a, Abundance of SR-B1, LDLR, and CD36 protein following RNAi knockdown of SR-B1, or following reconstitution of wild-type SR-B1 expression in cells depleted of the endogenous receptor. Expression of caveolin-1 (Cav1) was also evaluated. Findings for two samples per condition are shown. b, Alk1 transcript levels in cells manipulated as in a. n = 3, 4 and 4, respectively. c, Abundance of SR-B1, LDLR, and CD36 protein following RNAi knockdown of Alk1, SR-B1, or both. Findings for two samples per condition are shown. d, Alk1 transcript levels in cells manipulated as in c. n = 4 per group. e, Phosphorylation of SMAD1/5 in response to BMP9 (10 ng ml–1 for 0–120 min) after RNAi knockdown of SR-B1 or Alk1. The abundance of Ser463/465 phosphorylation of SMAD1/5 (p-SMAD1/5) and total SMAD1 (t-SMAD1) were evaluated by immunoblotting. f, Transcytosis of DiI–nLDL following RNAi knockdown of Alk1, SR-B1, or both. n = 9 per group. g, h, Uptake of nLDL was evaluated using 125I-nLDL in the absence or presence of a 50-fold excess of unlabelled nLDL (g), and following RNAi knockdown of SR-B1 or Dock4, or reconstitution of wild-type SR-B1 expression in cells depleted of the endogenous receptor (h). n = 8 per group. i, j, Transcytosis of nLDL was evaluated using 125I-nLDL in the absence or presence of a 50-fold excess of unlabelled nLDL (i), and following manipulation of SR-B1 or DOCK4 expression as in h (j). n = 3 per group. k, l, Transcytosis of nLDL was evaluated using TIRF microscopy in cells treated with Dyngo4A (k, 30 μM) or following RNAi knockdown of SR-B1 or Dock4 (l). n = 6 per group. m, Activation of RAC1 in response to oxLDL in cells expressing GFP control versus dominant-negative RAC1, and in untreated cells versus cells incubated with the RAC1 inhibitor NSC23766. Data are mean ± s.e.m.; P values calculated by ANOVA with Dunnett’s post-hoc test (d, f, h, j, l) or two-sided Student’s t-test (g, i, k). Source data