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@ARTICLE{Noethel:856433,
      author       = {Noethel, Barbara and Ramms, Lena and Dreissen, Georg and
                      Hoffmann, Marco and Springer, Ronald and Rübsam, Matthias
                      and Ziegler, Wolfgang H. and Niessen, Carien M. and Merkel,
                      Rudolf and Hoffmann, Bernd},
      title        = {{T}ransition of responsive mechanosensitive elements from
                      focal adhesions to adherens junctions on epithelial
                      differentiation},
      journal      = {Molecular biology of the cell},
      volume       = {29},
      number       = {19},
      issn         = {1939-4586},
      address      = {Bethesda, Md.},
      publisher    = {American Society for Cell Biology},
      reportid     = {FZJ-2018-05832},
      pages        = {2317 - 2325},
      year         = {2018},
      abstract     = {The skin’s epidermis is a multilayered epithelial tissue
                      and the first line of defense against mechanical stress. Its
                      barrier function depends on an integrated assembly and
                      reorganization of cell–matrix and cell–cell junctions in
                      the basal layer and on different intercellular junctions in
                      suprabasal layers. However, how mechanical stress is
                      recognized and which adhesive and cytoskeletal components
                      are involved are poorly understood. Here, we subjected
                      keratinocytes to cyclic stress in the presence or absence of
                      intercellular junctions. Both states not only recognized but
                      also responded to strain by reorienting actin filaments
                      perpendicular to the applied force. Using different
                      keratinocyte mutant strains that altered the mechanical link
                      of the actin cytoskeleton to either cell–matrix or
                      cell–cell junctions, we show that not only focal adhesions
                      but also adherens junctions function as mechanosensitive
                      elements in response to cyclic strain. Loss of paxillin or
                      talin impaired focal adhesion formation and only affected
                      mechanosensitivity in the absence but not presence of
                      intercellular junctions. Further analysis revealed the
                      adherens junction protein α-catenin as a main
                      mechanosensor, with greatest sensitivity conferred on
                      binding to vinculin. Our data reveal a mechanosensitive
                      transition from cell–matrix to cell–cell adhesions on
                      formation of keratinocyte monolayers with vinculin and
                      α-catenin as vital players.},
      cin          = {ICS-7},
      ddc          = {570},
      cid          = {I:(DE-Juel1)ICS-7-20110106},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30044710},
      UT           = {WOS:000451909400006},
      doi          = {10.1091/mbc.E17-06-0387},
      url          = {https://juser.fz-juelich.de/record/856433},
}