ArticleThe Journal of biological chemistry2014
Tumor necrosis factor (TNF)-α induction of CXCL10 in endothelial cells requires protein arginine methyltransferase 5 (PRMT5)-mediated nuclear factor (NF)-κB p65 methylation.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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.
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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
58 citing papers in PubMed, 75 citations in OpenAlex.
- S-Adenosylmethionine-Dependent Methylation, Protein Arginine Methyltransferases and Cardiovascular Diseases.Biomolecules · 2026Review
- Targeting PRMTs with small-molecule inhibitors: a comprehensive review.RSC medicinal chemistry · 2026Review
- Targeting the PRMT5/Nur77 methylation axis enhances endometrial decidualization capacity and female fertility in preclinical models.The Journal of clinical investigation · 2026Article
- PRMT5 promotes psoriatic inflammation through mediating dimethylation of p65 in keratinocytes.Molecular medicine (Cambridge, Mass.) · 2026Article
- LncRNA AFAP1-AS1 mediates therapy-dependent expression of CCL5, CXCL10 and MMP9 in multiple sclerosis.Biochemistry and biophysics reports · 2026Article
- TWEAK-induced alternative NF-κB signaling regulates Cxcl10 and Mymx to promote myoblast-to-myotube fusion and muscle regeneration.Communications biology · 2026Article
- T cell acute lymphoblastic leukemia exploits a neural proinflammatory pathway to colonize the meninges.The Journal of clinical investigation · 2026Article
- PRMT5 inhibition reduces hyperinflammation in a murine model of secondary hemophagocytic lymphohistiocytosis.Blood advances · 2025Article
- Role of CXCL10 released from osteocytes in response to TNF-α stimulation on osteoclasts.Scientific reports · 2025Article
- Immune suppression in MTAP-deficient cancers via glutamate metabolism and CXCL10 downregulation.Frontiers in immunology · 2025Article
- Lysine and arginine methylation of transcription factors.Cellular and molecular life sciences : CMLS · 2024Review
- A Supramolecular Antibiotic Targeting Drug-ResistantACS applied materials & interfaces · 2024Article
- Protein arginine methyltransferase 2 controls inflammatory signaling in acute myeloid leukemia.Communications biology · 2024Article
- Article
- Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024Review
- Altered Tumor Necrosis Factor Response in Neurologic Postacute SARS-CoV-2 Syndrome.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023Article
- PRMT5 inhibition induces pro-inflammatory macrophage polarization and increased hepatic triglyceride levels without affecting atherosclerosis in mice.Journal of cellular and molecular medicine · 2023Article
- Proinflammatory Responses in SARS-CoV-2 and Soluble Spike Glycoprotein S1 Subunit Activated Human Macrophages.Viruses · 2023Article
- The Role of PRMT5 in Immuno-Oncology.Genes · 2023Review
- (International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The chemokine CXCL10/IP-10 facilitates recruitment of Th1-type leukocytes to inflammatory sites. In this study, we show that the arginine methyltransferase PRMT5 is critical for CXCL10 transcription in TNF-α-activated human endothelial cells (EC). We found that depletion of PRMT5 results in significantly reduced levels of CXCL10 mRNA, demonstrating a positive role for PRMT5 in CXCL10 induction. Chromatin immunoprecipitation experiments revealed the presence of the symmetrical dimethylarginine modification catalyzed by PRMT5 associated with the CXCL10 promoter in response to TNF-α. However, symmetrical dimethylarginine-modified proteins were not detected at the promoter in the absence of PRMT5, indicating that PRMT5 is essential for methylation to occur. Furthermore, NF-κB p65, a critical driver of TNF-α-mediated CXCL10 induction, was determined to be methylated at arginine residues. Crucially, RNAi-mediated PRMT5 depletion abrogated p65 methylation and CXCL10 promoter binding. Mass spectrometric analysis in EC identified five dimethylated arginine residues in p65, four of which are uncharacterized in the literature. Expression of Arg-to-Lys point mutants of p65 demonstrated that both Arg-30 and Arg-35 must be dimethylated to achieve full CXCL10 expression. In conclusion, we have identified previously uncharacterized p65 post-translational modifications critical for CXCL10 induction.
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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.