{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhu JY"],"funding":["NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases","School of Medicine, University of Maryland"],"pagination":["dmm052178"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12352291"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(7)"],"pubmed_abstract":["People carrying two APOL1 risk alleles (RA) - G1 or G2 - are at greater risk of developing human immunodeficiency virus (HIV)-associated nephropathy (HIVAN). However, it remains unclear whether the encoded protein(s) (APOL1-RA) and HIV-1 Nef interact to induce podocyte cell death. Here, we generated transgenic flies that express APOL1-G1 (derived from a child with HIVAN) and HIV-1 nef specifically in the nephrocytes, the fly equivalent of mammalian podocytes, and assessed their individual and combined effects on the nephrocyte filtration structure and function. We found that HIV-1 Nef acts in synergy with APOL1-G1, resulting in nephrocyte structural and functional defects, and that Nef exacerbates the organelle acidification defects and autophagy reduction induced by APOL1-G1. The synergy "],"journal":["Disease models & mechanisms"],"pubmed_title":["HIV-1 Nef synergizes with APOL1-G1 to induce nephrocyte cell death in HIV-related kidney diseases."],"pmcid":["PMC12352291"],"funding_grant_id":["R01 DK103564","R01-DK120908","R01 DK098410","R01-DK103564","R01 DK115968","R01 DK120908","R01-DK098410","R01-DK115968"],"pubmed_authors":["Ray PE","Li J","Fu Y","Zhu JY","Han Z","Yu J","van de Leemput J"],"additional_accession":[]},"is_claimable":false,"name":"HIV-1 Nef synergizes with APOL1-G1 to induce nephrocyte cell death in HIV-related kidney diseases.","description":"People carrying two APOL1 risk alleles (RA) - G1 or G2 - are at greater risk of developing human immunodeficiency virus (HIV)-associated nephropathy (HIVAN). However, it remains unclear whether the encoded protein(s) (APOL1-RA) and HIV-1 Nef interact to induce podocyte cell death. Here, we generated transgenic flies that express APOL1-G1 (derived from a child with HIVAN) and HIV-1 nef specifically in the nephrocytes, the fly equivalent of mammalian podocytes, and assessed their individual and combined effects on the nephrocyte filtration structure and function. We found that HIV-1 Nef acts in synergy with APOL1-G1, resulting in nephrocyte structural and functional defects, and that Nef exacerbates the organelle acidification defects and autophagy reduction induced by APOL1-G1. The synergy ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-05-01T18:45:12.348Z","creation":"2026-04-07T17:09:49.085Z"},"accession":"S-EPMC12352291","cross_references":{"pubmed":["40747773"],"doi":["10.1242/dmm.052178"]}}