ArticleInternational journal of molecular sciences2015
RNase L Cleavage Products Promote Switch from Autophagy to Apoptosis by Caspase-Mediated Cleavage of Beclin-1.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 59 citations in OpenAlex.
- Autophagy-Apoptosis Crosstalk in Cancer: Mechanisms, Signaling Pathways, and Therapeutic Targeting.Cancers · 2026Review
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- A comparative transcriptomic analysis provides new insights into the ecological adaptations in Ichthyophis bannanicus.BMC genomics · 2025Article
- Fine-Tuning of the Endoplasmic Reticulum Stress Response Mechanism Plays a Key Role in Cellular Survival-A Mathematical Study.International journal of molecular sciences · 2025Article
- The Biological Role and Clinical Significance of BECLIN-1 in Cancer.International journal of molecular sciences · 2025Review
- Deciphering the Neuroprotective Action of Bee Venom Peptide Melittin: Insights into Mechanistic Interplay.Molecular neurobiology · 2025Review
- The integrated stress response engages a cell-autonomous, ligand-independent, DR5-driven apoptosis switch.Cell death & disease · 2025Article
- Anti-atherosclerotic effects and molecular targets of salvianolic acids fromFrontiers in pharmacology · 2025Review
- LncRNA-driven programmed cell death networks: new therapeutic targets for neurological disorders.Frontiers in molecular neuroscience · 2025Review
- Alterations ofCurrent Alzheimer research · 2025Article
- DHX15 and Rig-I Coordinate Apoptosis and Innate Immune Signaling by Antiviral RNase L.Viruses · 2024Article
- Group 2 innate lymphocytes protect the balance between autophagy and apoptosis in cardiomyocytes during sepsis-induced cardiac injury.Scientific reports · 2024Article
- Genomic Landscape of Susceptibility to Severe COVID-19 in the Slovenian Population.International journal of molecular sciences · 2024Article
- Beclin-1: a therapeutic target at the intersection of autophagy, immunotherapy, and cancer treatment.Frontiers in immunology · 2024Review
- Targeting autophagy and beyond: Deconvoluting the complexity of Beclin-1 from biological function to cancer therapy.Acta pharmaceutica Sinica. B · 2023Review
- Activation of cytosolic RNA sensors by endogenous ligands: roles in disease pathogenesis.Frontiers in immunology · 2023Review
- Regulatory insights into progression of cancer and Alzheimer's disorder from autophagy perspective.Molecular biology reports · 2021Review
- Over Fifty Years of Life, Death, and Cannibalism: A Historical Recollection of Apoptosis and Autophagy.International journal of molecular sciences · 2021Review
- RNase L limits host and viral protein synthesis via inhibition of mRNA export.Science advances · 2021Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Autophagy and apoptosis share regulatory molecules enabling crosstalk in pathways that affect cellular homeostasis including response to viral infections and survival of tumor cells. Ribonuclease L (RNase L) is an antiviral endonuclease that is activated in virus-infected cells and cleaves viral and cellular single-stranded RNAs to produce small double-stranded RNAs with roles in amplifying host responses. Activation of RNase L induces autophagy and apoptosis in many cell types. However, the mechanism by which RNase L mediates crosstalk between these two pathways remains unclear. Here we show that small dsRNAs produced by RNase L promote a switch from autophagy to apoptosis by caspase-mediated cleavage of Beclin-1, terminating autophagy. The caspase 3-cleaved C-terminal fragment of Beclin-1 enhances apoptosis by translocating to the mitochondria along with proapoptotic protein, Bax, and inducing release of cytochrome C to the cytosol. Cleavage of Beclin-1 determines switch to apoptosis since expression of caspase-resistant Beclin-1 inhibits apoptosis and sustains autophagy. Moreover, inhibiting RNase L-induced autophagy promotes cell death and inhibiting apoptosis prolongs autophagy in a cross-inhibitory mechanism. Our results demonstrate a novel role of RNase L generated small RNAs in cross-talk between autophagy and apoptosis that impacts the fate of cells during viral infections and cancer.
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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.