ArticleScientific reports2019
B1.12: a novel peptide interacting with the extracellular loop of the EBV oncoprotein LMP1.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Immune escape mechanisms and therapeutic advances in virus-associated hematological malignancies.Blood cancer journal · 2026Review
- Computational identification of PTPRJ peptide targeting the Epstein Barr virus latent membrane protein 1.Scientific reports · 2025Article
- Epstein-Barr virus-infected nasopharyngeal carcinoma therapeutics: oncoprotein targets and clinical implications.Medical oncology (Northwood, London, England) · 2025Review
- Anti-EBV: Artificial intelligence driven predictive modeling for repurposing drugs as potential antivirals against Epstein-Barr virus.Computational and structural biotechnology journal · 2025Article
- Molecular Characterisation of Epstein-Barr Virus in Classical Hodgkin Lymphoma.International journal of molecular sciences · 2022Article
- The roles of DNA methylation on the promotor of the Epstein-Barr virus (EBV) gene and the genome in patients with EBV-associated diseases.Applied microbiology and biotechnology · 2022Review
- The Role of EBV-Encoded LMP1 in the NPC Tumor Microenvironment: From Function to Therapy.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
9 authors.
Funding
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Abstract
Latent membrane protein 1 (LMP1) encoded by the Epstein-Barr virus (EBV) plays an important role in EBV-induced cell transformation. Down-regulation of the LMP1 expression had shown promising results on cancer cell therapy. In this study, we identified by Phage display a novel peptide called B1.12 (ACPLDLRSPCG) which selectively binds to the extracellular loop (B1) of the LMP1 oncoprotein as demonstrated by molecular docking, NMR and ITC. Using an LMP1 expressing cell line, we showed that B1.12 decreased cell viability, and induced G0/G1 cell cycle arrest. In addition, the expression of A20, pAkt, and pNFkb (pRelA536) in C666-1 cells treated with B1.12 decreased compared to the untreated cells. In conclusion, we selected a novel peptide able to bind specifically to the extracellular loop of LMP1 and thus modulate its oncogenic properties.
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