ArticleeLife2015
ATP hydrolysis by the viral RNA sensor RIG-I prevents unintentional recognition of self-RNA.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 61 papers.
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
61 citing papers in PubMed, 97 citations in OpenAlex.
- Human RIG-I Antiviral Deficiency Caused by a Dominant-Negative Variant Locked in a Signaling-Inactive State.medRxiv : the preprint server for health sciences · 2026Article
- Leigh Syndrome Pathomechanism Involves Region-Specific Innate Immune Activation in Ndufs4 Knockout Mice.Cellular and molecular neurobiology · 2026Article
- An autoinflammatory RIG-I variant causing Singleton-Merten syndrome associates with small non-coding Y-RNAs.Discovery immunology · 2026Article
- Toward unraveling molecular grammars for dsRNA-binding proteins: substrate recognition to binding mechanisms.BMB reports · 2025Review
- A two-step mechanism for RIG-I activation by influenza virus mvRNAs.Science advances · 2025Article
- Influenza virus antagonizes self sensing by RIG-I to enhance viral replication.bioRxiv : the preprint server for biology · 2025Article
- RAPIDASH: Tag-free enrichment of ribosome-associated proteins reveals composition dynamics in embryonic tissue, cancer cells, and macrophages.Molecular cell · 2024Article
- Type I interferon pathway in pediatric systemic lupus erythematosus.World journal of pediatrics : WJP · 2024Review
- Proofreading mechanisms of the innate immune receptor RIG-I: distinguishing self and viral RNA.Biochemical Society transactions · 2024Review
- Unraveling blunt-end RNA binding and ATPase-driven translocation activities of the RIG-I family helicase LGP2.Nucleic acids research · 2024Article
- RAPIDASH: A tag-free enrichment of ribosome-associated proteins reveals compositional dynamics in embryonic tissues and stimulated macrophages.bioRxiv : the preprint server for biology · 2023Article
- Characterization of RNA driven structural changes in full length RIG-I leading to its agonism or antagonism.Nucleic acids research · 2023Article
- Differential regulation of ATP hydrolysis of RIG-I-like receptors by transactivation response RNA-binding protein.Bioscience reports · 2023Article
- The RIG-I receptor adopts two different conformations for distinguishing host from viral RNA ligands.Molecular cell · 2022Article
- Measuring the impact of cofactors on RNA helicase activities.Methods (San Diego, Calif.) · 2022Article
- The intrinsically disordered CARDs-Helicase linker in RIG-I is a molecular gate for RNA proofreading.The EMBO journal · 2022Article
- The molecular mechanism of RIG-I activation and signaling.Immunological reviews · 2021Review
- Insights into the structure and RNA-binding specificity of Caenorhabditis elegans Dicer-related helicase 3 (DRH-3).Nucleic acids research · 2021Article
- Article
- Reciprocal regulation of RIG-I and XRCC4 connects DNA repair with RIG-I immune signaling.Nature communications · 2021Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
The cytosolic antiviral innate immune sensor RIG-I distinguishes 5' tri- or diphosphate containing viral double-stranded (ds) RNA from self-RNA by an incompletely understood mechanism that involves ATP hydrolysis by RIG-I's RNA translocase domain. Recently discovered mutations in ATPase motifs can lead to the multi-system disorder Singleton-Merten Syndrome (SMS) and increased interferon levels, suggesting misregulated signaling by RIG-I. Here we report that SMS mutations phenocopy a mutation that allows ATP binding but prevents hydrolysis. ATPase deficient RIG-I constitutively signals through endogenous RNA and co-purifies with self-RNA even from virus infected cells. Biochemical studies and cryo-electron microscopy identify a 60S ribosomal expansion segment as a dominant self-RNA that is stably bound by ATPase deficient RIG-I. ATP hydrolysis displaces wild-type RIG-I from this self-RNA but not from 5' triphosphate dsRNA. Our results indicate that ATP-hydrolysis prevents recognition of self-RNA and suggest that SMS mutations lead to unintentional signaling through prolonged RNA binding.
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.