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@ARTICLE{Schell:866149,
      author       = {Schell, Christoph and Sabass, Benedikt and Helmstaedter,
                      Martin and Geist, Felix and Abed, Ahmed and Yasuda-Yamahara,
                      Mako and Sigle, August and Maier, Jasmin I. and Grahammer,
                      Florian and Siegerist, Florian and Artelt, Nadine and
                      Endlich, Nicole and Kerjaschki, Dontscho and Arnold,
                      Hans-Henning and Dengjel, Jörn and Rogg, Manuel and Huber,
                      Tobias B.},
      title        = {{ARP}3 {C}ontrols the {P}odocyte {A}rchitecture at the
                      {K}idney {F}iltration {B}arrier},
      journal      = {Developmental cell},
      volume       = {47},
      number       = {6},
      issn         = {1534-5807},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {FZJ-2019-05345},
      pages        = {741 - 757.e8},
      year         = {2018},
      abstract     = {Podocytes, highly specialized epithelial cells, build the
                      outer part of the kidney filtration barrier and withstand
                      high mechanical forces through a complex network of cellular
                      protrusions. Here, we show that Arp2/3-dependent actin
                      polymerization controls actomyosin contractility and focal
                      adhesion maturation of podocyte protrusions and thereby
                      regulates formation, maintenance, and capacity to adapt to
                      mechanical requirements of the filtration barrier. We find
                      that N-WASP-Arp2/3 define the development of complex
                      arborized podocyte protrusions in vitro and in vivo. Loss of
                      dendritic actin networks results in a pronounced activation
                      of the actomyosin cytoskeleton and the generation of
                      over-maturated but less efficient adhesion, leading to
                      detachment of podocytes. Our data provide a model to explain
                      podocyte protrusion morphology and their mechanical
                      stability based on a tripartite relationship between actin
                      polymerization, contractility, and adhesion.},
      cin          = {ICS-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-2-20110106},
      pnm          = {553 - Physical Basis of Diseases (POF3-553)},
      pid          = {G:(DE-HGF)POF3-553},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30503751},
      UT           = {WOS:000453390700015},
      doi          = {10.1016/j.devcel.2018.11.011},
      url          = {https://juser.fz-juelich.de/record/866149},
}