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1 and the link between the sterol transporters ABCG5/8 and NPC1L1 and intestinal cholesterol absorption
8 Ppargamma, Angptl4), cholesterol metabolism (Abcg5/8), gastrointestinal homeostasis (RegIIIgamma), an
9 on, nonsynonymous and functional variants in ABCG5/8, and a combined weighted genotype score was calc
10 est the hypothesis that genetic variation in ABCG5/8, the transporter responsible for intestinal and
14 including ABCC3, ABCB6, ABCD1, ABCG1, ABCG4, ABCG5, ABCG8, ABCE1, ABCF1, ABCF2, and ABCF3, were expre
15 sion of cholesterol metabolism related genes Abcg5, Abcg8, Abcg11, Cyp7a1 and Cyp8b1; and (6) induced
17 uction, whereas reductions in Gata4 diminish Abcg5/Abcg8 expression and biliary cholesterol excretion
20 re human disease Sitosterolemia, the role of ABCG5/ABCG8 in sterol trafficking and how newer data imp
21 and the canalicular cholesterol transporter ABCG5/ABCG8 in the genetic susceptibility and pathogenes
22 re involved on pathogenesis, and the role of ABCG5/ABCG8 may extend into other metabolic processes by
27 irst, we quantified the effect of rs4299376 (ABCG5/ABCG8), which affects the intestinal cholesterol a
31 ccumulation of plant sterols in mice lacking ABCG5 and ABCG8 (G5G8-/- mice) profoundly perturbs chole
42 es with mice doubly transgenic for the human ABCG5 and ABCG8 genes rescued platelet counts and volume
43 hypothesis, a P1 clone containing the human ABCG5 and ABCG8 genes was used to generate transgenic mi
45 the ATP-binding cassette (ABC) transporters ABCG5 and ABCG8 have recently been shown to cause the au
49 the ATP-binding cassette (ABC) transporters ABCG5 and ABCG8 in patients with sitosterolemia suggests
50 These results establish a central role for ABCG5 and ABCG8 in promoting cholesterol excretion in vi
52 ndividual roles of hepatic versus intestinal ABCG5 and ABCG8 in sterol transport have not yet been in
53 Higher hepatic messenger RNA expression of Abcg5 and Abcg8 in strain PERA/Ei correlates positively
54 rated transgenic mice that overexpress human ABCG5 and ABCG8 in the liver but not intestine (liver G5
56 the ATP-binding cassette (ABC) transporters ABCG5 and ABCG8 lead to sitosterolemia, a disorder chara
61 lts demonstrate that increased expression of ABCG5 and ABCG8 selectively drives biliary neutral stero
62 strain PERA/Ei), colocalizes with the genes Abcg5 and Abcg8 that encode the canalicular cholesterol
64 allelic imbalance or allelic splicing of the ABCG5 and ABCG8 transcripts in human liver limited the s
69 lation in hepatic mRNA and protein levels of ABCG5 and ABCG8, and in hepatic mRNA levels of Niemann-P
71 Two ATP-binding cassette (ABC) transporters, ABCG5 and ABCG8, have been proposed to limit sterol abso
72 ol; it also upregulates liver and intestinal ABCG5 and ABCG8, helping to promote biliary and fecal ex
73 the ATP-binding cassette (ABC) transporters Abcg5 and Abcg8, is required for both the increase in st
74 sion of the biliary cholesterol transporters Abcg5 and Abcg8, resulting in an increase in biliary cho
76 in the role of ATP-binding cassette proteins ABCG5 and G8 in dietary sterol absorption, excretion and
78 ing cassette, subfamily G (WHITE), member 5 (ABCG5) and ATP-binding cassette, subfamily G (WHITE), me
80 ompletely known but involves the genes ABC1, ABCG5, and ABCG8, which are members of the ATP-binding c
81 lesterol transport or uptake (SCARB1, ABCA1, ABCG5, and LIPC), long-chain omega-3 fatty acid status (
82 significant down-regulation of BMI-1, ABCG2, ABCG5, and MDR1 expression and in a concomitant increase
86 of the bile salt tauroursodeoxycholic acid, Abcg5 became fully rate-limiting for biliary cholesterol
87 ation status of ABCG5; rather it accelerated ABCG5 degradation in an E3 activity-dependent manner.
89 > Sr-bI ko (-16%) > Abcg5 ko (-75%) > Sr-bI/Abcg5 dko (-94%), all at least P < 0.05, while biliary b
94 the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholester
98 The ATP-binding cassette half-transporters ABCG5 (G5) and ABCG8 (G8) promote secretion of neutral s
103 tone characteristics in male wild-type (WT), ABCG5(-/-)/G8(-/-), and ABCG8 (-/-) mice fed a lithogeni
105 n ATP hydrolysis in Pichia pastoris purified ABCG5/G8 and found that they stimulated hydrolysis appro
106 er attenuated bile acid induction of hepatic Abcg5/g8 and gallbladder cholesterol content, suggesting
111 ary cholesterol secretion is mediated by the ABCG5/G8 complex in vivo, and if so, whether LXRa is inv
114 y promote an active conformation of purified ABCG5/G8 either by global stabilization of the transport
117 there was no change in bile acid synthesis, ABCG5/G8 expression, or hepatic cholesterol concentratio
120 ne FTO2B, LXR-dependent transcription of the ABCG5/G8 genes was cycloheximide-resistant, indicating t
124 findings demonstrate that overexpression of ABCG5/G8 in the liver profoundly alters hepatic but not
125 xclusion from the body, we fed wild-type and ABCG5/G8 knockout mice a diet enriched with plant sterol
126 -phytosterol diet was extremely toxic to the ABCG5/G8 knockout mice but had no adverse effects on wil
130 from LXR agonist-treated mice revealed that ABCG5/G8 mRNA is located in hepatocytes and enterocytes
131 sterol in conjunction with decreased hepatic Abcg5/g8 mRNA, increased Npc1l1 mRNA, and decreased Hmgr
136 udies demonstrated that bile acids increased ABCG5/G8 specific cholesterol efflux in cell models.
137 determine the specific contribution of liver ABCG5/G8 to sterol transport and atherosclerosis, we gen
138 into bile is largely dependent on an intact ABCG5/G8 transporter complex, whereas LXRa is not critic
140 to bile induced by hepatic overexpression of ABCG5/G8 was not sufficient to alter hepatic cholesterol
141 binding cassette subfamily G member 5 and 8 (ABCG5/G8) and scavenger receptor class B type I (SR-BI)
142 transporters that function as heterodimers (ABCG5/G8) to reduce sterol absorption in the intestines
146 e-binding cassette (ABC) sterol transporter, Abcg5/g8, is Lith9 in mice, and two gallstone-associated
147 of lipid-lowering therapy (ie, HMGCR, PCSK9, ABCG5/G8, LDLR) are associated with the risk of type 2 d
148 rnative mechanism, independent of intestinal ABCG5/G8, to protect against the accumulation of dietary
149 ta demonstrate that (1) SR-BI contributes to ABCG5/G8-independent biliary cholesterol secretion under
150 pothesize that in the defect of ABCG5/G8, an ABCG5/G8-independent pathway is essential for regulating
153 cholesterol transport (RCT) independently of ABCG5/G8-mediated biliary cholesterol secretion, implyin
158 -stimulated conditions is fully dependent on ABCG5/G8; and (3) Sr-bI contributes to macrophage-to-fec
159 enosine triphosphate-binding cassette G5/G8 [ABCG5/G8], scavenger receptor class B, member 1) and bil
161 ATP)-binding cassette subfamily G, member 5 (Abcg5) gene, alters a tryptophan codon (UGG) to a premat
163 (ATP-binding cassette transporters ABCA1 and ABCG5, hydroxymethylglutaryl-CoA synthase and the LDL re
166 a new member of the ABC transporter family, ABCG5, is mutant in nine unrelated sitosterolemia patien
167 er family, named "sterolin-1" and encoded by ABCG5, is mutated in 9 unrelated families with sitostero
169 llowing order: wild type > Sr-bI ko (-16%) > Abcg5 ko (-75%) > Sr-bI/Abcg5 dko (-94%), all at least P
173 increased cholesterol secretion 3.1-fold in Abcg5(+/+) mice, whereas this response was severely blun
177 (1) mg(-)(1)), suggesting that expression of ABCG5 or ABCG8 alone yielded nonfunctional transporters.
178 osterolemic patients with a defect in either ABCG5 or ABCG8 and in either Abcg5/g8 double- or single-
180 5n-3 had no effect on the T1317 induction of ABCG5 or ABCG8 in the rat hepatoma cell line, FTO-2B.
183 phosphate-binding cassette transporter genes ABCG5 or ABCG8 that result in accumulation of xenosterol
185 osterolemia is caused by mutations in either ABCG5 or ABCG8, but simultaneous mutations of these gene
186 TP-binding cassette (ABC) half-transporters, ABCG5 or ABCG8, lead to reduced secretion of sterols int
187 sorder that results from mutations in either ABCG5 or G8 proteins, with hyperabsorption of dietary st
188 Mice homozygous for disruption of Abcg5 (Abcg5(-/-) ) or Lxra (Lxra(-/-) ) and their wild-type co
190 ing yielded two disease-associated variants: ABCG5-R50C (P = 4.94 x 10(-9) ) and ABCG8-D19H (P = 1.74
191 ight effect on the N-glycosylation status of ABCG5; rather it accelerated ABCG5 degradation in an E3
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