% 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{Zupancic:128242,
      author       = {T. Zupancic and G. Sersa and H. Törmä and E. B. Lane and
                      H. Herrmann$^*$ and R. Komel and M. Liovic},
      title        = {{K}eratin gene mutations influence the keratinocyte
                      response to {DNA} damage and cytokine induced apoptosis.},
      journal      = {Archives of dermatological research},
      volume       = {309},
      number       = {7},
      issn         = {1432-069X},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {DKFZ-2017-04259},
      pages        = {587 - 593},
      year         = {2017},
      abstract     = {The keratin filament cytoskeleton is vital to the normal
                      function of epithelial cells. It provides structural support
                      and regulates different aspects of cell metabolism.
                      Mutations in keratins 5 and 14 cause a skin fragility
                      disorder, epidermolysis bullosa simplex (EBS). Patients with
                      severe EBS have an increased cumulative risk for basal cell
                      carcinoma. In this study, we tested how keratin 5 and 14
                      mutant EBS patient-derived keratinocytes behave in the face
                      of two different types of stressors that are able to induce
                      cell death: ionizing radiation and cytokines TNF-α and
                      TRAIL. The data point out to a substantial difference
                      between how normal and keratin mutant keratinocytes deal
                      with such stresses. When case of DNA damage, the
                      ATM/Chk2-pathway is one of the two main tracks that can
                      prevent the progression of mitosis and so allow repair. This
                      was altered in all investigated keratin mutants with a
                      particular down-regulation of the activated form of
                      checkpoint kinase 2 (pChk2). Keratin mutants also appear
                      less sensitive than normal cells to treatment with TNF-α or
                      TRAIL, and this may be linked to the up-regulation of two
                      pro-survival proteins, Bcl-2 and FLIP. Such changes are
                      likely to have a profound effect on mutant keratinocytes
                      ability to survive and withstand stress, and in theory this
                      may be also a contributing factor to cell transformation.},
      cin          = {B065},
      ddc          = {610},
      cid          = {I:(DE-He78)B065-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28647894},
      doi          = {10.1007/s00403-017-1757-9},
      url          = {https://inrepo02.dkfz.de/record/128242},
}