Fig. 3: ZNF529 silencing induces LDLR expression and LDL uptake.
From: Loss-of-function genomic variants highlight potential therapeutic targets for cardiovascular disease

a Efficient silencing of ZNF529 in HepG2 cells via siRNA as shown by qPCR using GAPDH as reference (N = 21 biologically independent samples). b ZNF529 silencing in HepG2 cells induces LDLR mRNA as shown by qPCR using GAPDH as reference (N = 21 biologically independent samples), and (c and d) LDLR protein as shown by western blot using β-actin as loading control (N = 4 biologically independent samples). e ZNF529 silencing in HepG2 cells increases LDL uptake as evidenced by enhanced fluorescence of DiI-LDL (10 µg/ml, N = 9 biologically independent samples) which is inhibited in cells preloaded with 25-fold excess amounts of unlabeled-LDL (250 µg/ml, N = 3 biologically independent samples, scale bars = 200 µm), and (f) leads to increased intracellular cholesterol (N = 12 biologically independent samples). Values are presented as mean ± SD (vertical whiskers) showing all points and P values (two-tailed). Mann–Whitney U test was used for a, b and f. Student t test was used for d. Source data are provided as a Source Data file.