ArticleeLife2018
Unified mechanisms for self-RNA recognition by RIG-I Singleton-Merten syndrome variants.
Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- TOR3A represses type I interferon production and limits viral clearance during respiratory syncytial virus infection.Emerging microbes & infections · 2026Article
- 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
- HSPA6 is induced by RIG-I-like receptors and negatively regulates type-I interferon signaling.Cellular and molecular life sciences : CMLS · 2026Article
- An autoinflammatory RIG-I variant causing Singleton-Merten syndrome associates with small non-coding Y-RNAs.Discovery immunology · 2026Article
- Targeting a key disulfide linkage to regulate RIG-I condensation and cytosolic RNA-sensing.Nature cell biology · 2025Article
- A novel ADP-directed chaperone function facilitates the ATP-driven motor activity of SARS-CoV helicase.Nucleic acids research · 2025Article
- Proofreading mechanisms of the innate immune receptor RIG-I: distinguishing self and viral RNA.Biochemical Society transactions · 2024Review
- The molecular language of RNA 5' ends: guardians of RNA identity and immunity.RNA (New York, N.Y.) · 2024Review
- A conserved isoleucine in the binding pocket of RIG-I controls immune tolerance to mitochondrial RNA.Nucleic acids research · 2023Article
- Cellular functions of eukaryotic RNA helicases and their links to human diseases.Nature reviews. Molecular cell biology · 2023Review
- Universality in RNA and DNA deformations induced by salt, temperature change, stretching force, and protein binding.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Thymidine phosphorylase facilitates retinoic acid inducible gene-I induced endothelial dysfunction.Cell death & disease · 2023Article
- RNA-protein complexes and force field polarizability.Frontiers in chemistry · 2023Article
- The RIG-I receptor adopts two different conformations for distinguishing host from viral RNA ligands.Molecular cell · 2022Article
- The intrinsically disordered CARDs-Helicase linker in RIG-I is a molecular gate for RNA proofreading.The EMBO journal · 2022Article
- Cellular origins of dsRNA, their recognition and consequences.Nature reviews. Molecular cell biology · 2022Review
- Immune Regulator Retinoic Acid-Inducible Gene I (RIG-I) in the Pathogenesis of Cardiovascular Disease.Frontiers in immunology · 2022Review
- The molecular mechanism of RIG-I activation and signaling.Immunological reviews · 2021Review
- Cellular and molecular mechanisms breaking immune tolerance in inborn errors of immunity.Cellular & molecular immunology · 2021Review
- Regulation of RIG-I-like receptor-mediated signaling: interaction between host and viral factors.Cellular & molecular immunology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The innate immune sensor retinoic acid-inducible gene I (RIG-I) detects cytosolic viral RNA and requires a conformational change caused by both ATP and RNA binding to induce an active signaling state and to trigger an immune response. Previously, we showed that ATP hydrolysis removes RIG-I from lower-affinity self-RNAs (<xref ref-type="bibr" rid="bib19">Lässig et al., 2015</xref>), revealing how ATP turnover helps RIG-I distinguish viral from self-RNA and explaining why a mutation in a motif that slows down ATP hydrolysis causes the autoimmune disease Singleton-Merten syndrome (SMS). Here we show that a different, mechanistically unexplained SMS variant, C268F, which is localized in the ATP-binding P-loop, can signal independently of ATP but is still dependent on RNA. The structure of RIG-I C268F in complex with double-stranded RNA reveals that C268F helps induce a structural conformation in RIG-I that is similar to that induced by ATP. Our results uncover an unexpected mechanism to explain how a mutation in a P-loop ATPase can induce a gain-of-function ATP state in the absence of ATP.
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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.