompetent model of MCPyV-driven Merkel cell carcinoma reveals tumor evolution under immune selection.bioRxiv : the preprint server for biology · 2026Article
- Article
- Response of B Cells Specific for Polyomavirus-Derived Oncoprotein Is Predictive of Merkel Cell Carcinoma Tumor Control.Cancer immunology research · 2026Article
- Variable A-type lamin expression in Merkel cell carcinoma cell lines and its association with nuclear integrity.Scientific reports · 2026Article
- Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses.Journal of virology · 2026Review
- In vitro evaluation of bidirectional transcription levels of five types of non-coding control regions of Merkel cell polyomavirus.Virology journal · 2025Article
- MCPyV small T antigen enhances HPV16 oncogene expression, promotes Ca Ski cell proliferation, and reduces 5-fluorouracil-induced apoptosis in cervical cancer cells.Infectious medicine · 2025Article
- Review
- Kit-mediated autophagy suppression driven by a viral oncoprotein emerges as a crucial survival mechanism in Merkel cell carcinoma.Autophagy · 2025Article
- Article
- Review
- Small T Oncoprotein of Merkel Cell Polyomavirus Attenuates Cisplatin-Induced Apoptosis and Enhances E1, E6/E7, MMP-1, and Ki-67 Expression in HeLa Cervical Cancer Cells.Advanced pharmaceutical bulletin · 2025Article
- High-throughput screening identifies Aurora kinase B as a critical therapeutic target for Merkel cell carcinoma.Nature communications · 2025Article
- A Landscape of Cancer Initiation and Cancer Stem Cells.Cancers · 2025Article
- The pathogen's playbook in cancer: from oncogenesis to progression.Frontiers in oncology · 2025Review
- Merkel cell polyomavirus in lung carcinogenesis: evidence and controversy.Frontiers in oncology · 2025Review
- JC virus small tumor antigen promotes S phase entry and cell cycle progression.Tumour virus research · 2024Article
- Merkel Cell Polyomavirus targets SET/PP2A complex to promote cellular proliferation and migration.Virology · 2024Article
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
154 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Merkel cell polyomavirus (MCV) is the recently discovered cause of most Merkel cell carcinomas (MCCs), an aggressive form of nonmelanoma skin cancer. Although MCV is known to integrate into the tumor cell genome and to undergo mutation, the molecular mechanisms used by this virus to cause cancer are unknown. Here, we show that MCV small T (sT) antigen is expressed in most MCC tumors, where it is required for tumor cell growth. Unlike the closely related SV40 sT, MCV sT transformed rodent fibroblasts to anchorage- and contact-independent growth and promoted serum-free proliferation of human cells. These effects did not involve protein phosphatase 2A (PP2A) inhibition. MCV sT was found to act downstream in the mammalian target of rapamycin (mTOR) signaling pathway to preserve eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) hyperphosphorylation, resulting in dysregulated cap-dependent translation. MCV sT-associated 4E-BP1 serine 65 hyperphosphorylation was resistant to mTOR complex (mTORC1) and mTORC2 inhibitors. Steady-state phosphorylation of other downstream Akt-mTOR targets, including S6K and 4E-BP2, was also increased by MCV sT. Expression of a constitutively active 4E-BP1 that could not be phosphorylated antagonized the cell transformation activity of MCV sT. Taken together, these experiments showed that 4E-BP1 inhibition is required for MCV transformation. Thus, MCV sT is an oncoprotein, and its effects on dysregulated cap-dependent translation have clinical implications for the prevention, diagnosis, and treatment of MCV-related cancers.
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What OpenQuestion holds
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.