Fig. 7: CSA/B availability determines QPRT expression.
From: Cockayne syndrome mice reflect human kidney disease and are defective in de novo NAD biosynthesis
A CS mice kidney tissues were subjected to western blot for probing indicated antibodies. B Actin normalized mATF and mQPRT blot quantification data are shown (Blue bar, WT; Red bar, HO CSA/CSB). C HK-2 cells were transfected with two sets of CSA/B siRNAs. Cells were harvested 72 h post-transfection and subjected to qPCR. GAPDH-normalized expression values and (D) western blot analysis with indicated antibodies are shown. E Actin normalized blot quantification of CSA, CSB, hQPRT (human isoform) and hATF3 are shown. F siRNA-transfected HK2 cells were harvested and subjected to total protein-normalized NAD+ and NAD+/NADH quantification analyses. Data are presented as mean ± SD (n ≥ 3). An unpaired t test was used for comparing CS with WT and HK-2 Knockdown vs SCR. A two-way ANOVA Sidak test used for male vs female comparisons. A Mann–Whitney test used for ATF3 quantification. p values indicated.
