ArticleCell host & microbe2013
The unfolded protein response element IRE1α senses bacterial proteins invading the ER to activate RIG-I and innate immune signaling.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 66 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.
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
66 citing papers in PubMed, 95 citations in OpenAlex.
- IRE1α recognizes a structural motif in cholera toxin to activate an unfolded protein response.The Journal of cell biology · 2024Article
- Evolutionary Aspects of the Unfolded Protein Response.Cold Spring Harbor perspectives in biology · 2022Article
- Mesenchymal Stem Cell-Derived Exosomal MiRNAs Promote M2 Macrophages Polarization: Therapeutic Opportunities for Spinal Cord Injury.Frontiers in molecular neuroscience · 2022Review
- Endoplasmic Reticulum Stress-Associated Neuronal Death and Innate Immune Response in Neurological Diseases.Frontiers in immunology · 2021Review
- Sigma-1 Receptor: A Potential Therapeutic Target for Traumatic Brain Injury.Frontiers in cellular neuroscience · 2021Review
- Integrated stress response in hepatitis C promotes Nrf2-related chaperone-mediated autophagy: A novel mechanism for host-microbe survival and HCC development in liver cirrhosis.Seminars in cell & developmental biology · 2020Review
- A modified cholera toxin B subunit containing an ER retention motif enhances colon epithelial repairFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Distinct Subcellular Compartments of Dendritic Cells Used for Cross-Presentation.International journal of molecular sciences · 2019Review
- Viral priming of cell intrinsic innate antiviral signaling by the unfolded protein response.Nature communications · 2019Article
- Toxins Utilize the Endoplasmic Reticulum-Associated Protein Degradation Pathway in Their Intoxication Process.International journal of molecular sciences · 2019Review
- Modulation of the sigma-1 receptor-IRE1 pathway is beneficial in preclinical models of inflammation and sepsis.Science translational medicine · 2019Article
- PI3Kδ contributes to ER stress-associated asthma through ER-redox disturbances: the involvement of the RIDD-RIG-I-NF-κB axis.Experimental & molecular medicine · 2018Article
- tRNA fragmentation and protein translation dynamics in the course of kidney injury.RNA biology · 2018Review
- Endoplasmic Reticulum Stress Markers and Their Possible Implications in Leprosy's Pathogenesis.Disease markers · 2018Article
- Cellular Stress Responses and Gut Microbiota in Inflammatory Bowel Disease.Gastroenterology research and practice · 2018Review
- IRE1α Implications in Endoplasmic Reticulum Stress-Mediated Development and Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2018Review
- Regulation of Cytokine Production by the Unfolded Protein Response; Implications for Infection and Autoimmunity.Frontiers in immunology · 2018Review
- Orientia tsutsugamushi Modulates Endoplasmic Reticulum-Associated Degradation To Benefit Its Growth.Infection and immunity · 2018Article
- Lower temperatures reduce type I interferon activity and promote alphaviral arthritis.PLoS pathogens · 2017Article
- Therapeutic Potential of Cholera Toxin B Subunit for the Treatment of Inflammatory Diseases of the Mucosa.Toxins · 2017Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2018-04-11Unreliable Data · Unreliable Results and/or Conclusions ·
- Commented on by
- Retracted
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
The plasma membrane and all membrane-bound organelles except for the Golgi and endoplasmic reticulum (ER) are equipped with pattern-recognition molecules to sense microbes or their products and induce innate immunity for host defense. Here, we report that inositol-requiring-1α (IRE1α), an ER protein that signals in the unfolded protein response (UPR), is activated to induce inflammation by binding a portion of cholera toxin as it co-opts the ER to cause disease. Other known UPR transducers, including the IRE1α-dependent transcription factor XBP1, are dispensable for this signaling. The inflammatory response depends instead on the RNase activity of IRE1α to degrade endogenous mRNA, a process termed regulated IRE1α-dependent decay (RIDD) of mRNA. The mRNA fragments produced engage retinoic-acid inducible gene 1 (RIG-I), a cytosolic sensor of RNA viruses, to activate NF-κB and interferon pathways. We propose IRE1α provides for a generalized mechanism of innate immune surveillance originating within the ER lumen.
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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.