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stat, trim, acetylation, macrophages, fig, cells, cbp, analysis, article, data, google, scholar, expression, lys, cas, macrophage, ubiquitination, lysine, activity, polarization, gene, tumor, immunoblot, transcriptional, genes, cell, proteins, mice, stimulated, nature, protein, human, supplementary, cancer, immunity, transfected, immunoprecipitation, mutant, study, source, trimdeficient, antibodies, function, antitumor, assay, primary, activation, mouse, suggested, min,

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nature portfolio privacy policy critical editing bgi tech solutions advertising p300/creb-binding protein-mediated acetylation acetylation-dependent signal transduction thermo fisher scientific anti-csf-1r antibody reveals reprints nature 496 nature 513 nature 468 nature shanghai research center specific pathogen-free facility anti-ly-6g/ly6c antibodies nf-κb-mediated m1 underwent curative-intent surgery peer review reports tumour-derived lactic acid source data file stat6-induced luciferase activity /g-coupled agarose beads myeloid-derived suppressor cells diverse c-terminal domains key research program human pbmc-derived macrophages stat6-mediated trim24 downregulation macrophage-recruiting chemokine ccl24 luciferase activity driven acetyltransferase creb-binding protein 10-ml media trim24 deficiency-induced inhibition social media il-4-induced activated stat6 tsa/nam pretreatment suppressed ring domain-deleted mutant fluorescent-conjugated secondary antibodies il-4-induced signaling pathway functional domains-deleted trim24 tumor-killing immune cells donkey anti-goat igg human peripheral blood anti-ly-6g antibody il-4-stimulated trim24-deficient macrophages trim24-mediated cbp ubiquitination stat6 dramatically suppresses trim24-induced cbp ubiquitination cbp-mediated stat6 acetylation

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         headline:Modulation of M2 macrophage polarization by the crosstalk between Stat6 and Trim24
         description:Stat6 is known to drive macrophage M2 polarization. However, how macrophage polarization is fine-tuned by Stat6 is poorly understood. Here, we find that Lys383 of Stat6 is acetylated by the acetyltransferase CREB-binding protein (CBP) during macrophage activation to suppress macrophage M2 polarization. Mechanistically, Trim24, a CBP-associated E3 ligase, promotes Stat6 acetylation by catalyzing CBP ubiquitination at Lys119 to facilitate the recruitment of CBP to Stat6. Loss of Trim24 inhibits Stat6 acetylation and thus promotes M2 polarization in both mouse and human macrophages, potentially compromising antitumor immune responses. By contrast, Stat6 mediates the suppression of TRIM24 expression in M2 macrophages to contribute to the induction of an immunosuppressive tumor niche. Taken together, our findings establish Stat6 acetylation as an essential negative regulatory mechanism that curtails macrophage M2 polarization. Stat6 promotes M2 macrophage polarization. Here the authors characterize Trim24-CBP-Stat6 circuit regulating M2 macrophage polarization via Stat6 acetylation, and show it contributes to pro-tumorigenic macrophage activity in mice.
         datePublished:2019-09-25T00:00:00Z
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            Innate immune cells
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      headline:Modulation of M2 macrophage polarization by the crosstalk between Stat6 and Trim24
      description:Stat6 is known to drive macrophage M2 polarization. However, how macrophage polarization is fine-tuned by Stat6 is poorly understood. Here, we find that Lys383 of Stat6 is acetylated by the acetyltransferase CREB-binding protein (CBP) during macrophage activation to suppress macrophage M2 polarization. Mechanistically, Trim24, a CBP-associated E3 ligase, promotes Stat6 acetylation by catalyzing CBP ubiquitination at Lys119 to facilitate the recruitment of CBP to Stat6. Loss of Trim24 inhibits Stat6 acetylation and thus promotes M2 polarization in both mouse and human macrophages, potentially compromising antitumor immune responses. By contrast, Stat6 mediates the suppression of TRIM24 expression in M2 macrophages to contribute to the induction of an immunosuppressive tumor niche. Taken together, our findings establish Stat6 acetylation as an essential negative regulatory mechanism that curtails macrophage M2 polarization. Stat6 promotes M2 macrophage polarization. Here the authors characterize Trim24-CBP-Stat6 circuit regulating M2 macrophage polarization via Stat6 acetylation, and show it contributes to pro-tumorigenic macrophage activity in mice.
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         Innate immune cells
         Phagocytes
         Signal transduction
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         Humanities and Social Sciences
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      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
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      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
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      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
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      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
      name:CAS Key Laboratory of Tissue Microenvironment and Tumor, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine & Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China
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