ArticleInternational journal of molecular sciences2019
m6A Reader YTHDF2 Regulates LPS-Induced Inflammatory Response.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.
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Who cites it
149 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.
- The m6A epitranscriptome opens a new charter in immune system logic.Epigenetics · 2021Pooled it
- DecreasedBioMed research international · 2020Trial
- mRedox biology · 2026Review
- YTHDF2 in inflammation: Mechanisms and therapeutic strategies.Genes & diseases · 2026Review
- ALKBH5-Driven m6A Demethylation Boosts Inflammation and Autophagy in LPS-Stimulated Macrophages.Immunity, inflammation and disease · 2026Article
- RNA modifications in intestinal macrophages: Implications for gut immunity and inflammation.Genes & diseases · 2026Review
- Targeting intracellular mRNA mJournal of advanced research · 2026Review
- Emerging role of RNA modification reader YTHDF2 in hematopoiesis, immunity, and cancer.MedScience · 2026Review
- Emerging roles of tRNA modification-mediated codon-specific translational reprogramming in cancer biology.Cell death & disease · 2026Review
- Radiotherapy induces YTHDF2 in dendritic cells impairing cross-presentation and T cell function.The Journal of experimental medicine · 2026Article
- Epitranscriptomic regulation by m6A in immunity and autoimmune disorders: emerging mechanisms and clinical perspectives.Frontiers in immunology · 2026Review
- N6-methyladenosine as a potential epitranscriptomic immune rheostat during SARS-CoV-2 infection.Frontiers in immunology · 2026Review
- RNA stability: a novel perspective on gene regulatory networks in bovine mastitis.BMC genomics · 2025Article
- RBM25 Regulates p38 MAPK Pathway Activation via Exon 16 Skipping of MAP4K4 in a Rat Model of Post-Infarction Heart Failure.FASEB bioAdvances · 2025Article
- The m6A reader YTHDF2 protects vascular smooth muscle cells against the osteogenic differentiation through targeting Runx2.Renal failure · 2025Article
- N6-methyladenosine: a key regulator in ocular disease mechanisms and treatment.Cell death discovery · 2025Review
- Decoding the role of mNeurochemistry international · 2025Review
- Transcriptional Regulation ofInternational journal of molecular sciences · 2025Article
- Reduced Expression of mInternational journal of molecular sciences · 2025Article
- mCell · 2025Article
89 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
5 authors at 1 institution in 1 country.
Funding
Abstract
N6-methyladenosine (m6A) is an abundant mRNA modification that affects multiple biological processes, including those involved in the cell stress response and viral infection. YTH domain family 2 (YTHDF2) is an m6A-binding protein that affects the localization and stability of targeted mRNA. RNA-binding proteins (RBPs) can regulate the stability of inflammatory gene mRNA transcripts, thus participating in the regulation of inflammatory processes. As an RBP, the role of YTHDF2 in the LPS-induced inflammatory reaction has not been reported. To elucidate the function of YTHDF2 in the inflammatory response of macrophages, we first detected the expression level of YTHDF2 in RAW 264.7 cells, and found that it was upregulated after LPS stimulation. YTHDF2 knockdown significantly increased the LPS-induced IL-6, TNF-α, IL-1β, and IL-12 expression and the phosphorylation of p65, p38, and ERK1/2 in NF-κB and MAPK signaling. Moreover, the upregulated expression of TNF-α and IL-6 in cells with silenced YTHDF2 expression was downregulated by the NF-κB, p38, and ERK inhibitors. YTHDF2 depletion increased the expression and stability of MAP2K4 and MAP4K4 mRNAs. All of these results suggest that YTHDF2 knockdown increases mRNA expression levels of MAP2K4 and MAP4K4 via stabilizing the mRNA transcripts, which activate MAPK and NF-κB signaling pathways, which promote the expression of proinflammatory cytokines and aggravate the inflammatory response in LPS-stimulated RAW 264.7 cells.
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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.