ArticlePLoS genetics2013
Limiting of the innate immune response by SF3A-dependent control of MyD88 alternative mRNA splicing.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Genome-wide association study reveals a novel tuberculosis susceptibility locus in multiple East Asian and European populations.Genome medicine · 2026Pooled it
- Alternative splicing of toll-like receptor pathway mRNAs in lung immune cells from patients with ARDS.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Weakened macrophage antibacterial capacity in myelodysplastic syndrome.ImmunoHorizons · 2026Article
- Splicing-driven post-translational dysregulation: a new frontier for precision cancer medicine and immunotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- The emerging roles of alternative splicing in modulating tumor immune responses and immunotherapies.Cell death and differentiation · 2026Review
- Pharmacological targeting of SF3a1-MDM4 splicing vulnerability in ovarian cancer with rifaximin and antisense oligonucleotide.Journal of translational medicine · 2026Article
- The dynamic landscape of alternative splicing during silicosis progression.Respiratory research · 2026Article
- Downregulation of Tra2α and Tra2β suppresses lipopolysaccharide-induced inflammation in macrophages by regulating MyD88 mRNA alternative splicing.Molecular and cellular biochemistry · 2026Article
- Systemic Effects of Pesticides on Insectivorous Bats: A Proteomics Approach.Integrative and comparative biology · 2025Article
- Multimodal analysis stratifies genetic susceptibility and reveals the pathogenic mechanism of kidney injury in diabetic nephropathy.Cell reports. Medicine · 2025Article
- The potential impact of RNA splicing abnormalities on immune regulation in endometrial cancer.Cell death & disease · 2025Review
- Low-risk MDS-A spotlight on precision medicine forHemaSphere · 2025Review
- Covalent targeting of splicing in T cells.Cell chemical biology · 2025Article
- Review
- S-allylmercaptocysteine inhibits TLR4-mediated inflammation through enhanced formation of inhibitory MyD88 splice variant in mammary epithelial cells.Scientific reports · 2024Article
- Article
- The Many Roads from Alternative Splicing to Cancer: Molecular Mechanisms Involving Driver Genes.Cancers · 2024Review
- RNA Binding Proteins that Mediate LPS-induced Alternative Splicing of the MyD88 Innate Immune Regulator.Journal of molecular biology · 2024Article
- Treatment with β-Adrenoceptor Agonist Isoproterenol Reduces Non-parenchymal Cell Responses in LPS/D-GalN-Induced Liver Injury.Inflammation · 2024Article
- Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Controlling infectious disease without inducing unwanted inflammatory disease requires proper regulation of the innate immune response. Thus, innate immunity needs to be activated when needed during an infection, but must be limited to prevent damage. To accomplish this, negative regulators of innate immunity limit the response. Here we investigate one such negative regulator encoded by an alternative splice form of MyD88. MyD88 mRNA exists in two alternative splice forms: MyD88L, a long form that encodes a protein that activates innate immunity by transducing Toll-like receptor (TLR) signals; and a short form that encodes a different protein, MyD88S, that inhibits the response. We find that MyD88S levels regulate the extent of inflammatory cytokine production in murine macrophages. MyD88S mRNA levels are regulated by the SF3A and SF3B mRNA splicing complexes, and these mRNA splicing complexes function with TLR signaling to regulate MyD88S production. Thus, the SF3A mRNA splicing complex controls production of a negative regulator of TLR signaling that limits the extent of innate immune activation.
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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.