ArticleRNA (New York, N.Y.)2014
Translation control of TAK1 mRNA by hnRNP K modulates LPS-induced macrophage activation.
Article in RNA (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 33 citations in OpenAlex.
- HnRNPK suppresses macrophage-driven inflammation in autoimmune myocarditis by restraining NCF1-dependent oxidized phospholipid signaling and ferroptosis-related changes.Redox biology · 2026Article
- RNA-binding protein hnRNPK: a multifunctional regulator of skeletal muscle biology and disease.Biochemical Society transactions · 2026Review
- Article
- The role of eIF4F-driven mRNA translation in regulating the tumour microenvironment.Nature reviews. Cancer · 2023Review
- Role of Heterogeneous Nuclear Ribonucleoproteins in the Cancer-Immune Landscape.International journal of molecular sciences · 2023Review
- TheThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- LINC00162 regulates cell proliferation and apoptosis by sponging PAQR4-targeting miR-485-5p.Journal of cellular physiology · 2022Article
- Long Non-coding RNAs (lncRNAs), A New Target in Stroke.Cellular and molecular neurobiology · 2022Review
- P23 Acts as Functional RBP in the Macrophage Inflammation Response.Frontiers in molecular biosciences · 2021Article
- RNA-binding motifs of hnRNP K are critical for induction of antibody diversification by activation-induced cytidine deaminase.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- The Splicing Factor hnRNP M Is a Critical Regulator of Innate Immune Gene Expression in Macrophages.Cell reports · 2019Article
- On the optimal design of metabolic RNA labeling experiments.PLoS computational biology · 2019Article
- Review
- LncSSBP1 Functions as a Negative Regulator of IL-6 Through Interaction With hnRNPK in Bronchial Epithelial Cells Infected WithFrontiers in immunology · 2019Article
- Integrated Functional Analysis of the Nuclear Proteome of Classically and Alternatively Activated Macrophages.Mediators of inflammation · 2019Article
- RNA-Binding Proteins in the Control of LPS-Induced Macrophage Response.Frontiers in genetics · 2019Review
- Identification of RNA-binding Proteins in Macrophages by Interactome Capture.Molecular & cellular proteomics : MCP · 2016Article
- miR-155 targets Caspase-3 mRNA in activated macrophages.RNA biology · 2016Article
- Review
- CPEB regulation of TAK1 synthesis mediates cytokine production and the inflammatory immune response.Molecular and cellular biology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage activation by bacterial lipopolysaccharides (LPS) is induced through Toll-like receptor 4 (TLR4). The synthesis and activity of TLR4 downstream signaling molecules modulates the expression of pro- and anti-inflammatory cytokines. To address the impact of post-transcriptional regulation on that process, we performed RIP-Chip analysis. Differential association of mRNAs with heterogeneous nuclear ribonucleoprotein K (hnRNP K), an mRNA-specific translational regulator in differentiating hematopoietic cells, was studied in noninduced and LPS-activated macrophages. Analysis of interactions affected by LPS revealed several mRNAs encoding TLR4 downstream kinases and their modulators. We focused on transforming growth factor-β-activated kinase 1 (TAK1) a central player in TLR4 signaling. HnRNP K interacts specifically with a sequence in the TAK1 mRNA 3' UTR in vitro. Silencing of hnRNP K does not affect TAK1 mRNA synthesis or stability but enhances TAK1 mRNA translation, resulting in elevated TNF-α, IL-1β, and IL-10 mRNA expression. Our data suggest that the hnRNP K-3' UTR complex inhibits TAK1 mRNA translation in noninduced macrophages. LPS-dependent TLR4 activation abrogates translational repression and newly synthesized TAK1 boosts macrophage inflammatory response.
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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.