Liqing Yu

TL;DR: Data suggest that ABCG5 and ABCG8 normally cooperate to limit intestinal absorption and to promote biliary excretion of sterols, and that mutated forms of these transporters predispose to sterol accumulation and atherosclerosis.

TL;DR: It is indicated that ABCG5 and ABCG8 are required for efficient secretion of cholesterol into bile and that disruption of these genes increases dramatically the responsiveness of plasma and hepatic cholesterol levels to changes in dietary cholesterol content.

TL;DR: It is demonstrated that increased expression of ABCG5 and ABCG8 selectively drives biliaryneutral sterol secretion and reduces intestinal cholesterol absorption, leading to a selective increase in neutral sterol excretion and a compensatory increase in cholesterol synthesis.

TL;DR: It is confirmed, in vivo, that G5 is localized to the apical membranes of mouse enterocytes and hepatocytes and that adenoviral expression of G2 in the presence or absence of G5 or G8 failed to promote sterol excretion into bile.

TL;DR: It is shown that expression of two target genes of LXRα, the ATP-binding cassette (ABC) transportersAbcg5 and Abcg8, is required for both the increase in sterol excretion and the decrease in fractional cholesterol absorption associated with LXR agonist treatment.