ArticleProceedings of the National Academy of Sciences of the United States of America2019
Polymerase III transcription is necessary for T cell priming by dendritic cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
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- VPS34-IN1 potentiates STING-dependent activation in human CAL-1 cells.Cellular & molecular biology letters · 2026Article
- MAF1 inhibits hepatocarcinogenesis by fostering an immunostimulatory tumor microenvironment.Journal for immunotherapy of cancer · 2025Article
- Intestinal-pulmonary axis: a 'Force For Good' against respiratory viral infections.Frontiers in immunology · 2025Review
- Regulation of cancer progression by CK2: an emerging therapeutic target.Medical oncology (Northwood, London, England) · 2024Review
- Translatomics to explore dynamic differences in immunocytes in the tumor microenvironment.Molecular therapy. Nucleic acids · 2023Review
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
- Iron-sulfur clusters as inhibitors and catalysts of viral replication.Nature chemistry · 2022Review
- Emerging role of Protein Kinase CK2 in Tumor immunity.Frontiers in oncology · 2022Review
- The Immune Regulatory Role of Protein Kinase CK2 and Its Implications for Treatment of Cancer.Biomedicines · 2021Review
- The nuclear and cytoplasmic activities of RNA polymerase III, and an evolving transcriptome for surveillance.Nucleic acids research · 2021Article
- The role of Sp140 revealed in IgE and mast cell responses in Collaborative Cross mice.JCI insight · 2021Article
- Proteostasis in dendritic cells is controlled by the PERK signaling axis independently of ATF4.Life science alliance · 2021Article
- The MAF1 Phosphoregulatory Region Controls MAF1 Interaction with the RNA Polymerase III C34 Subunit and Transcriptional Repression in Plants.The Plant cell · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to microbe-associated molecular patterns (MAMPs) causes dendritic cells (DCs) to undergo a remarkable activation process characterized by changes in key biochemical mechanisms. These enhance antigen processing and presentation, as well as strengthen DC capacity to stimulate naïve T cell proliferation. Here, we show that in response to the MAMPS lipopolysaccharide and polyriboinosinic:polyribocytidylic acid (Poly I:C), RNA polymerase III (Pol lII)-dependent transcription and consequently tRNA gene expression are strongly induced in DCs. This is in part caused by the phosphorylation and nuclear export of MAF1 homolog negative regulator of Poll III (MAF1), via a synergistic casein kinase 2 (CK2)- and mammalian target of rapamycin-dependent signaling cascade downstream of Toll-like receptors (TLRs). De novo tRNA expression is necessary to augment protein synthesis and compensate for tRNA degradation driven by TLR-dependent DC exposure to type-I IFN. Although protein synthesis is not strongly inhibited in absence of RNA Pol III activity, it compromises the translation of key DC mRNAs, like those coding for costimulatory molecules and proinflammatory cytokines, which instead can be stored in stress granules, as shown for CD86 mRNA. TLR-dependent CK2 stimulation and subsequent RNA Pol III activation are therefore key for the acquisition by DCs of their unique T cell immune-stimulatory functions.
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