ADCK4 knockout Human podocyte iTRAQ

ABSTRACT: 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.The reduced form of CoQ (QH2) plays a role as a potent lipid-soluble antioxidant, scavenging free radicals and preventing lipid peroxidative damage. Although ADCK4 KO in itself did not affect the viability of cultured podocytes, we examined cell viability upon arachidonic acid (AA) treatment because CoQ-deficient yeast mutants were found to be more sensitive to polyunsaturated fatty acids such as AA, which are prone to autoxidation and breakdown into toxic products. To comprehensively understand the molecular changes induced by the KO of ADCK4, we performed proteomic analysis and quantified protein abundance changes by MS-based proteomics using isobaric tag for relative and absolute quantification (iTRAQ) in podocytes with and without AA treatment.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Kidney

SUBMITTER: SEYOUNG YU  

LAB HEAD: Heon Yung Gee

PROVIDER: PXD016725 | Pride | 2021-09-09

REPOSITORIES: Pride