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1 ABCG1 expression and cholesterol efflux are reduced in p
2 ABCG1 has a lesser role in cholesterol efflux and a negl
3 ABCG1 is highly expressed in macrophages and probably me
4 ABCG1 plays a crucial role in maintaining intracellular
5 ABCG1 transcripts are induced in vivo in multiple tissue
6 ABCG1 was present in macrophages from control subjects b
7 ABCG1, a member of the ATP-binding cassette transporter
9 xpression of LXR target genes such as ABCA1, ABCG1, APOE, SCD-1, and SREBP-1c in THP-1 differentiated
10 Peritoneal macrophages deficient in ABCA1, ABCG1, or both show enhanced expression of inflammatory
11 volved in lipid metabolism, including ABCA1, ABCG1, and sterol regulatory element-binding protein-1c
12 e identified a new beneficial role of ABCA1, ABCG1 and HDL in dampening the oxidative burst and prese
14 r (LXR) agonist induced expression of ABCA1, ABCG1, and cholesterol efflux in both LDLR(-/-) and wild
17 ved in reverse cholesterol transport (ABCA1, ABCG1 and 27-hydroxylase) and scavenger receptors, respo
19 apolipoprotein E (apoE) or increasing ABCA1/ABCG1-induced apoE lipoprotein association/lipidation.
20 terol (by activating the PPARgamma-LXR-ABCA1/ABCG1 pathway), thereby reducing inflammation and apopto
22 SPCs to promote cholesterol efflux via ABCA1/ABCG1 and decrease cell proliferation, monocytosis, and
23 transporters, including ABCC3, ABCB6, ABCD1, ABCG1, ABCG4, ABCG5, ABCG8, ABCE1, ABCF1, ABCF2, and ABC
24 cine residue in the Walker A motif abolished ABCG1-dependent cholesterol efflux and esterification an
26 for the first time a major role of adipocyte ABCG1 in adiposity and fat mass growth and suggests that
27 nd fat mass growth and suggests that adipose ABCG1 might represent a potential therapeutic target in
29 ote cholesterol efflux from foam cells in an ABCG1-dependent pathway due to an increased content of L
36 activation and increased levels of ABCA1 and ABCG1 could be useful in the treatment of human apoE4 ca
37 ith isolated macrophages, combined ABCA1 and ABCG1 deficiency resulted in impaired cholesterol efflux
38 ATP binding cassette transporters ABCA1 and ABCG1 displayed a dramatic increase in HSPC mobilization
41 crophage RCT from cells where both ABCA1 and ABCG1 expression were knocked down than from ABCG1-knock
45 ed at doses in which they elevated ABCA1 and ABCG1 gene expression in duodenum and liver at equal lev
46 ATP-binding cassette transporters ABCA1 and ABCG1 have a major role in promoting cholesterol efflux
49 ses the mRNA and protein levels of ABCA1 and ABCG1 in hippocampal neurons, but has no effect on the c
50 ting a dose-dependent induction of ABCA1 and ABCG1 in human monocyte-derived macrophages by cholester
52 ggest that the combined effects of ABCA1 and ABCG1 in mediating macrophage sterol efflux are central
53 ts were independent of any role of ABCA1 and ABCG1 in mediating oxidized phospholipid efflux but were
54 letion of cholesterol transporters ABCA1 and ABCG1 in microglia, leading to inflammaraft formation, i
55 tudy was to determine the roles of ABCA1 and ABCG1 in preserving the viability of macrophages during
56 addressing the individual roles of ABCA1 and ABCG1 in the development of atherosclerosis have produce
60 ent, post-translational control of ABCA1 and ABCG1 protein levels, mediated through a specific and st
61 inding cassette (ABC) transporters ABCA1 and ABCG1 regulate macrophage cholesterol efflux and hence p
62 rol efflux from macrophages by the ABCA1 and ABCG1 transporter systems hold great promise and may be
63 g cassette transporters A1 and G1 (ABCA1 and ABCG1) in macrophages (MAC-ABC(DKO) mice) but not in hem
64 nding cassette (ABC) transporters (ABCA1 and ABCG1) involved in cholesterol efflux is not affected in
67 These results demonstrate that ABCA1 and ABCG1, but not SR-BI, promote macrophage RCT in vivo and
68 Two macrophage ABC transporters, ABCA1 and ABCG1, have a major role in promoting cholesterol efflux
70 g cassette transporters A1 and G1 (ABCA1 and ABCG1, respectively) are the most important apoE-lipidat
71 dentify sequences in the 3' UTR of ABCA1 and ABCG1, sterol transporter genes both previously shown to
73 ATP-binding cassette transporters ABCA1 and ABCG1, which are responsible for initiating reverse chol
74 inding cassette (ABC) transporters ABCA1 and ABCG1, which promote cholesterol efflux from macrophages
75 ATP-binding cassette transporters ABCA1 and ABCG1, which promote efflux of cholesterol and oxysterol
86 ased scavenger receptor AI, CD36, ABCA1, and ABCG1 expression which led to suppression of cholesterol
88 mRNA and protein levels of apoE, ABCA1, and ABCG1 in young, naive apoE3- and apoE4-targeted replacem
90 -bound pool, where it acted in an ABCA1- and ABCG1-dependent fashion to decrease cell proliferation.
93 ing lipoprotein lipase, CD36, LXR alpha, and ABCG1 in thioglycolate-elicited peritoneal macrophages.
94 sterol transport (PPAR-gamma, LXR-alpha, and ABCG1) and macrophage emigration from lesions (CCR7) in
95 from wild-type, ABCA1(-/-), SR-BI(-/-), and ABCG1(-/-) adipocytes to apolipoprotein A-I (apoA-I) and
96 avenger receptor class B type I (SR-BI), and ABCG1 have been shown to promote cholesterol efflux to e
97 gh the various pathways (ABCA1-, SR-BI-, and ABCG1-mediated efflux); however, these subjects had no c
102 s between triglyceride levels and SREBF1 and ABCG1 were also found in adipose tissue of the Multiple
104 , SC4MOL), and efflux ( downward arrowABCA1, ABCG1), producing a molecular profile expected to increa
105 ion analysis revealed an association between ABCG1 methylation and lipid levels that might be partly
108 in intracellular cholesterol homeostasis by ABCG1 profoundly impact iNKT cell development and functi
112 with type 2 diabetes mellitus had decreased ABCG1 and/or ABCA1, impaired cholesterol efflux, and inc
114 ophage cholesterol efflux and that decreased ABCG1 function can facilitate foam cell formation in Typ
115 lucidation of the various roles of different ABCG1 isoforms will be important for our understanding o
116 zation to the endosome pathway distinguishes ABCG1 and/or ABCG4 from all other mammalian members of t
117 nt in glucose tolerance compared with either ABCG1 deletion or loss of ABCA1 in beta-cells alone.
118 ly obese individuals indicated that elevated ABCG1 expression in adipose tissue was associated with i
119 eritoneal macrophages showed that endogenous ABCG1 is intracellular and undetectable at the cell surf
120 ues in the TM domains that are important for ABCG1 to alter sterol efflux, induce sterol regulatory e
122 These findings indicate a specific role for ABCG1 in promoting efflux of 7-ketocholesterol and relat
125 at two ABC transporters of unknown function, ABCG1 and ABCG4, mediate isotopic and net mass efflux of
126 harbored C-phosphorus-G dinucleotides (e.g., ABCG1/cg06500161), which overlapped Encyclopedia of DNA
127 ing cassette transporters A1 (ABCA1) and G1 (ABCG1) in macrophages, thus promoting efflux of choleste
128 ing cassette transporters A1 (ABCA1) and G1 (ABCG1), and a consequent decrease in cellular cholestero
129 esterol transporter ATP binding cassette G1 (ABCG1) have pulmonary lipidosis and enhanced innate immu
130 The role of the ATP-binding cassette G1 (ABCG1) transporter in human pathophysiology is still lar
131 ing the ATP-binding cassette transporter G1 (ABCG1) develop chronic inflammation in the lungs, which
133 The ATP-binding cassette transporter G1 (ABCG1) has been shown to play a role in cholesterol effl
138 te that ATP-binding cassette transporter G1 (ABCG1) regulates cholesterol homeostasis in thymocytes a
142 ABCG1 degradation via lysosomes and hampered ABCG1-mediated cholesterol efflux and reverse cholestero
145 E1 and NEDD4-1 in cells overexpressing human ABCG1 significantly increased levels of the ABCG1 monome
148 omic organization and structure of the human ABCG1 gene demonstrates that: (i) the gene consists of 2
150 Using microarray analyses, we identified ABCG1, encoding an ABC transporter, as a gene responsive
152 and emphasizes recent studies that identify ABCG1 as a key regulator of cellular lipid homeostasis.
153 geted to endosomes and functional, and (iii) ABCG1 colocalizes with multiple proteins that mark late
157 the lungs of aged chow-fed mice deficient in ABCG1 show distinctive signs of inflammation that includ
158 e, indicating that the ATP binding domain in ABCG1 is essential for both lipid transport activity and
159 DL was largely derived from these domains in ABCG1 transfectants but not in cells lacking ABCG1.
165 In addition, ligase silencing increased ABCG1-mediated cholesterol export to HDL in cells overex
167 other LXR target genes were weakly induced (ABCG1 and SREBP-1c) or not induced (apoE and LXRalpha).
169 , implicating a role for regulation of islet ABCG1 expression in diabetes pathogenesis and treatment.
171 plementary roles in beta-cells, mice lacking ABCG1 and beta-cell ABCA1 were generated and glucose tol
172 nd inflammation, hyperlipidemic mice lacking ABCG1 develop smaller atherosclerotic lesions compared w
174 provide important information that may link ABCG1 to diseases of dysregulated tissue lipid homeostas
175 d provide critical information that may link ABCG1 to the reverse cholesterol transport pathway or di
178 ed while knockdown or knockout of macrophage ABCG1 expression significantly reduced macrophage RCT in
182 merase chain reaction, we identified a novel ABCG1 transcript that encodes a putative protein of 786
184 , our study demonstrates that the absence of ABCG1 inhibits tumour growth through modulation of macro
189 d critical residues within the TM domains of ABCG1 that are both essential for sterol transport and c
191 tato plants with downregulated expression of ABCG1 display major alterations in both root and tuber m
193 RNA interference reduced the expression of ABCG1 in liver X receptor-activated macrophages and caus
194 ear receptor LXR and that over expression of ABCG1 results in increased efflux of cellular cholestero
195 mouse embryos revealed strong expression of ABCG1 transcripts in the olfactory epithelium, hind brai
196 sterol esterification, induced expression of ABCG1, and stimulated HDL-dependent cholesterol efflux i
197 ell ABCA1 have increased islet expression of ABCG1, another cholesterol transporter implicated in bet
199 into HEK-293 cells conferred an induction of ABCG1 and SREBP-1c; 2) upon cholesterol loading, CYP27-e
200 l treatment results in >10-fold induction of ABCG1 transcripts that are derived from either exons 8-2
201 esterification and prevented localization of ABCG1 to the cell surface, indicating that the ATP bindi
203 ecent studies have demonstrated that loss of ABCG1 has wide-ranging consequences and impacts lymphocy
204 e, we investigated how the selective loss of ABCG1 in T cells impacts atherosclerosis in LDL receptor
212 s type 2, demonstrate that overexpression of ABCG1 specifically stimulates the efflux of cellular cho
214 ymes in the post-translational regulation of ABCG1 and ABCG4 protein levels and cellular cholesterol
216 al inhibitors blocked the down-regulation of ABCG1 expression and resulted in accumulation of phospho
217 ges were resistant to the down-regulation of ABCG1 protein, reduction in efflux, and increase in seri
218 , we were able to confirm down-regulation of ABCG1 using C57BL/6J peritoneal macrophages cultured in
219 e also shown that ABCG4, a close relative of ABCG1, controls platelet production, atherosclerosis, an
225 (ii) a chimeric protein containing the TM of ABCG1 and the cytoplasmic domains of the nonsterol trans
226 ter luciferase activity and transcription of ABCG1 and ABCA1 through peroxisome proliferator-activate
228 a HDL, cell lines stably expressing ABCA1 or ABCG1, and both mouse and human macrophages in which ABC
229 cell lines stably expressing human ABCA1 or ABCG1, we observed that the abundance of these proteins
235 ave enhanced transporter expression, reduced ABCG1 phosphorylation, and increased cholesterol efflux.
236 phages that overexpress 12/15LO have reduced ABCG1 expression, increased transporter phosphorylation,
239 ings provide evidence that 12/15LO regulates ABCG1 expression and function through p38- and JNK2-depe
242 fed a high-cholesterol diet, T cell-specific ABCG1 deficiency protected against atherosclerotic lesio
244 ne genes (SREBF1, SREBF2, PHOSPHO1, SYNGAP1, ABCG1, CPT1A, MYLIP, TXNIP and SLC7A11) and 2 intergenic
245 In mouse macrophages, miR-33 also targets ABCG1, reducing cholesterol efflux to nascent high-densi
249 In summary, our results demonstrate that ABCG1 plays essential roles in pulmonary lipid homeostas
251 Recent studies have also demonstrated that ABCG1 functions as an intracellular lipid transporter, l
252 ssed in adipose tissue, we hypothesized that ABCG1 is implicated in adipocyte TG storage and therefor
254 Early studies with Abcg1 mice indicated that ABCG1 was crucial for tissue lipid homeostasis, especial
265 in neuronal tissues and the eye suggest that ABCG1-dependent cholesterol efflux may be critical for n
266 (25 mM glucose for 7 days), suggesting that ABCG1 expression in diabetic macrophages is regulated by
267 of RNA interference plants, suggesting that ABCG1 is required for the export of suberin components.
270 cellular cholesterol levels mediated by the ABCG1 transporter increase ATP release by volume-regulat
271 ediating free cholesterol efflux to HDL, the ABCG1 transporter equally promotes lipid accumulation in
272 ABCG1 significantly increased levels of the ABCG1 monomeric and dimeric protein forms, however ABCA1
274 f a diet high in both fat and cholesterol to ABCG1 mice results in massive cholesterol accumulation i
275 as fully functional and of a similar size to ABCG1 expressed by cholesterol-loaded human monocyte-der
277 decreased expression of the ABC transporter ABCG1 and increased expression of the scavenger receptor
280 cently, the ATP-binding cassette transporter ABCG1, a macrophage liver X receptor (LXR) target, has b
282 P-binding cassette transmembrane transporter ABCG1 show progressive and age-dependent severe pulmonar
283 ession of a reverse cholesterol transporter (ABCG1; P=7.2E-28) and incident cardiovascular disease ev
286 ng to three well-characterized genes (TXNIP, ABCG1 and SAMD12) independently explained 7.8% of the he
291 involved in macrophage RCT in vivo, we used ABCG1-overexpressing, -knockdown, and -knockout macropha
292 effects by promoting cholesterol efflux via ABCG1 and ABCA1 with consequent attenuation of signaling
297 cidation of the molecular mechanism by which ABCG1 controls sterol flux should provide critical infor
298 d two HECT domain E3 ligases associated with ABCG1, named HUWE1 (HECT, UBA, and WWE domain containing
300 uggest that methylation of a CpG site within ABCG1 is associated with fasting insulin and merits furt