ABCG8 Proteine (ABCG8)

Human ATP-Binding Cassette, Sub-Family G (WHITE), Member 8 (ABCG8) Interaktionspartner

1. Risk trait of cholesterol metabolism (low phytosterols) in childhood favouring cholesterol gallstone disease later in adulthood is influenced by risk variant 19H of ABCG8 and obviously also other factors.

2. we identified a novel mutation in the ABCG8 gene, which in the homozygous form was associated with generalized xanthomatosis, and in the heterozygous form was associated with isolated xanthelasmas

3. Case Reports: compound heterozygous for nonsense mutations in ABCG8 responsible for sitosterolemia.

4. ABCG8 genetic variants may have role in the development of cholelithiasis in patients with Gaucher disease type 1.

5. Genetic polymorphism within the ABCG8 gene is a risk factor for diabetes.

6. crystallization in lipid bilayers to determine the X-ray structure of human G5G8 in a nucleotide-free state at 3.9 A resolution, generating the first atomic model of an ABC sterol transporter

7. A polymorphism of the sterol transporter ABCG8 has been associated with the prevalence of end-stage renal disease

8. Mutation in ABCG8 is associated with sitosterolaemia.

9. ATP-binding cassette (ABC) transporters G5 (ABCG5) and G8 (ABCG8) form an obligate heterodimer that limits intestinal absorption and facilitates biliary secretion of cholesterol and phytosterols.

10. ABCG5/8 variants are associated with susceptibility to coronary heart disease.

11. 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

12. HRD1 and RMA1 may therefore be negative regulators of disease-associated transporter ABCG5/ABCG8.

13. MI and gallstones, 2 seemingly unrelated diseases, are intrinsically linked via the function of the ABCG5/8 cholesterol transporter.

14. A single nucleotide polymorphism of ABCG8 is associated with fasting plasma glucose levels in a cross-sectional study but do not predict hyperglycemia or incident type 2 diabetes. [meta-analysis]

15. The evolutionary conserved region of ABCG8 were found to be responsive to the Liver-X-Receptor.

16. Recurrence of gallstones after cholecystectomy is associated with ABCG8 genotype.

17. ABCG8 (and ABO) variants are associated with high intestinal cholesterol absorption and cardiovascular disease.

18. Both gallstone disease and p.D19H of ABCG8 are associated with diminished cholesterol absorption.

19. ABCG8-D19H variant associated with cholesterol gallstone disease

20. The sterol transporters ABCA1, ABCG5, and ABCG8 may play a role in the pathogenesis of human cholesterol related gallbladder diseases.

Mouse (Murine) ATP-Binding Cassette, Sub-Family G (WHITE), Member 8 (ABCG8) Interaktionspartner

1. ABCG5 and ABCG8 mRNA levels were significantly increased in cholesterol group and less increased in myriocin group, relative to that in normal group.

2. 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.

3. ABCG5/G8 mediate mass biliary cholesterol secretion but not from a reverse cholesterol transport-relevant pool.

4. 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

5. 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.

6. 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

7. The absence of an ABCG5/ABCG8 expression.

8. biliary cholesterol mass secretion under maximal bile salt-stimulated conditions is fully dependent on ABCG5/G8

9. This study is the first to report such toxic effects of phytosterol accumulation in ABCG5/G8 knockout mice.

10. 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

11. The ABCG5 ABCG8 sterol transporter opposes the development of fatty liver disease and loss of glycemic control independently of phytosterol accumulation

12. ABCG5/G8 deficiency in mice markedly raises triglyceride levels by impairing triglyceride catabolism and by increasing liver and intestinal triglyceride secretion.

13. NPC2 is a positive regulator of biliary cholesterol secretion via stimulation of ABCG5/G8-mediated cholesterol transport.

14. NBD1, although not required for ATP hydrolysis, is essential for normal function of G5G8 in sterol transport

15. regulation by liver X receptors alpha and beta

16. 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

17. biliary cholesterol secretion by ABCG5 and ABCG8

18. expression, dimerization, and transport of ABCG5 and ABCG8

19. 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.

20. Abcg5 and Abcg8 are required for LXR agonist-associated changes in dietary and biliary sterol trafficking.

Cow (Bovine) ATP-Binding Cassette, Sub-Family G (WHITE), Member 8 (ABCG8) Interaktionspartner

1. high expression levels of both ATP-binding cassette sub-family G member 5 and 8 (ABCG5 and ABCG8) were present in bovine liver and digestive tract samples, and in the mammary gland