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@ARTICLE{Madej:280948,
      author       = {Madej, Magdalena and Ngoc, Phuong Cao Thi and Muthukumar,
                      Sowndarya and Konturek-Cieśla, Anna and Tucciarone, Silvia
                      and Germanos, Alexandre and Ashworth, Christian and
                      Kotarsky, Knut and Ghosh, Sudip and Fan, Zhimeng and Fritz,
                      Helena and Pascual-Gonzalez, Izei and Huerta, Alain and
                      Guzzi, Nicola and Colazzo, Anita and Beneventi, Giulia and
                      Lee, Hang-mao and Cieśla, Maciej and Douse, Christopher and
                      Kato, Hiroki and Swaminathan, Vinay and Agace, William W and
                      Castellanos-Rubio, Ainara and Salomoni, Paolo and Bryder,
                      David and Bellodi, Cristian},
      title        = {{PUS}10-induced t{RNA} fragmentation impacts
                      retrotransposon-driven inflammation.},
      journal      = {Cell reports},
      volume       = {44},
      number       = {6},
      issn         = {2211-1247},
      address      = {Maryland Heights, MO},
      publisher    = {Cell Press},
      reportid     = {DZNE-2025-01030},
      pages        = {115735},
      year         = {2025},
      abstract     = {Pseudouridine synthases (PUSs) catalyze the isomerization
                      of uridine (U)-to-pseudouridine (Ψ) and have emerging roles
                      in development and disease. How PUSs adapt gene expression
                      under stress remains mostly unexplored. We identify an
                      unconventional role for the Ψ 'writer' PUS10 impacting
                      intracellular innate immunity. Using Pus10 knockout mice, we
                      uncover cell-intrinsic upregulation of interferon (IFN)
                      signaling, conferring resistance to inflammation in vivo.
                      Pus10 loss alters tRNA-derived small RNAs (tdRs) abundance,
                      perturbing translation and endogenous retroelements
                      expression. These alterations promote proinflammatory
                      RNA-DNA hybrids accumulation, potentially activating cyclic
                      GMP-AMP synthase (cGAS)-stimulator of interferon gene
                      (STING). Supplementation with selected tdR pools partly
                      rescues these effects through interactions with RNA
                      processing factors that modulate immune responses, revealing
                      a regulatory circuit that counteracts cell-intrinsic
                      inflammation. By extension, we define a PUS10-specific
                      molecular fingerprint linking its dysregulation to human
                      autoimmune disorders, including inflammatory bowel diseases.
                      Collectively, these findings establish PUS10 as a viral
                      mimicry modulator, with broad implications for innate immune
                      homeostasis and autoimmunity.},
      keywords     = {Animals / Retroelements: genetics / Inflammation: genetics
                      / Inflammation: pathology / Inflammation: metabolism / Mice
                      / RNA, Transfer: metabolism / RNA, Transfer: genetics /
                      Mice, Knockout / Humans / Immunity, Innate / Intramolecular
                      Transferases: metabolism / Intramolecular Transferases:
                      genetics / Mice, Inbred C57BL / Hydro-Lyases: metabolism /
                      Hydro-Lyases: genetics / Interferons: metabolism / Signal
                      Transduction / Membrane Proteins: metabolism / CP: Molecular
                      biology (Other) / PUS10 (Other) / RNA-DNA hybrids (Other) /
                      cGAS-STING (Other) / hematopoietic stem cell (Other) /
                      inflammation (Other) / inflammatory bowel disease (Other) /
                      interferon (Other) / pseudouridine (Other) / tRNA-derived
                      small RNAs (Other) / transposable elements (Other) / viral
                      mimicry (Other) / Retroelements (NLM Chemicals) / RNA,
                      Transfer (NLM Chemicals) / pseudouridine synthases (NLM
                      Chemicals) / Intramolecular Transferases (NLM Chemicals) /
                      Hydro-Lyases (NLM Chemicals) / Interferons (NLM Chemicals) /
                      Membrane Proteins (NLM Chemicals)},
      cin          = {AG Salomoni},
      ddc          = {610},
      cid          = {I:(DE-2719)1013032},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40402745},
      doi          = {10.1016/j.celrep.2025.115735},
      url          = {https://pub.dzne.de/record/280948},
}