Recombinant Mouse ATP-binding cassette sub-family G member 5 (Abcg5)

1. ABCG5 and ABCG8 mRNA levels were significantly increased in cholesterol group and less increased in myriocin group, relative to that in normal group. PMID:28268212
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. PMID:27014967
3. ABCG5/G8 mediate mass biliary cholesterol secretion but not from a reverse cholesterol transport-relevant pool. PMID:26520893
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 PMID:26365598
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. PMID:25676339
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 PMID:24811295
7. The absence of an ABCG5/ABCG8 expression. PMID:25060694
8. Mice with deficient Abcg2 have features of inflammatory DCM and that the reversibility of myocardial T cell infiltration provides a novel model for investigating the progression of myocardial fibrosis. PMID:23129576
9. biliary cholesterol mass secretion under maximal bile salt-stimulated conditions is fully dependent on ABCG5/G8 PMID:23401258
10. This study is the first to report such toxic effects of phytosterol accumulation in ABCG5/G8 knockout mice. PMID:23380580
11. The ability of triiodothyronine to stimulate the secretion of cholesterol into bile is largely mediated by the ABCG5/G8 complex. PMID:22829162
12. 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 PMID:22669916
13. The ABCG5 ABCG8 sterol transporter opposes the development of fatty liver disease and loss of glycemic control independently of phytosterol accumulation PMID:22715101
14. ABCG5/G8 deficiency in mice markedly raises triglyceride levels by impairing triglyceride catabolism and by increasing liver and intestinal triglyceride secretion. PMID:21855652
15. NPC2 is a positive regulator of biliary cholesterol secretion via stimulation of ABCG5/G8-mediated cholesterol transport. PMID:21315718
16. NBD1, although not required for ATP hydrolysis, is essential for normal function of G5G8 in sterol transport PMID:21209088
17. Disruption in Abcg5 gene is associated with thrombocytopenia and cardiomyopathy. PMID:19846887
18. regulation by liver X receptors alpha and beta PMID:11901146
19. Although a large number of polymorphic variants were identified, strains reported to show significant differences in cholesterol absorption rates did not show significant genomic variations in Abcg5 or Abcg8. PMID:11907139
20. biliary cholesterol secretion by ABCG5 and ABCG8 PMID:12208859
21. expression, dimerization, and transport of ABCG5 and ABCG8 PMID:12208867
22. 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. PMID:12444248
23. A role for Abcg5 and Abcg8 in regulation of biliary cholesterol secretion. Also, existence of largely independent route of cholesterol secretion. PMID:12763362
24. endotoxin significantly decreased mRNA levels of ABCG5 and ABCG8 in the liver, but not in the small intestine PMID:12777468
25. ABCG5 and ABCG8 function as obligate heterodimers to promote sterol excretion into bile PMID:14504269
26. Disruption of the Abcg5 gene alone is sufficient to cause hyperabsorption of dietary plant sterols and sitosterolemia in mice, whereas the ability to secrete cholesterol into bile is maintained. PMID:14699507
27. Abcg5 and Abcg8 in the jejunum and ileum, but not in the duodenum, were main factors in determining, in part, variations in Ch absorption efficiency. PMID:15102882
28. The PERA allele of Abcg5/Abcg8, on chromosome 17, is responsible for lithogenicity underlying the Lith9 cholelithiasis QTL. PMID:16151694
29. aging significantly enhances cholesterol absorption by suppressing expression of the jejunal and ileal sterol efflux transporter Abcg5 PMID:16179600
30. Our data confirm that Abcg5, as part of the Abcg5/Abcg8 heterodimer, strongly controls hepatobiliary cholesterol secretion in mice. PMID:16614371
31. G5 and G8 are sufficient for reconstitution of sterol transfer activity in vitro and provide the first demonstration that sterols are direct transport substrates of the G5 and G8 heterodimer. PMID:16867993
32. distinct roles for liver and intestinal ABCG5/G8 in modulating sterol metabolism and atherosclerosis in abcg5 transgenic mice. PMID:17060690
33. levels of the ABCG5-ABCG8 sterol transporter in liver are regulated by the leptin axis PMID:17561514
34. Cholesterol secretion was highly bile salt dependent, whereas other cholesterol acceptors such as ApoAI, HDL or methyl-beta-cyclodextrin did not elicit Abcg5/g8 dependent cholesterol secretion PMID:17825296
35. Mutations in either ABCG5 or ABCG8 cause sitosterolemia, an inborn error of metabolism characterized by high plasma plant sterol concentrations. PMID:18156627
36. The cholesterol transporters Npc1l1, Abca1, Abcg5, and Abcg8 were found to be downregulated after 2, 4, and 8 wk on a cholesterol-free, high-fat diet. PMID:18356535
37. Both ABCG5 (G5) and ABCG8 (G8) have short but highly conserved cytoplasmic tails PMID:18402465
38. Increased biliary cholesterol excretion in Atp8b1-deficient mice is independent of Abcg5/8 activity. PMID:18466903
39. LXR activation stimulated the fecal excretion of labeled cholesterol after an intravenous injection of HDL-[(3)H]cholesteryl oleate in G5/G8(+/+) mice, but failed to enhance fecal [(3)H]cholesterol in G5/G8(-/-) mice. PMID:18509196
40. Abcg5 (-/-) mice, develop sitosterolemia, a genetic disorder characterized by the accumulation of phytosterols in blood and tissues PMID:18796403
41. In the liver, histone H3 in the proximal promoter of Abcg5 is hyperacetylated, whereas acetylation in the kidney and the cerebrum is minimal. PMID:19047482

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UNIGENE: Mm.289590

KEGG: mmu:27409

STRING: 10090.ENSMUSP00000069495