{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360021391874860544.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1096/fj.202301691rr"}},{"identifier":{"@type":"URI","@value":"https://faseb.onlinelibrary.wiley.com/doi/pdf/10.1096/fj.202301691RR"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"<scp>FilGAP</scp>\n                    controls cell‐extracellular matrix adhesion and process formation of kidney podocytes"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title>\n                  <jats:p>The function of kidney podocytes is closely associated with actin cytoskeleton regulated by Rho small GTPases. Loss of actin‐driven cell adhesions and processes is connected to podocyte dysfunction, proteinuria, and kidney diseases. FilGAP, a GTPase‐activating protein for Rho small GTPase Rac1, is abundantly expressed in kidney podocytes, and its gene is linked to diseases in a family with focal segmental glomerulosclerosis. In this study, we have studied the role of FilGAP in podocytes in vitro. Depletion of FilGAP in cultured podocytes induced loss of actin stress fibers and increased Rac1 activity. Conversely, forced expression of FilGAP increased stress fiber formation whereas Rac1 activation significantly reduced its formation. FilGAP localizes at the focal adhesion (FA), an integrin‐based protein complex closely associated with stress fibers, that mediates cell‐extracellular matrix (ECM) adhesion, and FilGAP depletion decreased FA formation and impaired attachment to the ECM. Moreover, in unique podocyte cell cultures capable of inducing the formation of highly organized processes including major processes and foot process‐like projections, FilGAP depletion or Rac1 activation decreased the formation of these processes. The reduction of FAs and process formations in FilGAP‐depleted podocyte cells was rescued by inhibition of Rac1 or P21‐activated kinase 1 (PAK1), a downstream effector of Rac1, and PAK1 activation inhibited their formations. Thus, FilGAP contributes to both cell‐ECM adhesion and process formation of podocytes by suppressing Rac1/PAK1 signaling.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380021391874860675","@type":"Researcher","foaf:name":[{"@value":"Koji Saito"}],"jpcoar:affiliationName":[{"@value":"Division of Cell Biology, Department of Biosciences, School of Science Kitasato University  Sagamihara Kanagawa Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021391874860673","@type":"Researcher","foaf:name":[{"@value":"Seiji Yokawa"}],"jpcoar:affiliationName":[{"@value":"Division of Cell Biology, Department of Biosciences, School of Science Kitasato University  Sagamihara Kanagawa Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021391874860546","@type":"Researcher","foaf:name":[{"@value":"Hidetake Kurihara"}],"jpcoar:affiliationName":[{"@value":"Department of Physical Therapy, Faculty of Health Sciences Aino University  Osaka Ibaraki Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021391874860549","@type":"Researcher","foaf:name":[{"@value":"Eishin Yaoita"}],"jpcoar:affiliationName":[{"@value":"Kidney Research Center Niigata University Graduate School of Medical and Dental Sciences  Niigata Niigata Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021391874860674","@type":"Researcher","foaf:name":[{"@value":"Sari Mizuta"}],"jpcoar:affiliationName":[{"@value":"Division of Cell Biology, Department of Biosciences, School of Science Kitasato University  Sagamihara Kanagawa Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021391874860548","@type":"Researcher","foaf:name":[{"@value":"Kanae Tada"}],"jpcoar:affiliationName":[{"@value":"Division of Cell Biology, Department of Biosciences, School of Science Kitasato University  Sagamihara Kanagawa Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021391874860672","@type":"Researcher","foaf:name":[{"@value":"Moemi Oda"}],"jpcoar:affiliationName":[{"@value":"Division of Cell Biology, Department of Biosciences, School of Science Kitasato University  Sagamihara Kanagawa Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021391874860545","@type":"Researcher","foaf:name":[{"@value":"Hiroyasu Hatakeyama"}],"jpcoar:affiliationName":[{"@value":"Department of Physiology, School of Medicine Kitasato University  Sagamihara Kanagawa Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021391874860544","@type":"Researcher","foaf:name":[{"@value":"Yasutaka Ohta"}],"jpcoar:affiliationName":[{"@value":"Division of Cell Biology, Department of Biosciences, School of Science Kitasato University  Sagamihara Kanagawa Japan"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"08926638"},{"@type":"EISSN","@value":"15306860"}],"prism:publicationName":[{"@value":"The FASEB Journal"}],"dc:publisher":[{"@value":"Wiley"}],"prism:publicationDate":"2024-02-29","prism:volume":"38","prism:number":"5"},"reviewed":"false","dc:rights":["http://onlinelibrary.wiley.com/termsAndConditions#vor"],"url":[{"@id":"https://faseb.onlinelibrary.wiley.com/doi/pdf/10.1096/fj.202301691RR"}],"createdAt":"2024-02-29","modifiedAt":"2025-10-28","project":[{"@id":"https://cir.nii.ac.jp/crid/1040291932584044544","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"22K06149"},{"@type":"JGN","@value":"JP22K06149"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22K06149/"}],"notation":[{"@language":"ja","@value":"腎糸球体上皮細胞の突起形成におけるRacの活性制御機構の解明"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360002217491669376","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"FilGAP, a Rho/Rho-associated protein kinase–regulated GTPase-activating protein for Rac, controls tumor cell 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