ArticleThe Journal of biological chemistry2015
Phosphorylation of Merkel cell polyomavirus large tumor antigen at serine 816 by ATM kinase induces apoptosis in host cells.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses.Journal of virology · 2026Review
- Review
- Phosphorylation of Human Polyomavirus Large and Small T Antigens: An Ignored Research Field.Viruses · 2023Review
- Regulation of Transcriptional Activity of Merkel Cell Polyomavirus Large T-Antigen by PKA-Mediated Phosphorylation.International journal of molecular sciences · 2023Article
- Identification of the Merkel Cell Polyomavirus Large Tumor Antigen Ubiquitin Conjugation Residue.International journal of molecular sciences · 2021Article
- From Merkel Cell Polyomavirus Infection to Merkel Cell Carcinoma Oncogenesis.Frontiers in microbiology · 2021Review
- Merkel Cell Polyomavirus Large T Antigen Unique Domain Regulates Its Own Protein Stability and Cell Growth.Viruses · 2020Article
- Merkel Cell Polyomavirus and Merkel Cell Carcinoma.Cancers · 2020Review
- Article
- Effect of the Large and Small T-Antigens of Human Polyomaviruses on Signaling Pathways.International journal of molecular sciences · 2019Review
- Mechanisms of persistence by small DNA tumor viruses.Current opinion in virology · 2018Review
- Take your PIKK: tumour viruses and DNA damage response pathways.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Protein-mediated viral latency is a novel mechanism for Merkel cell polyomavirus persistence.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Human Polyomaviruses: The Battle of Large and Small Tumor Antigens.Virology : research and treatment · 2017Review
- Merkel cell polyomavirus infection and Merkel cell carcinoma.Current opinion in virology · 2016Review
- Review
- Polyomavirus interaction with the DNA damage response.Virologica Sinica · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Merkel cell carcinoma is a highly aggressive form of skin cancer. Merkel cell polyomavirus (MCV) infection and DNA integration into the host genome correlate with 80% of all Merkel cell carcinoma cases. Integration of the MCV genome frequently results in mutations in the large tumor antigen (LT), leading to expression of a truncated LT that retains pRB binding but with a deletion of the C-terminal domain. Studies from our laboratory and others have shown that the MCV LT C-terminal helicase domain contains growth-inhibiting properties. Additionally, we have shown that host DNA damage response factors are recruited to viral replication centers. In this study, we identified a novel MCV LT phosphorylation site at Ser-816 in the C-terminal domain. We demonstrate that activation of the ATM pathway stimulated MCV LT phosphorylation at Ser-816, whereas inhibition of ATM kinase activity prevented LT phosphorylation at this site. In vitro phosphorylation experiments confirmed that ATM kinase is responsible for phosphorylating MCV LT at Ser-816. Finally, we show that ATM kinase-mediated MCV LT Ser-816 phosphorylation may contribute to the anti-tumorigenic properties of the MCV LT C-terminal domain.
Indexed as
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What Socratic 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 Socratic graph.