ArticleOncotarget2016
RB1 is the crucial target of the Merkel cell polyomavirus Large T antigen in Merkel cell carcinoma cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 110 citations in OpenAlex.
- An immunocompetent model of MCPyV-driven Merkel cell carcinoma reveals tumor evolution under immune selection.bioRxiv : the preprint server for biology · 2026Article
- E2F1-3 activate Merkel cell polyomavirus early transcription and replication.bioRxiv : the preprint server for biology · 2025Article
- HSPA5, a Host Cellular Heat-Shock Protein Required for Influenza a Virus Replication.International journal of molecular sciences · 2025Article
- Targeting an essential viral oncoprotein with an IL-7-enhanced mRNA vaccine induces durable immunity to Merkel cell carcinoma.Cell reports · 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
- Review
- Detection by Single-Cell RNA Sequencing of Virally Mediated Skin Diseases.JID innovations : skin science from molecules to population health · 2025Article
- Understanding Merkel Cell Carcinoma: Pathogenic Signaling, Extracellular Matrix Dynamics, and Novel Treatment Approaches.Cancers · 2025Review
- Ribosomal protein S25 promotes cell cycle entry for a productive BK polyomavirus infection.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Article
- Merkel Cell Polyomavirus Co-Infection in HIV/AIDS Individuals: Clinical Diagnosis, Consequences and Treatments.Pathogens (Basel, Switzerland) · 2025Review
- The role of pioneering transcription factors, chromatin accessibility and epigenetic reprogramming in oncogenic viruses.Frontiers in microbiology · 2025Review
- Review
- Therapeutic Approaches for Non-Melanoma Skin Cancer: Standard of Care and Emerging Modalities.International journal of molecular sciences · 2024Review
- The small tumor antigen of Merkel cell polyomavirus accomplishes cellular transformation by uniquely localizing to the nucleus despite the absence of a known nuclear localization signal.Virology journal · 2024Article
- Rubella virus chronic inflammatory disease and other unusual viral phenotypes in inborn errors of immunity.Immunological reviews · 2024Review
- Enhancing immunogenic responses through CDK4/6 and HIF2α inhibition in Merkel cell carcinoma.Heliyon · 2024Article
- Merkel Cell Polyomavirus T Antigen-Mediated Reprogramming in Adult Merkel Cell Progenitors.The Journal of investigative dermatology · 2023Article
3 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
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pocket protein (PP) family consists of the three members RB1, p107 and p130 all possessing tumor suppressive properties. Indeed, the PPs jointly control the G1/S transition mainly by inhibiting E2F transcription factors. Notably, several viral oncoproteins are capable of binding and inhibiting PPs. Merkel cell polyomavirus (MCPyV) is considered as etiological factor for Merkel cell carcinoma (MCC) with expression of the viral Large T antigen (LT) harboring an intact PP binding domain being required for proliferation of most MCC cells. Therefore, we analyzed the interaction of MCPyV-LT with the PPs. Co-IP experiments indicate that MCPyV-LT binds potently only to RB1. Moreover, MCPyV-LT knockdown-induced growth arrest in MCC cells can be rescued by knockdown of RB1, but not by p107 or p130 knockdown. Accordingly, cell cycle arrest and E2F target gene repression mediated by the single PPs can only in the case of RB1 be significantly reverted by MCPyV-LT expression. Moreover, data from an MCC patient indicate that loss of RB1 rendered the MCPyV-positive MCC cells LT independent. Thus, our results suggest that RB1 is the dominant tumor suppressor PP in MCC, and that inactivation of RB1 by MCPyV-LT is largely sufficient for its growth supporting function in established MCPyV-positive MCC cells.
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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 OpenQuestion graph.