{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T20:07:54Z","timestamp":1786133274275,"version":"build-2736575974"},"reference-count":71,"publisher":"Ovid Technologies (Wolters Kluwer Health)","license":[{"start":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T00:00:00Z","timestamp":1779062400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["DK083294"],"award-info":[{"award-number":["DK083294"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["DK093629"],"award-info":[{"award-number":["DK093629"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000062","name":"National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"crossref","award":["F30DK142452"],"award-info":[{"award-number":["F30DK142452"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Loss of podocyte-associated cyclin G\u2013associated kinase resulted in mistrafficking of lysosomal hydrolases.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Loss of podocyte-associated cyclin G\u2013associated kinase induced immune modulation.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Given the postmitotic nature of podocytes, adapting to both physiologic and pathologic stress is crucial to prevent podocyte loss. An important component of maintaining cellular homeostasis are lysosomes, which are membrane-bound organelles responsible for degradation and recycling of damaged organelles and other macromolecules. Lysosome impairment has been shown to cause cellular and organ dysfunction, highlighting its crucial role in homeostasis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We previously showed that podocyte-specific loss of cyclin G\u2013associated kinase knockout (\n                      <jats:italic toggle=\"yes\">Gak<\/jats:italic>\n                      -KO) leads to severe proteinuria, podocyte injury, and kidney failure. To interrogate which GAK domains are necessary for its function, we used a transgenic mouse expressing a truncated 62-kDa\n                      <jats:italic toggle=\"yes\">C<\/jats:italic>\n                      -terminal GAK protein (GAK C62), which consists of the clathrin-binding and J domains. We evaluated the functional role of GAK C62 in podocytes using immunofluorescence, western blotting, and\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      transcriptomic analysis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Our findings revealed significant accumulation of autophagic vesicles in\n                      <jats:italic toggle=\"yes\">Gak<\/jats:italic>\n                      -KO podocytes. By systematically probing for potential causes of autophagosome accumulation, we showed that loss of\n                      <jats:italic toggle=\"yes\">Gak<\/jats:italic>\n                      resulted in impaired lysosomal degradation, secondary to mistrafficking of lysosomal hydrolases. Notably, GAK C62 expression completely rescued these phenotypes at the cellular and organismal levels. Moreover,\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      translating ribosome affinity purification sequencing and cytokine profiling demonstrated enrichment of immune-related pathways and IL-11 production in\n                      <jats:italic toggle=\"yes\">Gak<\/jats:italic>\n                      -KO podocytes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      GAK, specifically its\n                      <jats:italic toggle=\"yes\">C<\/jats:italic>\n                      -terminal domains, plays an important role in podocyte lysosome homeostasis. Lysosomal dysfunction due to loss of\n                      <jats:italic toggle=\"yes\">Gak<\/jats:italic>\n                      led podocytes to adopt immune-like properties characterized by the release of proinflammatory cytokine IL-11.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.0000001130","type":"journal-article","created":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T16:01:22Z","timestamp":1779120082000},"update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Loss of Cyclin G\u2013Associated Kinase Leads to Lysosome Dysfunction and Immune Modulation in Podocytes"],"prefix":"10.1681","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7047-3266","authenticated-orcid":false,"given":"Patricia","family":"Bunda","sequence":"first","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, Connecticut"},{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4235-0896","authenticated-orcid":false,"given":"Xuefei","family":"Tian","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2080-4391","authenticated-orcid":false,"given":"Soichiro","family":"Nagata","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0286-9597","authenticated-orcid":false,"given":"Gabriel","family":"Lerner","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"},{"name":"Department of Pathology, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2919-7575","authenticated-orcid":false,"given":"Paulina","family":"Medina-Rangel","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9337-5017","authenticated-orcid":false,"given":"Jianlei","family":"Gu","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Yale University, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1195-9607","authenticated-orcid":false,"given":"Hongyu","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Yale University, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lois E.","family":"Greene","sequence":"additional","affiliation":[{"name":"Laboratory of Cell Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3092-7718","authenticated-orcid":false,"given":"Shawn M.","family":"Ferguson","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7149-6651","authenticated-orcid":false,"given":"Kazunori","family":"Inoue","sequence":"additional","affiliation":[{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"},{"name":"Department of Nephrology, The University of Osaka Graduate School of Medicine, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3212-641X","authenticated-orcid":false,"given":"Shuta","family":"Ishibe","sequence":"additional","affiliation":[{"name":"Department of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, Connecticut"},{"name":"Section of Nephrology, Department of Internal Medicine, Yale School of Medicine, New Haven, Connecticut"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2026,5,18]]},"reference":[{"issue":"4","key":"B1-20260713","doi-asserted-by":"crossref","first-page":"604","DOI":"10.1042\/bj0600604","article-title":"Tissue fractionation studies. 6. 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