ArticleJournal of virology2009
The minimum replication origin of merkel cell polyomavirus has a unique large T-antigen loading architecture and requires small T-antigen expression for optimal replication.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
What it found
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Who cites it
97 citing papers in PubMed, 155 citations in OpenAlex.
- Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses.Journal of virology · 2026Review
- Molecular analysis of the interaction between ubiquitin-specific protease 7 and large T antigen of Merkel cell polyomavirus.Journal of microbiology (Seoul, Korea) · 2026Article
- 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
- Kit-mediated autophagy suppression driven by a viral oncoprotein emerges as a crucial survival mechanism in Merkel cell carcinoma.Autophagy · 2025Article
- 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
- JC virus small tumor antigen promotes S phase entry and cell cycle progression.Tumour virus research · 2024Article
- Review
- Polyomavirus ALTOs, but not MTs, downregulate viral early gene expression by activating the NF-κB pathway.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling.PLoS pathogens · 2024Article
- Iron‑sulfur clusters in viral proteins: Exploring their elusive nature, roles and new avenues for targeting infections.Biochimica et biophysica acta. Molecular cell research · 2024Review
- Polyomavirus ALTOs, but not MTs, downregulate viral early gene expression by activating the NF-κB pathway.bioRxiv : the preprint server for biology · 2024Article
- Merkel cell carcinoma: updates in tumor biology, emerging therapies, and preclinical models.Frontiers in oncology · 2024Review
- Membrane-bound Merkel cell polyomavirus middle T protein constitutively activates PLCγ1 signaling through Src-family kinases.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities.Molecular pharmaceutics · 2023Review
- Characterization of molecular mechanisms driving Merkel cell polyomavirus oncogene transcription and tumorigenic potential.PLoS pathogens · 2023Article
- Unlicensed origin DNA melting by MCV and SV40 polyomavirus LT proteins is independent of ATP-dependent helicase activity.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Merkel cell polyomavirus small T antigen is a viral transcription activator that is essential for viral genome maintenance.PLoS pathogens · 2022Article
- Review
- Merkel cell polyomavirus and associated Merkel cell carcinoma.Tumour virus research · 2022Review
37 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
7 authors at 2 institutions in 1 country.
Funding
Abstract
Merkel cell polyomavirus (MCV) is a recently discovered human polyomavirus causing the majority of human Merkel cell carcinomas. We mapped a 71-bp minimal MCV replication core origin sufficient for initiating eukaryotic DNA replication in the presence of wild-type MCV large T protein (LT). The origin includes a poly(T)-rich tract and eight variably oriented, GAGGC-like pentanucleotide sequences (PS) that serve as LT recognition sites. Mutation analysis shows that only four of the eight PS are required for origin replication. A single point mutation in one origin PS from a naturally occurring, tumor-derived virus reduces LT assembly on the origin and eliminates viral DNA replication. Tumor-derived LT having mutations truncating either the origin-binding domain or the helicase domain also prevent LT-origin assembly. Optimal MCV replication requires coexpression of MCV small T protein (sT), together with LT. An intact DnaJ domain on the LT is required for replication but is dispensable on the sT. In contrast, PP2A targeting by sT is required for enhanced replication. The MCV origin provides a novel model for eukaryotic replication from a defined DNA element and illustrates the selective pressure within tumors to abrogate independent MCV replication.
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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.