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hu6-mcs-ubiquitin-egfp-ires-puromycin nature portfolio privacy policy ubi-mcs-3flag-cmv-egfp inhibiting hif-1α-mediated glycolysis online bioinformatics tools pe-cy7 anti-mouse i-ab scientific investigation board editing strengthened tlr4/nf-κb signaling middle-salt washing buffer published research dendritic cell development advertising tlr4/nf-κb signaling pathway specialized antigen-presenting cells pe-cy7 anti-mouse cd4 antigen-specific t-cell responses nature communications pe-cy7 anti-mouse cd40 professional apcs flag-tagged wild-type mettl3 tlr4/nf-κb pathway reprints research design facilitates hippocampus-dependent learning prevalent post-transcriptional modification rna n6-methyladenosine methyltransferase n6-methyladenosine-dependent regulation research nf-κb signaling pathway n6-methyladenosine rna demethylase cfse-labeled ot-ii cd4+ full size image source data file early cell-fate decisions52 mettl3-mediated m6a modification bone marrow-derived dc post-transcriptional gene regulation dual-luciferase reporter assay high-salt washing buffer low-salt washing buffer ngs library preparation acute myeloid leukemia peer review nf-κb subunit p65 bone marrow-derived imdc a-demethylated antiviral transcripts il-7/stat5/socs pathways plasmids bearing wild-type

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      description:N6-methyladenosine (m6A) modification plays important roles in various cellular responses by regulating mRNA biology. However, how m6A modification is involved in innate immunity via affecting the translation of immune transcripts remains to be further investigated. Here we report that RNA methyltransferase Mettl3-mediated mRNA m6A methylation promotes dendritic cell (DC) activation and function. Specific depletion of Mettl3 in DC resulted in impaired phenotypic and functional maturation of DC, with decreased expression of co-stimulatory molecules CD40, CD80 and cytokine IL-12, and reduced ability to stimulate T cell responses both in vitro and in vivo. Mechanistically, Mettl3-mediated m6A of CD40, CD80 and TLR4 signaling adaptor Tirap transcripts enhanced their translation in DC for stimulating T cell activation, and strengthening TLR4/NF-κB signaling-induced cytokine production. Our findings identify a new role for Mettl3-mediated m6A modification in increasing translation of certain immune transcripts for physiological promotion of DC activation and DC-based T cell response. Here the authors examine how m6A modification is involved in innate immunity. They show that RNA methyltransferase Mettl3-mediated mRNA m6A methylation promotes dendritic cell (DC) activation and function, and in promoting DC-based T cells responses.
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      name:Westlake Institute for Advanced Study, Hangzhou, China
      name:State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China
      name:Department of Immunology & Center for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China
      name:National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China
      name:College of Life Science, Nankai University, Tianjin, China
      name:Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, China

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