-
ABCG5 and ABCG8 mRNA levels were significantly increased in cholesterol group and less increased in myriocin group, relative to that in normal group.
-
The ABCG5/G8-independent pathway plays an important role in regulating biliary cholesterol secretion, and gallstone formation, which works independently of the ABCG5/G8 pathway.
-
ABCG5/G8 mediate mass biliary cholesterol secretion but not from a reverse cholesterol transport-relevant pool.
-
AdGRP78 reduced expression of lipogenic genes and plasma triglycerides in the db/db strain. Both G5 and G8 protein levels increased as did total biliary cholesterol
-
The data demonstrate that Abcg5/Abcg8 deficiency reduces the uptake and secretion of both dietary triacylglycerols and cholesterol by the intestine, suggesting a novel role for the sterol transporter in the formation and secretion of chylomicrons.
-
Sitosterolemia is caused by a genetic defect of sterolins (ABCG5/ABCG8) mapped to the STSL locus. Polymorphic variations in STSL have been linked to lipid levels and gallstone disease
-
The absence of an ABCG5/ABCG8 expression.
-
biliary cholesterol mass secretion under maximal bile salt-stimulated conditions is fully dependent on ABCG5/G8
-
This study is the first to report such toxic effects of phytosterol accumulation in ABCG5/G8 knockout mice.
-
handling of sterols by the intestine involves both G5G8 and ACAT2 but that an additional factor (possibly Niemann-Pick C1-like 1) may be key in determining absorption efficiency
-
The ABCG5 ABCG8 sterol transporter opposes the development of fatty liver disease and loss of glycemic control independently of phytosterol accumulation
-
ABCG5/G8 deficiency in mice markedly raises triglyceride levels by impairing triglyceride catabolism and by increasing liver and intestinal triglyceride secretion.
-
NPC2 is a positive regulator of biliary cholesterol secretion via stimulation of ABCG5/G8-mediated cholesterol transport.
-
NBD1, although not required for ATP hydrolysis, is essential for normal function of G5G8 in sterol transport
-
regulation by liver X receptors alpha and beta
-
Alternatively spliced forms for Abcg8 were identified, resulting from a CAG repeat at the intron 1 splice-acceptor site, causing a deletion of a glutamine
-
biliary cholesterol secretion by ABCG5 and ABCG8
-
expression, dimerization, and transport of ABCG5 and ABCG8
-
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.
-
Abcg5 and Abcg8 are required for LXR agonist-associated changes in dietary and biliary sterol trafficking.