ArticleProceedings of the National Academy of Sciences of the United States of America2024
Polyomavirus ALTOs, but not MTs, downregulate viral early gene expression by activating the NF-κB pathway.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed.
- Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses.Journal of virology · 2026Review
- Review
- Molecular analysis of the interaction between ubiquitin-specific protease 7 and large T antigen of Merkel cell polyomavirus.Journal of microbiology (Seoul, Korea) · 2026Article
- A short intrinsically disordered domain of MCPyV ALTO regulates TBK1 signaling during MCPyV infection.Journal of virology · 2025Article
- E2F1-3 activate Merkel cell polyomavirus early transcription and replication.bioRxiv : the preprint server for biology · 2025Article
- Complete Genomes of DNA Viruses in Fecal Samples from Small Terrestrial Mammals in Spain.Viruses · 2024Article
- Novel polyomavirus in the endangered garden dormouse Eliomys quercinus.Virology journal · 2024Article
- 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
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Abstract
Polyomaviruses are small, circular dsDNA viruses that can cause cancer. Alternative splicing of polyomavirus early transcripts generates large and small tumor antigens (LT, ST) that play essential roles in viral replication and tumorigenesis. Some polyomaviruses also express middle tumor antigens (MTs) or alternate LT open reading frames (ALTOs), which are evolutionarily related but have distinct gene structures. MTs are a splice variant of the early transcript whereas ALTOs are overprinted on the second exon of the LT transcript in an alternate reading frame and are translated via an alternative start codon. Merkel cell polyomavirus (MCPyV), the only human polyomavirus that causes cancer, encodes an ALTO but its role in the viral lifecycle and tumorigenesis has remained elusive. Here, we show MCPyV ALTO acts as a tumor suppressor and is silenced in Merkel cell carcinoma (MCC). Rescuing ALTO in MCC cells induces growth arrest and activates NF-κB signaling. ALTO activates NF-κB by binding SQSTM1 and TRAF2&3 via two
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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 Socratic graph.