ArticleScience immunology2024
GGNBP2 regulates MDA5 sensing triggered by self double-stranded RNA following loss of ADAR1 editing.
Article in Science immunology, 2024. 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 7 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
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Who cites it
7 citing papers in PubMed.
- Tumour-associated dsRNA accumulation and innate immune activation: mechanistic basis and therapeutic strategies.EBioMedicine · 2026Review
- A cytoplasmic index for quantifying immune-related A-to-I RNA editing.Genome biology · 2026Article
- RNA-binding proteins and ribonucleoproteins as determinants of immunity.Nature reviews. Immunology · 2026Review
- Minute amounts of helicase-deficient truncated RECQL4 are sufficient for DNA replication.EMBO reports · 2026Article
- Regulators of interferon-responsive microglia uncovered by Genome-wide CRISPRi screening.NPJ dementia · 2026Article
- The CCR4-NOT complex: a multifaceted sensor of molecular signals instructing eukaryotic mRNA translation and stability.Nucleic acids research · 2025Review
- Leveraging genetics to understand ADAR1-mediated RNA editing in health and disease.Nature reviews. Genetics · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
Abstract
Adenosine-to-inosine (A-to-I) editing of double-stranded RNA (dsRNA) by ADAR1 is an essential modifier of the immunogenicity of cellular dsRNA. The role of MDA5 in sensing unedited cellular dsRNA and the downstream activation of type I interferon (IFN) signaling are well established. However, we have an incomplete understanding of pathways that modify the response to unedited dsRNA. We performed a genome-wide CRISPR screen and showed that GGNBP2, CNOT10, and CNOT11 interact and regulate sensing of unedited cellular dsRNA. We found that GGNBP2 acts between dsRNA transcription and its cytoplasmic sensing by MDA5. GGNBP2 loss prevented induction of type I IFN and autoinflammation after the loss of ADAR1 editing activity by modifying the subcellular distribution of endogenous A-to-I editing substrates and reducing cytoplasmic dsRNA load. These findings reveal previously undescribed pathways to modify diseases associated with
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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.