% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Khan:145064,
      author       = {Khan, Nida S and Lukason, Daniel P and Feliu, Marianela and
                      Ward, Rebecca A and Lord, Allison K and Reedy, Jennifer L
                      and Ramirez-Ortiz, Zaida G and Tam, Jenny M and
                      Kasperkovitz, Pia V and Negoro, Paige E and Vyas, Tammy D
                      and Xu, Shuying and Brinkmann, Melanie M and Acharaya, Mridu
                      and Artavanis-Tsakonas, Katerina and Frickel, Eva-Maria and
                      Becker, Christine E and Dagher, Zeina and Kim, You-Me and
                      Latz, Eicke and Ploegh, Hidde L and Mansour, Michael K and
                      Miranti, Cindy K and Levitz, Stuart M and Vyas, Jatin M},
      title        = {{CD}82 controls {C}p{G}-dependent {TLR}9 signaling.},
      journal      = {The FASEB journal},
      volume       = {33},
      number       = {11},
      issn         = {0892-6638},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DZNE-2020-00423},
      pages        = {12500-12514},
      year         = {2019},
      abstract     = {The tetraspanin CD82 is a potent suppressor of tumor
                      metastasis and regulates several processes including signal
                      transduction, cell adhesion, motility, and aggregation.
                      However, the mechanisms by which CD82 participates in innate
                      immunity are unknown. We report that CD82 is a key regulator
                      of TLR9 trafficking and signaling. TLR9 recognizes
                      unmethylated cytosine-phosphate-guanine (CpG) motifs present
                      in viral, bacterial, and fungal DNA. We demonstrate that
                      TLR9 and CD82 associate in macrophages, which occurs in the
                      endoplasmic reticulum (ER) and post-ER. Moreover, CD82 is
                      essential for TLR9-dependent myddosome formation in response
                      to CpG stimulation. Finally, CD82 modulates TLR9-dependent
                      NF-κB nuclear translocation, which is critical for
                      inflammatory cytokine production. To our knowledge, this is
                      the first time a tetraspanin has been implicated as a key
                      regulator of TLR signaling. Collectively, our study
                      demonstrates that CD82 is a specific regulator of TLR9
                      signaling, which may be critical in cancer immunotherapy
                      approaches and coordinating the innate immune response to
                      pathogens.},
      keywords     = {Active Transport, Cell Nucleus: drug effects / Active
                      Transport, Cell Nucleus: genetics / Active Transport, Cell
                      Nucleus: immunology / Animals / Cell Nucleus: genetics /
                      Cell Nucleus: immunology / Cytokines: genetics / Cytokines:
                      immunology / Endoplasmic Reticulum: genetics / Endoplasmic
                      Reticulum: immunology / Endoplasmic Reticulum: pathology /
                      Inflammation: genetics / Inflammation: immunology /
                      Inflammation: pathology / Kangai-1 Protein: genetics /
                      Kangai-1 Protein: immunology / Macrophages: immunology /
                      Macrophages: pathology / Mice / Mice, Knockout / NF-kappa B:
                      genetics / NF-kappa B: immunology /
                      Oligodeoxyribonucleotides: pharmacology / RAW 264.7 Cells /
                      Signal Transduction: drug effects / Signal Transduction:
                      genetics / Signal Transduction: immunology / Toll-Like
                      Receptor 9: genetics / Toll-Like Receptor 9: immunology /
                      CPG-oligonucleotide (NLM Chemicals) / Cd82 antigen, mouse
                      (NLM Chemicals) / Cytokines (NLM Chemicals) / Kangai-1
                      Protein (NLM Chemicals) / NF-kappa B (NLM Chemicals) /
                      Oligodeoxyribonucleotides (NLM Chemicals) / Tlr9 protein,
                      mouse (NLM Chemicals) / Toll-Like Receptor 9 (NLM
                      Chemicals)},
      cin          = {Bonn common / AG Latz},
      ddc          = {570},
      cid          = {I:(DE-2719)6000011 / I:(DE-2719)1013024},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31408613},
      pmc          = {pmc:PMC6988855},
      doi          = {10.1096/fj.201901547R},
      url          = {https://pub.dzne.de/record/145064},
}