ArticleProceedings of the National Academy of Sciences of the United States of America2014
Nucleolin is important for Epstein-Barr virus nuclear antigen 1-mediated episome binding, maintenance, and transcription.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Nucleolin a Central Player in Host Virus Interactions and its Role in Viral Progeny Production.Molecular biotechnology · 2026Review
- The multifaceted roles of nucleolin in viral entry, replication, and antiviral therapy.Molecular biology reports · 2025Review
- The Epstein-Barr virus EBNA1 protein binds to G-quadruplexes in its own mRNA hence controlling its expression and immune evasion of the virus.Nucleic acids research · 2025Article
- Nucleolin binds to and regulates transcription of hepatitis B virus covalently closed circular DNA minichromosome.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Momordica anti-HIV protein MAP30 abrogates the Epstein-Barr virus nuclear antigen 1 dependent functions in host cells.Heliyon · 2023Article
- Article
- Nucleolin Promotes IRES-Driven Translation of Foot-and-Mouth Disease Virus by Supporting the Assembly of Translation Initiation Complexes.Journal of virology · 2021Article
- Infection-induced epigenetic changes and their impact on the pathogenesis of diseases.Seminars in immunopathology · 2020Article
- Rainbow Kaposi's Sarcoma-Associated Herpesvirus Revealed Heterogenic Replication with Dynamic Gene Expression.Journal of virology · 2020Article
- B Cell-Specific Transcription Activator PAX5 Recruits p300 To Support EBNA1-Driven Transcription.Journal of virology · 2020Article
- STUB1 is targeted by the SUMO-interacting motif of EBNA1 to maintain Epstein-Barr Virus latency.PLoS pathogens · 2020Article
- Epigenetic specifications of host chromosome docking sites for latent Epstein-Barr virus.Nature communications · 2020Article
- Control of Viral Latency by Episome Maintenance Proteins.Trends in microbiology · 2020Review
- Nucleolin (NCL) inhibits the growth of peste des petits ruminants virus.The Journal of general virology · 2020Article
- Epstein-Barr Virus Nuclear Antigen 1 Recruits Cyclophilin A to Facilitate the Replication of Viral DNA Genome.Frontiers in microbiology · 2019Article
- The Hsp70 inhibitor 2-phenylethynesulfonamide inhibits replication and carcinogenicity of Epstein-Barr virus by inhibiting the molecular chaperone function of Hsp70.Cell death & disease · 2018Article
- Review
- Article
- Nucleolin directly mediates Epstein-Barr virus immune evasion through binding to G-quadruplexes of EBNA1 mRNA.Nature communications · 2017Article
- The cellular protein nucleolin preferentially binds long-looped G-quadruplex nucleic acids.Biochimica et biophysica acta. General subjects · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1) is essential for EBV episome maintenance, replication, and transcription. These effects are mediated by EBNA1 binding to cognate oriP DNA, which comprise 20 imperfect copies of a 30-bp dyad symmetry enhancer and an origin for DNA replication. To identify cell proteins essential for these EBNA1 functions, EBNA1 associated cell proteins were immune precipitated and analyzed by liquid chromatography-tandem mass spectrometry. Nucleolin (NCL) was identified to be EBNA1 associated. EBNA1's N-terminal 100 aa and NCL's RNA-binding domains were critical for EBNA1/NCL interaction. Lentivirus shRNA-mediated NCL depletion substantially reduced EBNA1 recruitment to oriP DNA, EBNA1-dependent transcription of an EBV oriP luciferase reporter, and EBV genome maintenance in lymphoblastoid cell lines. NCL RNA-binding domain K429 was critical for ATP and EBNA1 binding. NCL overexpression increased EBNA1 binding to oriP and transcription, whereas NCL K429A was deficient. Moreover, NCL silencing impaired lymphoblastoid cell line growth. These experiments reveal a surprisingly critical role for NCL K429 in EBNA1 episome maintenance and transcription, which may be a target for therapeutic intervention.
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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.