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@ARTICLE{Breitkopf:148843,
      author       = {D. M. Breitkopf and V. Jankowski and K. Ohl and J. Hermann
                      and D. Hermert and K. Tenbrock and X. Liu and I. V. Martin
                      and J. Wang and F. Groll and E. Gröne$^*$ and J. Floege and
                      T. Ostendorf and T. Rauen and U. Raffetseder},
      title        = {{T}he {YB}-1:{N}otch-3 axis modulates immune cell responses
                      and organ damage in systemic lupus erythematosus.},
      journal      = {Kidney international},
      volume       = {97},
      number       = {2},
      issn         = {0085-2538},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2020-00035},
      pages        = {289-303},
      year         = {2020},
      note         = {2020 Feb;97(2):289-303},
      abstract     = {Systemic lupus erythematosus (SLE) is an autoimmune disease
                      and lupus nephritis is a major risk factor for morbidity and
                      mortality. Notch-3 signaling induced by membrane-bound or
                      soluble ligands such as YB-1 constitutes an evolutionarily
                      conserved pathway that determines major decisions in cell
                      fate. Mass spectrometry of extracellular YB-1 in sera from
                      patients with SLE and lupus-prone mice revealed specific
                      post-translational guanidinylation of two lysine residues
                      within the highly conserved cold-shock domain of YB-1
                      (YB-1-G). These modifications highly correlated with SLE
                      disease activity, especially in patients with lupus
                      nephritis and resulted in enhanced activation of Notch-3
                      signaling in T lymphocytes. The importance of YB-1:Notch-3
                      interaction in T cells was further evidenced by increased
                      interleukin (Il)10 expression following YB-1-G stimulation
                      and detection of both, YB-1-G and Notch-3, in kidneys of
                      MRL.lpr mice by mass spectrometry imaging. Notch-3
                      expression and activation was significantly up-regulated in
                      kidneys of 20-week-old MRL.lpr mice. Notably, lupus-prone
                      mice with constitutional Notch-3 depletion
                      (B6.Faslpr/lprNotch3-/-) exhibited an aggravated lupus
                      phenotype with significantly increased mortality, enlarged
                      lymphoid organs and aggravated nephritis. Additionally,
                      these mice displayed fewer regulatory T cells and reduced
                      amounts of anti-inflammatory IL-10. Thus, our results
                      indicate that the YB-1:Notch-3 axis exerts protective
                      effects in SLE and that Notch-3 deficiency exacerbates the
                      SLE phenotype.},
      cin          = {G130},
      ddc          = {610},
      cid          = {I:(DE-He78)G130-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31882173},
      doi          = {10.1016/j.kint.2019.09.031},
      url          = {https://inrepo02.dkfz.de/record/148843},
}