{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T20:06:38Z","timestamp":1786133198563,"version":"build-2736575974"},"reference-count":77,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01DK088826-03"],"award-info":[{"award-number":["R01DK088826-03"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T32 DK007726 NRSA"],"award-info":[{"award-number":["T32 DK007726 NRSA"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2021,2]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      FSGS caused by mutations in\n                      <jats:italic toggle=\"yes\">INF2<\/jats:italic>\n                      is characterized by a podocytopathy with mistrafficked nephrin, an essential component of the slit diaphragm. Because INF2 is a formin-type actin nucleator, research has focused on its actin-regulating function, providing an important but incomplete insight into how these mutations lead to podocytopathy. A yeast two-hybridization screen identified the interaction between INF2 and the dynein transport complex, suggesting a newly recognized role of INF2 in regulating dynein-mediated vesicular trafficking in podocytes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Live cell and quantitative imaging, fluorescent and surface biotinylation-based trafficking assays in cultured podocytes, and a new puromycin aminoglycoside nephropathy model of\n                      <jats:italic toggle=\"yes\">INF2<\/jats:italic>\n                      transgenic mice were used to demonstrate altered dynein-mediated trafficking of nephrin in INF2 associated podocytopathy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Pathogenic\n                      <jats:italic toggle=\"yes\">INF2<\/jats:italic>\n                      mutations disrupt an interaction of INF2 with dynein light chain 1, a key dynein component. The best-studied mutation, R218Q, diverts dynein-mediated postendocytic sorting of nephrin from recycling endosomes to lysosomes for degradation. Antagonizing dynein-mediated transport can rescue this effect. Augmented dynein-mediated trafficking and degradation of nephrin underlies puromycin aminoglycoside-induced podocytopathy and FSGS\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">INF2<\/jats:italic>\n                      mutations enhance dynein-mediated trafficking of nephrin to proteolytic pathways, diminishing its recycling required for maintaining slit diaphragm integrity. The recognition that dysregulated dynein-mediated transport of nephrin in R218Q knockin podocytes opens an avenue for developing targeted therapy for INF2-mediated FSGS.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2020081109","type":"journal-article","created":{"date-parts":[[2020,12,23]],"date-time":"2020-12-23T13:08:31Z","timestamp":1608728911000},"page":"307-322","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":30,"title":["Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy"],"prefix":"10.1681","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8233-7755","authenticated-orcid":false,"given":"Hua","family":"Sun","sequence":"first","affiliation":[{"name":"Division of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"},{"name":"Renal Division, Boston Children\u2019s Hospital, Harvard Medical School, Boston, Massachusetts"},{"name":"Stead Family Department of Pediatrics, University of Iowa, Iowa City, Iowa"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chandra","family":"Perez-Gill","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9973-9731","authenticated-orcid":false,"given":"Johannes S","family":"Schl\u00f6ndorff","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Balajikarthick","family":"Subramanian","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin R.","family":"Pollak","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2020,12,22]]},"reference":[{"issue":"Suppl 1","key":"B1-20240826","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1159\/000481633","article-title":"A review of podocyte biology","volume":"47","author":"Garg","year":"2018","journal-title":"Am J Nephrol"},{"key":"B2-20240826","doi-asserted-by":"crossref","first-page":"302","DOI":"10.3389\/fendo.2018.00302","article-title":"Nephrin signaling in the podocyte: An updated view of signal regulation at the slit diaphragm and beyond","volume":"9","author":"Martin","year":"2018","journal-title":"Front Endocrinol 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