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anti-Human ABCG5 Antibodies:
anti-Mouse (Murine) ABCG5 Antibodies:
anti-Rat (Rattus) ABCG5 Antibodies:
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Human Polyclonal ABCG5 Primary Antibody for IF (p), IHC (p) - ABIN708371
Wang, Xiaoling, Pingting, Shuqiang, Yuaner: Chronic unpredictable mild stress combined with a high-fat diets aggravates atherosclerosis in rats. in Lipids in health and disease 2014
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Human Polyclonal ABCG5 Primary Antibody for IHC, IHC (p) - ABIN4277248
Ahn, Jang, Jun, Lee, Shin: Expression of liver X receptor correlates with intrahepatic inflammation and fibrosis in patients with nonalcoholic fatty liver disease. in Digestive diseases and sciences 2014
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Human Monoclonal ABCG5 Primary Antibody for FACS, IHC - ABIN1724857
Johnson, Lee, Pickert, Urbatsch: Bile acids stimulate ATP hydrolysis in the purified cholesterol transporter ABCG5/G8. in Biochemistry 2010
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Human Polyclonal ABCG5 Primary Antibody for WB - ABIN4892532
Huang, Wang, Quan, Wang, Yang, Zhong: Lactobacillus acidophilus ATCC 4356 prevents atherosclerosis via inhibition of intestinal cholesterol absorption in apolipoprotein E-knockout mice. in Applied and environmental microbiology 2014
SNPs rs6720173 (ABCG5), rs3808607 (CYP7A1), and rs760241 (DHCR7) may work in conjunction with each other to amplify individual genotyping impacts on serum cholesterol responses to dairy consumption.
Case Report/Review: novel variants of the ABCG5 gene causing xanthelasmas and macrothrombocytopenia in sitosterolemia.
Mutation-negative familial hypercholesterolemia subjects accumulate an excess of rare and common gene variations in ABCG5/G8 genes
Case Reports: compound heterozygous for nonsense mutations in ABCG5 responsible for sitosterolemia.
ABCG5 gene variants were not associated with cholelithiasis in patients with Gaucher disease type 1.
Genetic variations in ABCG5, CYP7A1, and DHCR7 may contribute to differing responses of serum cholesterol to dairy intake among healthy adults.
ABCG5 Gene Variants are associated with Sitosterolemia and Familial Mediterranean Fever.
first case of a Mexican family with sitosterolemia carrying two new ABCG5 gene mutations
Genetic polymorphism within the ABCG5 gene is a risk factor for diabetes.
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
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.
ABCG5/8 variants are associated with susceptibility to coronary heart disease.
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
HRD1 and RMA1 may therefore be negative regulators of disease-associated transporter ABCG5/ABCG8.
No association of T400K and Y54C polymorphism with hepatic ABCG8/G5 mRNA expression.
MI and gallstones, 2 seemingly unrelated diseases, are intrinsically linked via the function of the ABCG5/8 cholesterol transporter.
A novel mutation of ABCG5 gene in a Turkish boy with phytosterolemia presenting with macrotrombocytopenia and stomatocytosis.
The evolutionary conserved region of ABCG5 were found to be responsive to the Liver-X-Receptor.
ABCG5-R50C variant associated with cholesterol gallstone disease
The sterol transporters ABCA1, ABCG5, and ABCG8 may play a role in the pathogenesis of human cholesterol related gallbladder diseases.
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
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.
The absence of an ABCG5/ABCG8 expression.
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.
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.
The ability of triiodothyronine to stimulate the secretion of cholesterol into bile is largely mediated by the ABCG5/G8 complex.
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
Disruption in Abcg5 gene is associated with thrombocytopenia and cardiomyopathy.
regulation by liver X receptors alpha and beta
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.
biliary cholesterol secretion by ABCG5 and ABCG8
The protein encoded by this gene is a member of the superfamily of ATP-binding cassette (ABC) transporters. ABC proteins transport various molecules across extra- and intra-cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). This protein is a member of the White subfamily. The protein encoded by this gene functions as a half-transporter to limit intestinal absorption and promote biliary excretion of sterols. It is expressed in a tissue-specific manner in the liver, colon, and intestine. This gene is tandemly arrayed on chromosome 2, in a head-to-head orientation with family member ABCG8. Mutations in this gene may contribute to sterol accumulation and atheroschlerosis, and have been observed in patients with sitosterolemia.
ATP-binding cassette, sub-family G (WHITE), member 5 (sterolin 1)
, ATP-binding cassette sub-family G member 5
, sterolin 1
, ATP-binding cassette transporter
, ATP-binding cassette, sub-family G (WHITE), member 5
, ATP-binding cassette sub-family G member 5-like
, ATP-binding cassette, subfamily G, member 5
, ATP-binding cassette sub-family G (WHITE) member 5 (sterolin 1)