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@ARTICLE{Seidel:130537,
      author       = {P. Seidel and M. Remus and M. Delacher$^*$ and P.
                      Grigaravicius$^*$ and D. E. Reuss and L. Frappart and A. von
                      Deimling$^*$ and M. Feuerer$^*$ and A. Abdollahi$^*$ and
                      P.-O. Frappart$^*$},
      title        = {{E}pidermal {N}bn deletion causes premature hair loss and a
                      phenotype resembling psoriasiform dermatitis.},
      journal      = {OncoTarget},
      volume       = {7},
      number       = {17},
      issn         = {1949-2553},
      address      = {[S.l.]},
      publisher    = {Impact Journals LLC},
      reportid     = {DKFZ-2017-05616},
      pages        = {23006 - 23018},
      year         = {2016},
      abstract     = {Nijmegen Breakage Syndrome is a disease caused by NBN
                      mutations. Here, we report a novel function of Nbn in skin
                      homeostasis. We found that Nbn deficiency in hair follicle
                      (HF) progenitors promoted increased DNA damage signaling,
                      stimulating p16Ink4a up-regulation, Trp53 stabilization and
                      cytokines secretion leading to HF-growth arrest and hair
                      loss. At later stages, the basal keratinocytes layer
                      exhibited also enhanced DNA damage response but in contrast
                      to the one in HF progenitor was not associated with
                      pro-inflammatory cytokines expression, but rather increased
                      proliferation, lack of differentiation and immune response
                      resembling psoriasiform dermatitis. Simultaneous Nbn and
                      Trp53 inactivation significantly exacerbated this phenotype,
                      due to the lack of inhibition of pro-inflammatory cytokines
                      secretion by Trp53. Altogether, we demonstrated novel
                      functions of Nbn in HF maintenance and prevention of skin
                      inflammation and we provide a mechanistic explanation that
                      links cell intrinsic DNA maintenance with large scale
                      morphological tissue alterations.},
      cin          = {D100 / E210 / G380 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)D100-20160331 / I:(DE-He78)E210-20160331 /
                      I:(DE-He78)G380-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27050272},
      pmc          = {pmc:PMC5029606},
      doi          = {10.18632/oncotarget.8470},
      url          = {https://inrepo02.dkfz.de/record/130537},
}