ArticleNucleic acids research2021
The N6-methyladenosine RNA-binding protein YTHDF1 modulates the translation of TRAF6 to mediate the intestinal immune response.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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73 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.
- To Systematically Evaluate and Analyze the Efficacy and Safety of Transcatheter Arterial Chemoembolization (TACE) in the Treatment of Primary Liver Cancer.Journal of healthcare engineering · 2022Pooled it
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- Epitranscriptomics in kidney disease: insights and therapeutic potential.Kidney research and clinical practice · 2026Article
- Poxvirus infection triggers remodeling of host m⁶A epitranscriptome and benefits from the m⁶A regulatory responses.Virology journal · 2026Article
- RNA modifications in intestinal macrophages: Implications for gut immunity and inflammation.Genes & diseases · 2026Review
- N6-methyladenosine (miScience · 2026Article
- N6-methyladenosine improves porcine longissimus dorsi muscle quality by regulating myofiber differentiation.BMC genomics · 2025Article
- Pathological α-synuclein dysregulates epitranscriptomic writer METTL3 to drive neuroinflammation in microglia.Cell reports · 2025Article
- Comprehensive characterization of lncRNA NJournal of animal science and biotechnology · 2025Article
- Elevated SPARC Disrupts the Intestinal Barrier Integrity in Crohn's Disease by Interacting with OTUD4 and Activating the MYD88/NF-κB Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Comparative analysis of improved m6A sequencing based on antibody optimization for low-input samples.Scientific reports · 2025Article
- YTHDF2-mediated mFrontiers in cellular and infection microbiology · 2025Article
- Analysis of METTL14 expression in pancreatic cancer and adjacent tissues and its prognostic value for patient outcomes.Clinical and experimental medicine · 2024Article
- KIFC1 depends on TRIM37-mediated ubiquitination of PLK4 to promote centrosome amplification in endometrial cancer.Cell death discovery · 2024Article
- CDK1 promotes the phosphorylation of KIFC1 to regulate the tumorgenicity of endometrial carcinoma.Journal of gynecologic oncology · 2024Article
- Article
- Sevoflurane augments neuroinflammation by regulating DUSP6 via YTHDF1 in postoperative cognitive dysfunction.Toxicology research · 2024Article
- Nurturing gut health: role of m6A RNA methylation in upholding the intestinal barrier.Cell death discovery · 2024Review
13 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intestinal invasion of pathogenic microorganisms can have serious health consequences. Recent evidence has shown that the N6-methyladenosine (m6A) mRNA modification is closely associated with innate immunity; however, the underlying mechanism is poorly understood. Here, we examined the function and mechanism of m6A mRNA modification and the YTH domain-containing protein YTHDF1 (YTH N6-methyladenosine RNA-binding protein 1) in the innate immune response against bacterial pathogens in the intestine. Ribo-seq and m6A-seq analyses revealed that YTHDF1 directs the translation of Traf6 mRNA, which encodes tumor necrosis factor receptor-associated factor 6, thereby regulating the immune response via the m6A modification near the transcript's stop codon. Furthermore, we identified a unique mechanism by which the P/Q/N-rich domain in YTHDF1 interacts with the DEAD domain in the host factor DDX60, thereby regulating the intestinal immune response to bacterial infection by recognizing the target Traf6 transcript. These results provide novel insights into the mechanism by which YTHDF1 recognizes its target and reveal YTHDF1 as an important driver of the intestinal immune response, opening new avenues for developing therapeutic strategies designed to modulate the intestinal immune response to bacterial infection.
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