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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2018,3,27]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    Two common variants in the\n                    <jats:italic>APOL1<\/jats:italic>\n                    gene explain most of the high rate of kidney disease in people of recent African ancestry. However, not all\n                    <jats:italic>APOL1<\/jats:italic>\n                    high-risk individuals develop kidney disease. Here we identified the\n                    <jats:italic>UBD<\/jats:italic>\n                    locus as a genetic modifier of\n                    <jats:italic>APOL1<\/jats:italic>\n                    kidney disease using admixture mapping. Focal segmental glomerulosclerosis patients have significantly increased African ancestry at the\n                    <jats:italic>UBD<\/jats:italic>\n                    locus, which associates with lower\n                    <jats:italic>UBD<\/jats:italic>\n                    gene expression. Using a cell-based system, we show that UBD and APOL1 interact functionally and that higher levels of\n                    <jats:italic>UBD<\/jats:italic>\n                    expression mitigate\n                    <jats:italic>APOL1<\/jats:italic>\n                    -mediated cell death. These findings are important for understanding the genetic and functional modifiers of the human\n                    <jats:italic>APOL1<\/jats:italic>\n                    -associated phenotype and the biological pathways relevant to\n                    <jats:italic>APOL1<\/jats:italic>\n                    -associated cell damage.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1716113115","type":"journal-article","created":{"date-parts":[[2018,3,12]],"date-time":"2018-03-12T15:41:12Z","timestamp":1520869272000},"page":"3446-3451","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":66,"title":["<i>UBD<\/i>\n                    modifies\n                    <i>APOL1<\/i>\n                    -induced kidney disease risk"],"prefix":"10.1073","volume":"115","author":[{"given":"Jia-Yue","family":"Zhang","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215;"},{"name":"Department of Medicine, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minxian","family":"Wang","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215;"},{"name":"Department of Medicine, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Tian","sequence":"additional","affiliation":[{"name":"Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giulio","family":"Genovese","sequence":"additional","affiliation":[{"name":"Stanley Center for Psychiatric Research, Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Yan","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215;"},{"name":"Department of Medicine, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G.","family":"Wilson","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ravi","family":"Thadhani","sequence":"additional","affiliation":[{"name":"Department of Medicine, Massachusetts General Hospital, Boston, MA 02114;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy K.","family":"Mottl","sequence":"additional","affiliation":[{"name":"University of North Carolina Kidney Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerald B.","family":"Appel","sequence":"additional","affiliation":[{"name":"Center for Glomerular Diseases, Columbia University Medical Center, New York, NY 10032;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5824-9595","authenticated-orcid":false,"given":"Alexander G.","family":"Bick","sequence":"additional","affiliation":[{"name":"Department of Medicine, Massachusetts General Hospital, Boston, MA 02114;"},{"name":"Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew G.","family":"Sampson","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Michigan School of Medicine, Ann Arbor, MI 48109"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seth L.","family":"Alper","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215;"},{"name":"Department of Medicine, Harvard Medical School, Boston, MA 02115;"},{"name":"Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David J.","family":"Friedman","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215;"},{"name":"Department of Medicine, Harvard Medical School, Boston, MA 02115;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin R.","family":"Pollak","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215;"},{"name":"Department of Medicine, Harvard Medical School, Boston, MA 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J Am Soc Nephrol 22, 2129\u20132137 (2011).","journal-title":"J Am Soc Nephrol"},{"key":"e_1_3_4_4_2","doi-asserted-by":"crossref","first-page":"2882","DOI":"10.1681\/ASN.2014050469","article-title":"APOL1 risk variants are strongly associated with HIV-associated nephropathy in black South Africans","volume":"26","author":"Kasembeli AN","year":"2015","unstructured":"AN Kasembeli, , APOL1 risk variants are strongly associated with HIV-associated nephropathy in black South Africans. J Am Soc Nephrol 26, 2882\u20132890 (2015).","journal-title":"J Am Soc Nephrol"},{"key":"e_1_3_4_5_2","doi-asserted-by":"crossref","first-page":"1008","DOI":"10.1681\/ASN.2016111262","article-title":"Identifying the intracellular function of APOL1","volume":"28","author":"Bruggeman LA","year":"2017","unstructured":"LA Bruggeman, JF O\u2019Toole, JR Sedor, Identifying the intracellular function of APOL1. 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