BAP and ADCK4 interactor proteomic data LC-MS/MS

Although identification of single gene mutations associated with SRNS have yielded insights into pathogenic mechanisms and localized its pathogenesis to glomerular podocytes, the disease mechanisms of SRNS remain obscure. ADCK4 mutations usually manifest as steroid-resistant nephrotic syndrome, and cause coenzyme Q10 (CoQ10) deficiency. We performed proteomic analysis to understand the function of ADCK4 via the identification of its interactome. We generated HEK293 cells that stably overexpressed C-terminal FLAG-tagged bacterial alkaline phosphatase (BAP; BAP-3xFLAG) and ADCK4 (ADCK4-3xFLAG). We confirmed that ADCK4-3xFLAG mostly localized to the mitochondria. Following affinity purification using anti-FLAG beads, protein eluates were analyzed using a liquid chromatograph coupled to a high-resolution mass spectrometer (LC-MS/MS). In total, 612 proteins were identified as interactors of ADCK4. Among them, the cytoplasmic proteins, including myosin (MYH10, MYH11, MYO1B, and MYO1C), filamin (FLNC), and kinase proteins (STK24, STK25, STK38 and ROCK1) were detected. In addition, the mitochondrial proteins, including ATP synthase subunit (ATP5L), cytochrome c oxidase subunit (COX6A1 and UQCRQ), and COQ5, were also identified as interactors.