ArticleJournal of virology2014
Regulation of autophagic activation by Rta of Epstein-Barr virus via the extracellular signal-regulated kinase pathway.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- A System-Level Perspective on Epstein-Barr Virus Persistence: The Partial Lytic Reactivation.International journal of molecular sciences · 2026Review
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- Exploring the interplay between EBV and autophagy-related gene expression patterns in nasopharyngeal carcinoma.Frontiers in oncology · 2025Article
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- Autophagy and Inflammation: Regulatory Roles in Viral Infections.Biomolecules · 2023Review
- The autophagy machinery interacts with EBV capsids during viral envelope release.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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- Subcellular Distribution of BALF2 and the Role of Rab1 in the Formation of Epstein-Barr Virus Cytoplasmic Assembly Compartment and Virion Release.Microbiology spectrum · 2023Article
- The role of autophagy in viral infections.Journal of biomedical science · 2023Review
- Autophagy as a dual-faced host response to viral infections.Frontiers in cellular and infection microbiology · 2023Review
- The roles of autophagy and mitophagy in corneal pathology: current knowledge and future perspectives.Frontiers in medicine · 2023Review
- Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022Article
- New Look of EBV LMP1 Signaling Landscape.Cancers · 2021Review
- BHRF1, a BCL2 viral homolog, disturbs mitochondrial dynamics and stimulates mitophagy to dampen type I IFN induction.Autophagy · 2021Article
- Autophagy in Viral Development and Progression of Cancer.Frontiers in oncology · 2021Review
- Lytic Induction Therapy against Epstein-Barr Virus-Associated Malignancies: Past, Present, and Future.Cancers · 2020Review
- Regulation of Autophagy in Cells Infected With Oncogenic Human Viruses and Its Impact on Cancer Development.Frontiers in cell and developmental biology · 2020Review
- CXCR4 induces cell autophagy and maintains EBV latent infection in EBVaGC.Theranostics · 2020Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Autophagy is an intracellular degradation pathway that provides a host defense mechanism against intracellular pathogens. However, many viruses exploit this mechanism to promote their replication. This study shows that lytic induction of Epstein-Barr virus (EBV) increases the membrane-bound form of LC3 (LC3-II) and LC3-containing punctate structures in EBV-positive cells. Transfecting 293T cells with a plasmid that expresses Rta also induces autophagy, revealing that Rta is responsible for autophagic activation. The activation involves Atg5, a key component of autophagy, but not the mTOR pathway. The expression of Rta also activates the transcription of the genes that participate in the formation of autophagosomes, including LC3A, LC3B, and ATG9B genes, as well as those that are involved in the regulation of autophagy, including the genes TNF, IRGM, and TRAIL. Additionally, treatment with U0126 inhibits the Rta-induced autophagy and the expression of autophagy genes, indicating that the autophagic activation is caused by the activation of extracellular signal-regulated kinase (ERK) signaling by Rta. Finally, the inhibition of autophagic activity by an autophagy inhibitor, 3-methyladenine, or Atg5 small interfering RNA, reduces the expression of EBV lytic proteins and the production of viral particles, revealing that autophagy is critical to EBV lytic progression. This investigation reveals how an EBV-encoded transcription factor promotes autophagy to affect viral lytic development.
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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.