ArticleNature immunology2017
NLRX1 promotes immediate IRF1-directed antiviral responses by limiting dsRNA-activated translational inhibition mediated by PKR.
Article in Nature immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 101 citations in OpenAlex.
- Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- IRF1 regulates apoptosis and osteogenic differentiation of bone marrow mesenchymal stem cells and ameliorates osteoporosis by activating the PI3K/AKT signaling pathway.Journal of advanced research · 2026Article
- Molecular Evolution of the NLR Gene Family Reveals Diverse Innate Immune Strategies in Bats.Biomolecules · 2025Article
- Harnessing NLRX1: a new frontier in mitigating inflammation in pulmonary hypertension.Respiratory research · 2025Article
- Promising Cancer Vaccine for Glioblastoma Therapy: A Focus on mRNA Vaccine.Cancer medicine · 2025Review
- The ELF3-TRIM22-MAVS signaling axis regulates type I interferon and antiviral responses.Journal of virology · 2025Article
- Article
- Mystery machine: the complex roles of NLRX1 in viral infection.Frontiers in immunology · 2025Review
- mRNA vaccines as cancer therapies.Chinese medical journal · 2024Review
- Insights into the structure of NLR family member X1: Paving the way for innovative drug discovery.Computational and structural biotechnology journal · 2024Article
- An NLR family member X1 mutation (p.Arg707Cys) suppresses hepatitis B virus infection in hepatocytes and favors the interaction of retinoic acid-inducible gene 1 with mitochondrial antiviral signaling protein.Archives of virology · 2024Article
- The Role of Interferon Regulatory Factors in Liver Diseases.International journal of molecular sciences · 2024Review
- Review
- Recent Progress in Innate Immune Responses to Enterovirus A71 and Viral Evasion Strategies.International journal of molecular sciences · 2024Review
- The NLR family of innate immune and cell death sensors.Immunity · 2024Review
- A zebrafish NLRX1 isoform downregulates fish IFN responses by targeting the adaptor STING.Journal of virology · 2024Article
- Identification of Cellular Interactions in the Tumor Immune Microenvironment Underlying CD8 T Cell Exhaustion.bioRxiv : the preprint server for biology · 2023Article
- The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023Review
- MAVI1, an endoplasmic reticulum-localized microprotein, suppresses antiviral innate immune response by targeting MAVS on mitochondrion.Science advances · 2023Article
- Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
NLRX1 is unique among the nucleotide-binding-domain and leucine-rich-repeat (NLR) proteins in its mitochondrial localization and ability to negatively regulate antiviral innate immunity dependent on the adaptors MAVS and STING. However, some studies have suggested a positive regulatory role for NLRX1 in inducing antiviral responses. We found that NLRX1 exerted opposing regulatory effects on viral activation of the transcription factors IRF1 and IRF3, which might potentially explain such contradictory results. Whereas NLRX1 suppressed MAVS-mediated activation of IRF3, it conversely facilitated virus-induced increases in IRF1 expression and thereby enhanced control of viral infection. NLRX1 had a minimal effect on the transcription of IRF1 mediated by the transcription factor NF-kB and regulated the abundance of IRF1 post-transcriptionally by preventing translational shutdown mediated by the double-stranded RNA (dsRNA)-activated kinase PKR and thereby allowed virus-induced increases in the abundance of IRF1 protein.
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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.