{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T02:15:47Z","timestamp":1789179347044,"version":"build-2803163510"},"reference-count":83,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:p>\n                    <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                    harbors C\u2013terminal sequence variants (G1 and G2), which account for much of the increased risk for kidney disease in sub\u2013Saharan African ancestry populations. Expression of the risk variants has also been shown to cause injury to podocytes and other cell types, but the underlying mechanisms are not understood. We used\n                    <jats:italic toggle=\"yes\">Drosophila melanogaster<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">Saccharomyces cerevisiae<\/jats:italic>\n                    to help clarify these mechanisms. Ubiquitous expression of the human APOL1 G1 and G2 disease risk alleles caused near-complete lethality in\n                    <jats:italic toggle=\"yes\">D. melanogaster<\/jats:italic>\n                    , with no effect of the G0 nonrisk\n                    <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                    allele, corresponding to the pattern of human disease risk. We also observed a congruent pattern of cellular damage with tissue-specific expression of APOL1. In particular, expression of APOL1 risk variants in\n                    <jats:italic toggle=\"yes\">D. melanogaster<\/jats:italic>\n                    nephrocytes caused cell-autonomous accumulation of the endocytic tracer atrial natriuretic factor-red fluorescent protein at early stages and nephrocyte loss at later stages. We also observed differential toxicity of the\n                    <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                    risk variants compared with the\n                    <jats:italic toggle=\"yes\">APOL1<\/jats:italic>\n                    nonrisk variants in\n                    <jats:italic toggle=\"yes\">S. cerevisiae<\/jats:italic>\n                    , including impairment of vacuole acidification. Yeast strains defective in endosomal trafficking or organelle acidification but not those defective in autophagy displayed augmented APOL1 toxicity with all isoforms. This pattern of differential injury by the APOL1 risk alleles compared with the nonrisk alleles across evolutionarily divergent species is consistent with an impairment of conserved core intracellular endosomal trafficking processes. This finding should facilitate the identification of cell injury pathways and corresponding therapeutic targets of interest in these amenable experimental platforms.\n                  <\/jats:p>","DOI":"10.1681\/asn.2016050546","type":"journal-article","created":{"date-parts":[[2016,11,18]],"date-time":"2016-11-18T22:30:28Z","timestamp":1479508228000},"page":"1117-1130","source":"Crossref","is-referenced-by-count":95,"title":["APOL1\u2013Mediated Cell Injury Involves Disruption of Conserved Trafficking Processes"],"prefix":"10.1681","volume":"28","author":[{"given":"Etty","family":"Kruzel-Davila","sequence":"first","affiliation":[{"name":"Department of Nephrology, Rambam Health Care Campus, Haifa, Israel; Departments of"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Revital","family":"Shemer","sequence":"additional","affiliation":[{"name":"Genetics and Developmental Biology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayala","family":"Ofir","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Rambam Health Care Campus, Haifa, Israel; Departments of"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ira","family":"Bavli-Kertselli","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Rambam Health Care Campus, Haifa, Israel; Departments of"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilona","family":"Darlyuk-Saadon","sequence":"additional","affiliation":[{"name":"Genetics and Developmental Biology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pazit","family":"Oren-Giladi","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Rambam Health Care Campus, Haifa, Israel; Departments of"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Walter G.","family":"Wasser","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Rambam Health Care Campus, Haifa, Israel; Departments of"},{"name":"Department of Nephrology, Mayanei HaYeshua Medical Center, Bnei Brak, Israel;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniella","family":"Magen","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Rambam Health Care Campus, Haifa, Israel; Departments of"},{"name":"Genetics and Developmental Biology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eid","family":"Zaknoun","sequence":"additional","affiliation":[{"name":"Genetics and Developmental Biology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maya","family":"Schuldiner","sequence":"additional","affiliation":[{"name":"Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adi","family":"Salzberg","sequence":"additional","affiliation":[{"name":"Genetics and Developmental Biology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Kornitzer","sequence":"additional","affiliation":[{"name":"Microbiology and Inflammation, Rappaport Faculty of Medicine and Research Institute, Technion\u2014Israel Institute of Technology, Haifa, Israel;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zvonimir","family":"Marelja","sequence":"additional","affiliation":[{"name":"Imagine Institute, Paris Descartes University\u2013Sorbonne Paris Cit\u00e9, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matias","family":"Simons","sequence":"additional","affiliation":[{"name":"Imagine Institute, Paris Descartes University\u2013Sorbonne Paris Cit\u00e9, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl","family":"Skorecki","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Rambam Health Care Campus, Haifa, Israel; Departments of"},{"name":"Genetics and Developmental Biology and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2016,11,18]]},"reference":[{"key":"B1-20230829","doi-asserted-by":"crossref","first-page":"841","DOI":"10.1126\/science.1193032","article-title":"Association of trypanolytic ApoL1 variants with kidney disease in African Americans.","volume":"329","author":"Genovese","year":"2010","journal-title":"Science"},{"key":"B2-20230829","doi-asserted-by":"crossref","first-page":"345","DOI":"10.1007\/s00439-010-0861-0","article-title":"Missense mutations in the APOL1 gene are highly associated with end stage kidney disease risk previously attributed to the MYH9 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