ArticleCell host & microbe2015
RIP3 Regulates Autophagy and Promotes Coxsackievirus B3 Infection of Intestinal Epithelial Cells.
Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 65 citations in OpenAlex.
- The c-Abl-RIPK3 Axis Drives Mitochondrial Dysfunction and Impaired Mitophagy in Gaucher Disease Models.Antioxidants (Basel, Switzerland) · 2026Article
- The gut virome and regulatory T cell axis in health and systemic disease.Microbiome research reports · 2026Review
- Autophagy-Induced Microglial Death Contributes to Neuroinflammation in Acute Optic Nerve Injury.Investigative ophthalmology & visual science · 2025Article
- PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue.Microorganisms · 2025Article
- Evolutionary and functional analyses reveal a role for the RHIM in tuning RIPK3 activity across vertebrates.eLife · 2025Article
- Article
- Cigarette smoke exposure triggers dendritic cell-derived exosome-mediated Th17 and Treg polarization through an autophagy- and necroptosis-associated SIRT1-dependent mechanism in vitro.Frontiers in immunology · 2025Article
- ROS: Executioner of regulating cell death in spinal cord injury.Frontiers in immunology · 2024Review
- Autophagy: Regulator of cell death.Cell death & disease · 2023Review
- Astrovirus replication is dependent on induction of double-membrane vesicles through a PI3K-dependent, LC3-independent pathway.Journal of virology · 2023Article
- Engineering organ-on-a-chip systems to model viral infections.Biofabrication · 2023Review
- RIP3 knockdown inhibits necroptosis of human intestinal epithelial cells via TLR4/MyD88/NF-κB signaling and ameliorates murine colitis.BMC gastroenterology · 2022Article
- TNF-induced necroptosis initiates early autophagy events via RIPK3-dependent AMPK activation, but inhibits late autophagy.Autophagy · 2021Article
- Article
- Innate immune evasion mediated by picornaviral 3C protease: Possible lessons for coronaviral 3C-like protease?Reviews in medical virology · 2021Review
- Article
- RIP3 impedes transcription factor EB to suppress autophagic degradation in septic acute kidney injury.Cell death & disease · 2021Article
- TNF-mediated alveolar macrophage necroptosis drives disease pathogenesis during respiratory syncytial virus infection.The European respiratory journal · 2021Article
- FUS/TLS Suppresses Enterovirus Replication and Promotes Antiviral Innate Immune Responses.Journal of virology · 2021Article
- Necroptosis restricts influenza A virus as a stand-alone cell death mechanism.The Journal of experimental medicine · 2020Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Receptor interacting protein kinase-3 (RIP3) is an essential kinase for necroptotic cell death signaling and has been implicated in antiviral cell death signaling upon DNA virus infection. Here, we performed high-throughput RNAi screening and identified RIP3 as a positive regulator of coxsackievirus B3 (CVB) replication in intestinal epithelial cells (IECs). RIP3 regulates autophagy, a process utilized by CVB for viral replication factory assembly, and depletion of RIP3 inhibits autophagic flux and leads to the accumulation of autophagosomes and amphisomes. Additionally, later in infection, RIP3 is cleaved by the CVB-encoded cysteine protease 3C(pro), which serves to abrogate RIP3-mediated necrotic signaling and induce a nonnecrotic form of cell death. Taken together, our results show that temporal targeting of RIP3 allows CVB to benefit from its roles in regulating autophagy while inhibiting the induction of necroptotic cell death.
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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.