ArticleCellular & molecular immunology2017
Inducible Rubicon facilitates viral replication by antagonizing interferon production.
Article in Cellular & molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Interplay between Cellular Autophagy and Hepatitis B Virus Replication: A Systematic Review.Cells · 2020Pooled it
- Identification ofFrontiers in immunology · 2018Trial
- The monkeypox virus suppresses autophagy by modulating Rubicon expression.Cell death discovery · 2025Article
- The space-time continuum in neurological disorders of the autophagosome-lysosome fusion machinery.Autophagy reports · 2025Review
- All-trans retinoic acid induces lipophagy by reducing Rubicon in Hepa1c1c7 cells.Journal of lipid research · 2024Article
- Lnc-AIFM2-1 promotes HBV immune escape by acting as a ceRNA for miR-330-3p to regulate CD244 expression.Frontiers in immunology · 2023Article
- LC3-associated endocytosis and the functions of Rubicon and ATG16L1.Science advances · 2022Review
- IFITM3 Interacts with the HBV/HDV Receptor NTCP and Modulates Virus Entry and Infection.Viruses · 2022Article
- CCDC88A/GIV promotes HBV replication and progeny secretion via enhancing endosomal trafficking and blocking autophagic degradation.Autophagy · 2022Article
- HSP90AA1 interacts with CSFV NS5A protein and regulates CSFV replicationFrontiers in immunology · 2022Article
- Interferon Alpha Induces Cellular Autophagy and Modulates Hepatitis B Virus Replication.Frontiers in cellular and infection microbiology · 2022Article
- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
- The roles of the inhibitory autophagy regulator Rubicon in the heart: A new therapeutic target to prevent cardiac cell death.Experimental & molecular medicine · 2021Review
- Effect of oxidative stress and calcium deregulation on FAM26F (CALHM6) expression during hepatitis B virus infection.BMC infectious diseases · 2021Article
- Rubicon in Metabolic Diseases and Ageing.Frontiers in cell and developmental biology · 2021Review
- Hepatitis B Virus DNA is a Substrate for the cGAS/STING Pathway but is not Sensed in Infected Hepatocytes.Viruses · 2020Article
- Article
- Rubicon: a facilitator of viral immune evasion.Cellular & molecular immunology · 2019Article
- Hepatitis B Virus-Hepatocyte Interactions and Innate Immune Responses: Experimental Models and Molecular Mechanisms.Seminars in liver disease · 2019Review
- LAP it up, fuzz ball: a short history of LC3-associated phagocytosis.Current opinion in immunology · 2018Review
Corrections and comments
- Commented on by
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RUN domain Beclin-1-interacting cysteine-rich-containing (Rubicon) protein is involved in the maturation step of autophagy and the endocytic pathway as a Beclin-1-binding partner, but little is known regarding the role of Rubicon during viral infection. Here, we performed functional studies of the identified target in interferon (IFN) signaling pathways associated with Rubicon to elucidate the mechanisms of viral resistance to IFN. The Rubicon protein levels were elevated in peripheral blood mononuclear cells, sera and liver tissues from patients with hepatitis B virus (HBV) infection relative to those in healthy individuals. Assays of the overexpression and knockdown of Rubicon showed that Rubicon significantly promoted HBV replication. In addition, Rubicon knockdown resulted in the inhibition of enterovirus 71, influenza A virus and vesicular stomatitis virus. The expression o0f Rubicon led to the suppression of virus-induced type-I interferon (IFN-α and IFN-β) and type-III interferon (IFN-λ1). Translocation of activated IRF3 and IRF7 from the cytoplasm to the nucleus was involved in this process, and the NF-κB essential modulator (NEMO), a key factor in the IFN pathway, was the target with which Rubicon interacted. Our results reveal a previously unrecognized function of Rubicon as a virus-induced protein that binds to NEMO, leading to the inhibition of type-I interferon production. Rubicon thus functions as an important negative regulator of the innate immune response, enhances viral replication and may play a role in viral immune evasion.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.