ArticleCell discovery2021
The RNA-binding protein LUC7L2 mediates MITA/STING intron retention to negatively regulate innate antiviral response.
Article in Cell discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed.
- ASAP1 gene InDel variants are associated with enhanced goat resistance against Brucella infection.Animal bioscience · 2026Article
- RETRACTED: Endogenous Retroviruses as Regulators of Innate Immune Signaling and InflammationViruses · 2026Review
- Intron Retention: A Reemerging Paradigm in RNA Biology and Post-Transcriptional Gene Regulation.Genes · 2025Review
- Targeting the cGAS-STING pathway: emerging strategies and challenges for the treatment of inflammatory skin diseases.Frontiers in pharmacology · 2025Review
- Regulation and Function of the cGAS-STING Pathway: Mechanisms, Post-Translational Modifications, and Therapeutic Potential in Immunotherapy.Drug design, development and therapy · 2025Review
- Let's make it personal: CRISPR tools in manipulating cell death pathways for cancer treatment.Cell biology and toxicology · 2024Review
- LUC7L3 is a downstream factor of SRSF1 and prevents genomic instability.Cell insight · 2024Article
- Histone H3K9 Lactylation Confers Temozolomide Resistance in Glioblastoma via LUC7L2-Mediated MLH1 Intron Retention.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- CRISPR-Cas9-Mediated Cytosine Base Editing Screen for the Functional Assessment ofInternational journal of molecular sciences · 2023Article
- STING strengthens host anti-hantaviral immunity through an interferon-independent pathway.Virologica Sinica · 2023Article
- Virus usurps alternative splicing to clear the decks for infection.Virology journal · 2023Review
- Multifaceted functions of STING in human health and disease: from molecular mechanism to targeted strategy.Signal transduction and targeted therapy · 2022Review
- Cytogenetic and Genetic Abnormalities with Diagnostic Value in Myelodysplastic Syndromes (MDS): Focus on the Pre-Messenger RNA Splicing Process.Diagnostics (Basel, Switzerland) · 2022Review
- Time-course RNA-Seq profiling reveals isoform-level gene expression dynamics of the cGAS-STING pathway.Computational and structural biotechnology journal · 2022Article
- Mitotic inactivation of the cGAS‒MITA/STING pathways.Journal of molecular cell biology · 2021Review
- The Regulatory Network of Cyclic GMP-AMP Synthase-Stimulator of Interferon Genes Pathway in Viral Evasion.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
MITA (also known as STING) is an ER-located adaptor protein, which mediates DNA-triggered innate immune response and is critically involved in autoimmune diseases and tumorigenesis. MITA is regulated by post-translational modifications, but how post-transcriptional mechanisms are involved in the regulation of MITA is still largely unknown. Here, we identified the RNA-binding protein LUC7L2 as a negative regulator of DNA virus-triggered innate immune response. LUC7L2-deficient mice exhibited resistance to lethal herpes simplex virus 1 (HSV-1) infection and reduced HSV-1 loads in the brain. Mechanistically, LUC7L2 directly bound to intron 3 of MITA precursor messenger RNA, inhibited its splicing and promoted its nonsense-mediated decay, leading to its downregulation at protein level. LUC7L2-deficient cells had markedly increased MITA level, leading to heightened innate antiviral response. Finally, LUC7L2 was induced following HSV-1 infection. Our findings reveal a feedback negative post-transcriptional regulatory mechanism for regulation of MITA-mediated innate immune response to viral and aberrant cellular DNA.
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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.