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@ARTICLE{Lvenich:894715,
      author       = {Lövenich, Lukas and Dreissen, Georg and Hoffmann,
                      Christina and Konrad, Jens and Springer, Ronald and
                      Höhfeld, Jörg and Merkel, Rudolf and Hoffmann, Bernd},
      title        = {{S}train induced mechanoresponse depends on cell
                      contractility and {BAG}3-mediated autophagy},
      journal      = {Molecular biology of the cell},
      volume       = {32},
      number       = {20},
      issn         = {1939-4586},
      address      = {Bethesda, Md.},
      publisher    = {American Society for Cell Biology},
      reportid     = {FZJ-2021-03367},
      pages        = {},
      year         = {2021},
      abstract     = {Basically, all mammalian tissues are constantly exposed to
                      a variety of environmental mechanical signals. Depending on
                      the signal strength, mechanics intervenes in a multitude of
                      cellular processes and is thus capable of inducing simple
                      cellular adaptations but also complex differentiation
                      processes and even apoptosis. The underlying recognition
                      typically depends on mechanosensitive proteins, which most
                      often sense the mechanical signal for the induction of a
                      cellular signaling cascade by changing their protein
                      conformation. However, the fate of mechanosensors after
                      mechanical stress application is still poorly understood,
                      and it remains unclear whether protein degradation pathways
                      affect the mechanosensitivity of cells. Here, we show that
                      cyclic stretch induces autophagosome formation in a
                      time-dependent manner. Formation depends on the cochaperone
                      BAG family molecular chaperone regulator 3 (BAG3) and thus
                      likely involves BAG3-mediated chaperone-assisted selective
                      autophagy. Furthermore, we demonstrate that strain-induced
                      cell reorientation is clearly delayed upon inhibition of
                      autophagy, suggesting a bidirectional cross-talk between
                      mechanotransduction and autophagic degradation. The strength
                      of the observed delay depends on stable adhesion structures
                      and stress fiber formation in a Ras homologue family member
                      A (RhoA)-dependent manner.},
      cin          = {IBI-2},
      ddc          = {570},
      cid          = {I:(DE-Juel1)IBI-2-20200312},
      pnm          = {5241 - Molecular Information Processing in Cellular Systems
                      (POF4-524) / DFG project 388932620 - FOR 2743: Zelluläre
                      Schutzmechanismen gegen mechanischen Stress},
      pid          = {G:(DE-HGF)POF4-5241 / G:(GEPRIS)388932620},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34379447},
      UT           = {WOS:000743181900005},
      doi          = {10.1091/mbc.E21-05-0254},
      url          = {https://juser.fz-juelich.de/record/894715},
}