{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T15:17:23Z","timestamp":1761664643118,"version":"3.41.2"},"reference-count":63,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2024,1,1]],"date-time":"2024-01-01T00:00:00Z","timestamp":1704067200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000191","name":"Kidney Foundation of Canada","doi-asserted-by":"publisher","award":["n\/a"],"award-info":[{"award-number":["n\/a"]}],"id":[{"id":"10.13039\/501100000191","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Physiological Reports"],"published-print":{"date-parts":[[2024,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>SLK controls the cytoskeleton, cell adhesion, and migration. Podocyte\u2010specific deletion of SLK in mice leads to podocyte injury as mice age and exacerbates injury in experimental focal segment glomerulosclerosis (FSGS; adriamycin nephrosis). We hypothesized that adhesion proteins may be substrates of SLK. In adriamycin nephrosis, podocyte ultrastructural injury was exaggerated by SLK deletion. Analysis of a protein kinase phosphorylation site dataset showed that podocyte adhesion proteins\u2014paxillin, vinculin, and talin\u20101 may be potential SLK substrates. In cultured podocytes, deletion of SLK increased adhesion to collagen. Analysis of paxillin, vinculin, and talin\u20101 showed that SLK deletion reduced focal adhesion complexes (FACs) containing these proteins mainly in adriamycin\u2010induced injury; there was no change in FAC turnover (focal adhesion kinase Y397 phosphorylation). In podocytes, paxillin S250 showed basal phosphorylation that was slightly enhanced by SLK; however, SLK did not phosphorylate talin\u20101. In adriamycin nephrosis, SLK deletion did not alter glomerular expression\/localization of talin\u20101 and vinculin, but increased focal adhesion kinase phosphorylation modestly. Therefore, SLK decreases podocyte adhesion, but FAC proteins in podocytes are not major substrates of SLK in health and disease.<\/jats:p>","DOI":"10.14814\/phy2.15897","type":"journal-article","created":{"date-parts":[[2024,1,2]],"date-time":"2024-01-02T01:25:13Z","timestamp":1704158713000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Role of the Ste20\u2010like kinase <scp>SLK<\/scp> in podocyte adhesion"],"prefix":"10.14814","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4348-2348","authenticated-orcid":false,"given":"Andrey V.","family":"Cybulsky","sequence":"first","affiliation":[{"name":"Department of Medicine McGill University Health Centre Research Institute, McGill University  Montreal Quebec Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joan","family":"Papillon","sequence":"additional","affiliation":[{"name":"Department of Medicine McGill University Health 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