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We began analyzing https://www.tandfonline.com/doi/full/10.1080/15548627.2022.2076192, but it redirected us to https://www.tandfonline.com/doi/full/10.1080/15548627.2022.2076192. The analysis below is for the second page.

Title[redir]:
Full article: UXT attenuates the CGAS-STING1 signaling by targeting STING1 for autophagic degradation
Description:
The CGAS-STING1 signaling is critical for mediating the production of type I interferons and other proinflammatory cytokines in innate immunity. Upon cytosolic DNA stimulation, CGAS produces an end...

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Keywords {🔍}

uxt, open, sting, expression, science, signaling, control, source, cell, autophagy, cgassting, sle, figure, windowgoogle, scholar, windowpubmed, windowweb, cgamp, cells, citation, type, mefs, mice, stimulated, transfected, patients, degradation, pathway, analysis, data, cko, htdna, gene, lupus, negative, isgs, autophagic, activation, sqstm, genes, lysates, irf, plasmids, ifn, pbmcs, significantly, collected, immune, china, interferon,

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crispr-cas9-mediated homologous recombination social care medicine including aicardi–goutières syndrome/ags disclosure statement specific pathogen-free conditions anti-interferon-α monoclonal antibody supplemental material acknowledgments age-matched uxtfl/fl mice references paludan sr additional information funding mice expressing lyz2/lysm-cre google scholar reprints sting-mediated ifn-β production methods mol biol bone marrow-derived macrophages basic medical sciences gram-negative bacterial peptidoglycan graph-based genome alignment nf-kappab transcriptional enhanceosome sciences dna sensing 2 × 150 bp paired-end layout cyclic gmp-amp synthase cyclic gmp‐amp synthase cgas-sting pathway controls double membrane-bound autophagosomes state key laboratory sting1-mediated autophagic vesicle cgas–sting signalling source ptk-renilla reporter plasmid autophagy-dependent secretion original rna-seq data analyze rna-seq data remove low-quality reads display full size heightened tmpd-induced expression tmpd-induced mice model apparent cell-type specificity raw rna-seq data 25% na-deoxycholate [sigma-aldrich suppressing sting1-mediated type cgas-sting1 signaling response cgas-sting1 signaling [citation23] cgas-sting1 signaling responses anti-actb/β-actin autophagy-lysosome pathway [citation25 cgas-sting1 signaling pathway request academic permissions lc3-interacting region motifs placebo-controlled study source innate immune response

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Complex disease=complex trial?
Editorial: Interferon‐Targeted Therapy for Systemic Lupus Erythematosus: Are the Trials on Target?
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What is damaging the kidney in lupus nephritis?
What is damaging the kidney in lupus nephritis?
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      articleSection:Research Paper
      name:UXT attenuates the CGAS-STING1 signaling by targeting STING1 for autophagic degradation
      headline:UXT attenuates the CGAS-STING1 signaling by targeting STING1 for autophagic degradation
      abstract:STING1 (stimulator of interferon response cGAMP interactor 1), the pivotal adaptor protein of CGAS (cyclic GMP-AMP synthase)-STING1 signaling, is critical for type I IFN production of innate immunity. However, excessive or prolonged activation of STING1 is associated with autoinflammatory and autoimmune diseases. Thus, preventing STING1 from over-activation is important to maintain immune homeostasis. Here, we reported that UXT (ubiquitously expressed prefoldin like chaperone), a small chaperone-like protein, was essential to prevent the excessive activation of STING1-mediated type I IFN signaling through autophagic degradation of STING1 via SQSTM1 (sequestosome 1). Upon DNA mimics or cyclic GMP-AMP (cGAMP) stimulation, UXT specifically interacted with STING1 and promoted STING1 degradation through selective macroautophagy/autophagy. Moreover, UXT was required for more efficient autophagic degradation of STING1 by facilitating the interaction of SQSTM1 and STING1. The in vivo role of UXT in attenuating the CGAS-STING1 signaling was further confirmed in the mouse model of DNA-virus infection and the TMPD (2,6,10,14-tetramethylpentadecane)-induced murine lupus model. Intriguingly, the expression of UXT was consistently impaired and exhibited a remarkable inverse correlation with type I IFN signature in the leukocytes and PBMCs (peripheral blood mononuclear cells) of several large SLE (systemic lupus erythematosus) cohorts. Importantly, the replenishment of UXT effectively suppressed the production of IFNs and ISGs in the PBMCs of SLE patients. Taken together, our study reveals a novel regulatory role of UXT in autophagic degradation of STING1 to maintain immune homeostasis. UXT might be a potential therapeutic target for alleviating aberrant type I IFNs in autoimmune diseasesAbbreviations: 3-MA: 3-methyladenine; BMDMs: bone marrow-derived macrophages; cGAMP: cyclic GMP-AMP; CGAS: cyclic gmp-amp synthase; cKO: conditional knockout; CXCL10: C-X-C motif chemokine ligand 10; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HSV-1: herpes simplex virus type 1; HTDNA: herring testes DNA; IFIT1: interferon induced protein with tetratricopeptide repeats 1; IFNA4: interferon alpha 4; IFNB: interferon beta; IRF3: interferon regulatory factor 3; ISD: interferon stimulatory DNA; ISGs: IFN-stimulated genes; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MEFs: mouse embryonic fibroblasts; RNA-seq: RNA sequencing; PBMCs: peripheral blood mononuclear cells; RSAD2: radical S-adenosyl methionine domain containing 2; SLE: systemic lupus erythematosus; SQSTM1: sequestosome 1; STING1: stimulator of interferon response cGAMP interactor 1; TBK1: TANK binding kinase 1; TMPD: 2,6,10,14-tetramethylpentadecane; UXT: ubiquitously expressed prefoldin like chaperone.
      description:STING1 (stimulator of interferon response cGAMP interactor 1), the pivotal adaptor protein of CGAS (cyclic GMP-AMP synthase)-STING1 signaling, is critical for type I IFN production of innate immunity. However, excessive or prolonged activation of STING1 is associated with autoinflammatory and autoimmune diseases. Thus, preventing STING1 from over-activation is important to maintain immune homeostasis. Here, we reported that UXT (ubiquitously expressed prefoldin like chaperone), a small chaperone-like protein, was essential to prevent the excessive activation of STING1-mediated type I IFN signaling through autophagic degradation of STING1 via SQSTM1 (sequestosome 1). Upon DNA mimics or cyclic GMP-AMP (cGAMP) stimulation, UXT specifically interacted with STING1 and promoted STING1 degradation through selective macroautophagy/autophagy. Moreover, UXT was required for more efficient autophagic degradation of STING1 by facilitating the interaction of SQSTM1 and STING1. The in vivo role of UXT in attenuating the CGAS-STING1 signaling was further confirmed in the mouse model of DNA-virus infection and the TMPD (2,6,10,14-tetramethylpentadecane)-induced murine lupus model. Intriguingly, the expression of UXT was consistently impaired and exhibited a remarkable inverse correlation with type I IFN signature in the leukocytes and PBMCs (peripheral blood mononuclear cells) of several large SLE (systemic lupus erythematosus) cohorts. Importantly, the replenishment of UXT effectively suppressed the production of IFNs and ISGs in the PBMCs of SLE patients. Taken together, our study reveals a novel regulatory role of UXT in autophagic degradation of STING1 to maintain immune homeostasis. UXT might be a potential therapeutic target for alleviating aberrant type I IFNs in autoimmune diseasesAbbreviations: 3-MA: 3-methyladenine; BMDMs: bone marrow-derived macrophages; cGAMP: cyclic GMP-AMP; CGAS: cyclic gmp-amp synthase; cKO: conditional knockout; CXCL10: C-X-C motif chemokine ligand 10; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HSV-1: herpes simplex virus type 1; HTDNA: herring testes DNA; IFIT1: interferon induced protein with tetratricopeptide repeats 1; IFNA4: interferon alpha 4; IFNB: interferon beta; IRF3: interferon regulatory factor 3; ISD: interferon stimulatory DNA; ISGs: IFN-stimulated genes; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MEFs: mouse embryonic fibroblasts; RNA-seq: RNA sequencing; PBMCs: peripheral blood mononuclear cells; RSAD2: radical S-adenosyl methionine domain containing 2; SLE: systemic lupus erythematosus; SQSTM1: sequestosome 1; STING1: stimulator of interferon response cGAMP interactor 1; TBK1: TANK binding kinase 1; TMPD: 2,6,10,14-tetramethylpentadecane; UXT: ubiquitously expressed prefoldin like chaperone.
      author:
            type:Person
            name:Mingyu Pan
            type:Person
            name:Yue Yin
            type:Person
            name:Tongyu Hu
            type:Person
            name:Xinxia Wang
            type:Person
            name:Tian Jia
            type:Person
            name:Jing Sun
            type:Person
            name:Quanyi Wang
            type:Person
            name:Wei Meng
            type:Person
            name:Juanjuan Zhu
            type:Person
            name:Chunsun Dai
            type:Person
            name:Haiyang Hu
            type:Person
            name:Chen Wang
      keywords:UXT, STING1, SQSTM1, SLE, Autophagic degradation
      pageStart:440
      pageEnd:456
      datePublished:2022-05-30
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      name:Tian Jia
      name:Jing Sun
      name:Quanyi Wang
      name:Wei Meng
      name:Juanjuan Zhu
      name:Chunsun Dai
      name:Haiyang Hu
      name:Chen Wang
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