<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Schell, Christoph</dc:creator>
  <dc:creator>Sabass, Benedikt</dc:creator>
  <dc:creator>Helmstaedter, Martin</dc:creator>
  <dc:creator>Geist, Felix</dc:creator>
  <dc:creator>Abed, Ahmed</dc:creator>
  <dc:creator>Yasuda-Yamahara, Mako</dc:creator>
  <dc:creator>Sigle, August</dc:creator>
  <dc:creator>Maier, Jasmin I.</dc:creator>
  <dc:creator>Grahammer, Florian</dc:creator>
  <dc:creator>Siegerist, Florian</dc:creator>
  <dc:creator>Artelt, Nadine</dc:creator>
  <dc:creator>Endlich, Nicole</dc:creator>
  <dc:creator>Kerjaschki, Dontscho</dc:creator>
  <dc:creator>Arnold, Hans-Henning</dc:creator>
  <dc:creator>Dengjel, Jörn</dc:creator>
  <dc:creator>Rogg, Manuel</dc:creator>
  <dc:creator>Huber, Tobias B.</dc:creator>
  <dc:date>2018-12-17</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">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.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/307333</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/307333/files/den_acp.pdf</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/307333/files/den_acp_sm1.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.devcel.2018.11.011</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>Developmental Cell. - 2018, vol. 47, no. 6, p. 741-757.e8</dc:source>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns1="xml" ns1:lang="en">Arp3 controls the podocyte architecture at the kidney filtration barrier</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
