ライフサイエンスコーパス: ABCG1

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

8 t ATP-binding cassette subfamily G member 1 (ABCG1), cholesterol transporters in this process.

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

13 XRbeta, resulting in the induction of ABCA1, ABCG1, and apolipoprotein E expression.

14 r (LXR) agonist induced expression of ABCA1, ABCG1, and cholesterol efflux in both LDLR(-/-) and wild

15 crophages had reduced basal levels of ABCA1, ABCG1, and cholesterol efflux.

16 The findings indicate that ABCA1, ABCG1, and HDL inhibit the proliferation of hematopoieti

17 ved in reverse cholesterol transport (ABCA1, ABCG1 and 27-hydroxylase) and scavenger receptors, respo

18 apolipoprotein E (apoE) or increasing ABCA1/ABCG1-induced apoE lipoprotein association/lipidation.

19 terol (by activating the PPARgamma-LXR-ABCA1/ABCG1 pathway), thereby reducing inflammation and apopto

20 lipidation of apoE4, then induction of ABCA1/ABCG1 may be beneficial.

21 SPCs to promote cholesterol efflux via ABCA1/ABCG1 and decrease cell proliferation, monocytosis, and

22 transporters, including ABCC3, ABCB6, ABCD1, ABCG1, ABCG4, ABCG5, ABCG8, ABCE1, ABCF1, ABCF2, and ABC

23 cine residue in the Walker A motif abolished ABCG1-dependent cholesterol efflux and esterification an

24 A 638-amino acid ABCG1, which lacked the 40 N-terminal amino acids of the

25 for the first time a major role of adipocyte ABCG1 in adiposity and fat mass growth and suggests that

26 nd fat mass growth and suggests that adipose ABCG1 might represent a potential therapeutic target in

27 ction and active eNOS dimer disruption in an ABCG1-dependent manner.

28 ote cholesterol efflux from foam cells in an ABCG1-dependent pathway due to an increased content of L

29 ransporters ATP binding cassette (ABC)A1 and ABCG1.

30 Combined deficiency of ABCA1 and ABCG1 also resulted in significant islet inflammation as

31 phages had decreased expression of ABCA1 and ABCG1 and reduced lipid efflux.

32 Deletion of ABCA1 and ABCG1 causes an increased cholesterol content on the inn

33 ABCA1 and ABCG1 control the proliferation of hematopoietic stem an

34 activation and increased levels of ABCA1 and ABCG1 could be useful in the treatment of human apoE4 ca

35 ith isolated macrophages, combined ABCA1 and ABCG1 deficiency resulted in impaired cholesterol efflux

36 ATP binding cassette transporters ABCA1 and ABCG1 displayed a dramatic increase in HSPC mobilization

37 These data suggest that ABCA1 and ABCG1 each make complimentary and important contribution

38 ABCA1 and ABCG1 export excess cellular cholesterol into the HDL pa

39 crophage RCT from cells where both ABCA1 and ABCG1 expression were knocked down than from ABCG1-knock

40 by increased PPARalpha, LXRalpha, ABCA1 and ABCG1 expressions in the liver.

41 ABCA1 and ABCG1 facilitate macrophage chemotaxis by promoting PM t

42 ABCA1 and ABCG1 facilitate the efflux of cholesterol from macropha

43 ed at doses in which they elevated ABCA1 and ABCG1 gene expression in duodenum and liver at equal lev

44 ATP-binding cassette transporters ABCA1 and ABCG1 have a major role in promoting cholesterol efflux

45 To determine whether ABCA1 and ABCG1 have complementary roles in beta-cells, mice lacki

46 efflux-promoting ABC transporters ABCA1 and ABCG1 in BM cells.

47 ses the mRNA and protein levels of ABCA1 and ABCG1 in hippocampal neurons, but has no effect on the c

48 ting a dose-dependent induction of ABCA1 and ABCG1 in human monocyte-derived macrophages by cholester

49 radation of endogenously expressed ABCA1 and ABCG1 in human THP-1 macrophages.

50 ggest that the combined effects of ABCA1 and ABCG1 in mediating macrophage sterol efflux are central

51 ts were independent of any role of ABCA1 and ABCG1 in mediating oxidized phospholipid efflux but were

52 tudy was to determine the roles of ABCA1 and ABCG1 in preserving the viability of macrophages during

53 addressing the individual roles of ABCA1 and ABCG1 in the development of atherosclerosis have produce

54 Thus, lack of both ABCA1 and ABCG1 induces greater defects in beta-cell function than

55 Turnover of ABCA1 and ABCG1 is strongly inhibited by proteasomal inhibitors an

56 l in post-translational control of ABCA1 and ABCG1 protein expression.

57 ent, post-translational control of ABCA1 and ABCG1 protein levels, mediated through a specific and st

58 inding cassette (ABC) transporters ABCA1 and ABCG1 regulate macrophage cholesterol efflux and hence p

59 rol efflux from macrophages by the ABCA1 and ABCG1 transporter systems hold great promise and may be

60 g cassette transporters A1 and G1 (ABCA1 and ABCG1) in macrophages (MAC-ABC(DKO) mice) but not in hem

61 nding cassette (ABC) transporters (ABCA1 and ABCG1) involved in cholesterol efflux is not affected in

62 ATP-binding cassette transporters (ABCA1 and ABCG1) that mediate cellular cholesterol efflux.

63 cholesterol uptake (LDLR), efflux (ABCA1 and ABCG1), and inflammation (DHCR24).

64 These results demonstrate that ABCA1 and ABCG1, but not SR-BI, promote macrophage RCT in vivo and

65 Two macrophage ABC transporters, ABCA1 and ABCG1, have a major role in promoting cholesterol efflux

66 ATP-binding cassette transporters, ABCA1 and ABCG1, in beta-cells (beta-DKO mice).

67 g cassette transporters A1 and G1 (ABCA1 and ABCG1, respectively) are the most important apoE-lipidat

68 dentify sequences in the 3' UTR of ABCA1 and ABCG1, sterol transporter genes both previously shown to

69 inding cassette (ABC) transporters ABCA1 and ABCG1, which are membrane lipid translocases.

70 ATP-binding cassette transporters ABCA1 and ABCG1, which are responsible for initiating reverse chol

71 inding cassette (ABC) transporters ABCA1 and ABCG1, which promote cholesterol efflux from macrophages

72 ATP-binding cassette transporters ABCA1 and ABCG1, which promote efflux of cholesterol and oxysterol

73 tivation upregulated the levels of ABCA1 and ABCG1.

74 xpression of the ABC transporters, ABCA1 and ABCG1.

75 ATP-binding cassette transporters ABCA1 and ABCG1.

76 anol, also caused up-regulation of ABCA1 and ABCG1.

77 n of the cholesterol transporters, ABCA1 and ABCG1.

78 anisms by which RAGE downregulates ABCA1 and ABCG1.

79 nding cassette (ABC) transporters, ABCA1 and ABCG1.

80 loading inhibits ubiquitination of ABCA1 and ABCG1.

81 ng cassette subfamily A member 1 (ABCA1) and ABCG1.

82 binding cassette transporter A1 (ABCA1) and ABCG1.

83 ased scavenger receptor AI, CD36, ABCA1, and ABCG1 expression which led to suppression of cholesterol

84 he coordinate regulation of apoE, ABCA1, and ABCG1 expression.

85 mRNA and protein levels of apoE, ABCA1, and ABCG1 in young, naive apoE3- and apoE4-targeted replacem

86 sm, such as the ATP transporters, ABCA1, and ABCG1, and the scavenger receptor, SRB1.

87 -bound pool, where it acted in an ABCA1- and ABCG1-dependent fashion to decrease cell proliferation.

88 This occurs through an ABCA1- and ABCG1-dependent mechanism and is reversible by intervent

89 ake while concomitantly promoting ABCA1- and ABCG1-mediated reverse cholesterol transport.

90 ing lipoprotein lipase, CD36, LXR alpha, and ABCG1 in thioglycolate-elicited peritoneal macrophages.

91 sterol transport (PPAR-gamma, LXR-alpha, and ABCG1) and macrophage emigration from lesions (CCR7) in

92 from wild-type, ABCA1(-/-), SR-BI(-/-), and ABCG1(-/-) adipocytes to apolipoprotein A-I (apoA-I) and

93 avenger receptor class B type I (SR-BI), and ABCG1 have been shown to promote cholesterol efflux to e

94 gh the various pathways (ABCA1-, SR-BI-, and ABCG1-mediated efflux); however, these subjects had no c

95 CETP and ABCG1 may be important mediators of these effects throug

96 CETP and ABCG1, both of which participate in the HDL-mediated rev

97 es in the recently reported HIF3A, CPT1A and ABCG1 regions.

98 CAV-1, CYP2b10, and ABCG1 were significantly induced in ABCA1-overexpressing

99 s between triglyceride levels and SREBF1 and ABCG1 were also found in adipose tissue of the Multiple

100 ated with Alzheimer's disease: TOMM40, APOE, ABCG1 and MEF2C.

101 , SC4MOL), and efflux ( downward arrowABCA1, ABCG1), producing a molecular profile expected to increa

102 ion analysis revealed an association between ABCG1 methylation and lipid levels that might be partly

103 Because both ABCG1 and LPL are expressed in adipose tissue, we hypoth

104 Lack of both ABCG1 and beta-cell ABCA1 resulted in increased fasting

105 in intracellular cholesterol homeostasis by ABCG1 profoundly impact iNKT cell development and functi

106 ipid levels that might be partly mediated by ABCG1 expression.

107 In transfected 293 cells, ABCG1 and ABCG4 stimulate cholesterol efflux to both sma

108 Consistent with these data, ABCG1 had a major role in promoting efflux of cholestero

109 with type 2 diabetes mellitus had decreased ABCG1 and/or ABCA1, impaired cholesterol efflux, and inc

110 lso studied and were found to have decreased ABCG1 expression without an increase in CD36.

111 ophage cholesterol efflux and that decreased ABCG1 function can facilitate foam cell formation in Typ

112 lucidation of the various roles of different ABCG1 isoforms will be important for our understanding o

113 zation to the endosome pathway distinguishes ABCG1 and/or ABCG4 from all other mammalian members of t

114 nt in glucose tolerance compared with either ABCG1 deletion or loss of ABCA1 in beta-cells alone.

115 ly obese individuals indicated that elevated ABCG1 expression in adipose tissue was associated with i

116 eritoneal macrophages showed that endogenous ABCG1 is intracellular and undetectable at the cell surf

117 ues in the TM domains that are important for ABCG1 to alter sterol efflux, induce sterol regulatory e

118 have demonstrated an intracellular role for ABCG1 in beta cells.

119 These findings indicate a specific role for ABCG1 in promoting efflux of 7-ketocholesterol and relat

120 Analysis of two frequent ABCG1 single nucleotide polymorphisms (rs1893590 [A/C] a

121 ABCG1 expression were knocked down than from ABCG1-knockdown cells.

122 at two ABC transporters of unknown function, ABCG1 and ABCG4, mediate isotopic and net mass efflux of

123 harbored C-phosphorus-G dinucleotides (e.g., ABCG1/cg06500161), which overlapped Encyclopedia of DNA

124 ing cassette transporters A1 (ABCA1) and G1 (ABCG1) in macrophages, thus promoting efflux of choleste

125 ing cassette transporters A1 (ABCA1) and G1 (ABCG1), and a consequent decrease in cellular cholestero

126 esterol transporter ATP binding cassette G1 (ABCG1) have pulmonary lipidosis and enhanced innate immu

127 The role of the ATP-binding cassette G1 (ABCG1) transporter in human pathophysiology is still lar

128 ing the ATP-binding cassette transporter G1 (ABCG1) develop chronic inflammation in the lungs, which

129 ATP-binding cassette transporter G1 (ABCG1) effluxes cholesterol from macrophages and plays a

130 The ATP-binding cassette transporter G1 (ABCG1) has been shown to play a role in cholesterol effl

131 ATP binding cassette transporter G1 (ABCG1) mediates the transport of cholesterol from cells

132 ATP-binding cassette transporter G1 (ABCG1) plays a role in the intracellular transport of ch

133 ATP-binding cassette transporter G1 (ABCG1) promotes cholesterol accumulation and alters T ce

134 ATP-binding cassette transporter G1 (ABCG1) promotes cholesterol efflux from cells and regula

135 te that ATP-binding cassette transporter G1 (ABCG1) regulates cholesterol homeostasis in thymocytes a

136 riphosphate-binding cassette transporter G1 (ABCG1).

137 -dependent expression of other target genes, ABCG1 and SREBP-1c.

138 Last, we found that higher ABCG1 expression in Tregs was associated with a higher f

139 mice that express both the murine and human ABCG1 genes.

140 E1 and NEDD4-1 in cells overexpressing human ABCG1 significantly increased levels of the ABCG1 monome

141 Here we show that human ABCG1 overexpressed in baby hamster kidney cells in the

142 In conclusion, the human ABCG1 gene contains multiple promoters, spans more than

143 omic organization and structure of the human ABCG1 gene demonstrates that: (i) the gene consists of 2

144 The human ABCG1 gene encodes a member of the ATP-binding cassette

145 Using microarray analyses, we identified ABCG1, encoding an ABC transporter, as a gene responsive

146 These findings identify ABCG1 as a novel integrator of cholesterol homeostasis a

147 and emphasizes recent studies that identify ABCG1 as a key regulator of cellular lipid homeostasis.

148 geted to endosomes and functional, and (iii) ABCG1 colocalizes with multiple proteins that mark late

149 This impaired ABCG1-mediated cholesterol efflux significantly correlat

150 These results implicate ABCG1 as an important negative regulator of lymphocyte p

151 Thymic iNKT cells deficient in ABCG1 had reduced membrane lipid raft content, and showe

152 the lungs of aged chow-fed mice deficient in ABCG1 show distinctive signs of inflammation that includ

153 e, indicating that the ATP binding domain in ABCG1 is essential for both lipid transport activity and

154 DL was largely derived from these domains in ABCG1 transfectants but not in cells lacking ABCG1.

155 CpG cg06500161, located in ABCG1, was associated in opposite directions with both h

156 es, respectively, with no effect observed in ABCG1(-/-) adipocytes.

157 rol content and rescued insulin secretion in ABCG1-deficient islets.

158 Methylation of a CpG site in ABCG1 on chromosome 21 was significantly associated with

159 G sites annotated to various genes including ABCG1, MIR33B/SREBF1, and TNIP1 were identified.

160 In addition, ligase silencing increased ABCG1-mediated cholesterol export to HDL in cells overex

161 k293 cells with plasmids encoding individual ABCG1 isoforms.

162 other LXR target genes were weakly induced (ABCG1 and SREBP-1c) or not induced (apoE and LXRalpha).

163 Furthermore, islet ABCG1 expression was reduced in diabetic mice and restor

164 , implicating a role for regulation of islet ABCG1 expression in diabetes pathogenesis and treatment.

165 ABCG1 transfectants but not in cells lacking ABCG1.

166 plementary roles in beta-cells, mice lacking ABCG1 and beta-cell ABCA1 were generated and glucose tol

167 nd inflammation, hyperlipidemic mice lacking ABCG1 develop smaller atherosclerotic lesions compared w

168 Like ABCG1, ABCG4 protein levels and cholesterol export activ

169 provide important information that may link ABCG1 to diseases of dysregulated tissue lipid homeostas

170 d provide critical information that may link ABCG1 to the reverse cholesterol transport pathway or di

171 tudies reveal a critical role for macrophage ABCG1 in lung inflammation and homeostasis.

172 We show that increased macrophage ABCG1 expression significantly promoted while knockdown

173 ed while knockdown or knockout of macrophage ABCG1 expression significantly reduced macrophage RCT in

174 To investigate whether macrophage ABCG1 is involved in macrophage RCT in vivo, we used ABC

175 implicate adipocyte SR-BI and ABCA1, but not ABCG1, in this process.

176 merase chain reaction, we identified a novel ABCG1 transcript that encodes a putative protein of 786

177 The absence of ABCG1 in CD4 T cells results in hyperproliferation in vi

178 , our study demonstrates that the absence of ABCG1 inhibits tumour growth through modulation of macro

179 In the absence of ABCG1, intracellular cholesterol accumulation led to dow

180 The mechanism of action of ABCG1 is controversial and it has been proposed to act a

181 ular localization studies showed the bulk of ABCG1 protein to be present in insulin granules.

182 eicosatetranoic acid-mediated degradation of ABCG1.

183 d critical residues within the TM domains of ABCG1 that are both essential for sterol transport and c

184 ls was completely dependent on expression of ABCG1 and the presence of HDL in media.

185 tato plants with downregulated expression of ABCG1 display major alterations in both root and tuber m

186 Macrophage expression of ABCG1 in both patients and control subjects was induced

187 RNA interference reduced the expression of ABCG1 in liver X receptor-activated macrophages and caus

188 ear receptor LXR and that over expression of ABCG1 results in increased efflux of cellular cholestero

189 mouse embryos revealed strong expression of ABCG1 transcripts in the olfactory epithelium, hind brai

190 sterol esterification, induced expression of ABCG1, and stimulated HDL-dependent cholesterol efflux i

191 ell ABCA1 have increased islet expression of ABCG1, another cholesterol transporter implicated in bet

192 The in-vivo importance of ABCG1 has recently been demonstrated with both loss-of-f

193 into HEK-293 cells conferred an induction of ABCG1 and SREBP-1c; 2) upon cholesterol loading, CYP27-e

194 l treatment results in >10-fold induction of ABCG1 transcripts that are derived from either exons 8-2

195 esterification and prevented localization of ABCG1 to the cell surface, indicating that the ATP bindi

196 Loss of ABCG1 expression impaired insulin secretion both in vivo

197 ecent studies have demonstrated that loss of ABCG1 has wide-ranging consequences and impacts lymphocy

198 e, we investigated how the selective loss of ABCG1 in T cells impacts atherosclerosis in LDL receptor

199 Loss of ABCG1 led to altered granule morphology and reduced gran

200 Loss of ABCG1 results in increased levels of specific oxysterols

201 Loss of ABCG1 results in severe pulmonary lipidosis in mice, wit

202 b macrophages was due to a selective loss of ABCG1-mediated efflux to high density lipoprotein.

203 DNA methylation of ABCG1 might also play a role in previous hospitalized my

204 Overexpression of ABCG1 also increased cholesterol esterification, which w

205 Genetic knockdown or overexpression of ABCG1 showed that increased cholesterol efflux to CETP-D

206 s type 2, demonstrate that overexpression of ABCG1 specifically stimulates the efflux of cellular cho

207 s the turnover and serine phosphorylation of ABCG1.

208 ymes in the post-translational regulation of ABCG1 and ABCG4 protein levels and cellular cholesterol

209 ceptor activator results in up-regulation of ABCG1 and increases cholesterol efflux to HDL.

210 al inhibitors blocked the down-regulation of ABCG1 expression and resulted in accumulation of phospho

211 ges were resistant to the down-regulation of ABCG1 protein, reduction in efflux, and increase in seri

212 , we were able to confirm down-regulation of ABCG1 using C57BL/6J peritoneal macrophages cultured in

213 e also shown that ABCG4, a close relative of ABCG1, controls platelet production, atherosclerosis, an

214 m macrophages and have evaluated the role of ABCG1 and other factors in this process.

215 Here we demonstrate a role of ABCG1 as a mediator of tumour immunity.

216 val by HDL, consistent with a direct role of ABCG1 in cellular cholesterol transport.

217 offer a comprehensive review on the role of ABCG1 in cellular sterol homeostasis.

218 The critical role of ABCG1 in obesity was further confirmed in independent po

219 (ii) a chimeric protein containing the TM of ABCG1 and the cytoplasmic domains of the nonsterol trans

220 ter luciferase activity and transcription of ABCG1 and ABCA1 through peroxisome proliferator-activate

221 ouse and human macrophages in which ABCA1 or ABCG1 expression was deleted.

222 a HDL, cell lines stably expressing ABCA1 or ABCG1, and both mouse and human macrophages in which ABC

223 cell lines stably expressing human ABCA1 or ABCG1, we observed that the abundance of these proteins

224 Genetic variants in SREBF1, PHOSPHO1, ABCG1 and CPT1A were also associated with lipid profile.

225 d resulted in accumulation of phosphorylated ABCG1.

226 aortic CD36 expression and increased plaque ABCG1 expression and signs of plaque stability.

227 ave enhanced transporter expression, reduced ABCG1 phosphorylation, and increased cholesterol efflux.

228 phages that overexpress 12/15LO have reduced ABCG1 expression, increased transporter phosphorylation,

229 found that chronic elevated glucose reduces ABCG1 expression.

230 However, lipoproteins regulated ABCG1 expression similarly in LDLR(-/-) and wild type ma

231 ings provide evidence that 12/15LO regulates ABCG1 expression and function through p38- and JNK2-depe

232 te the mechanisms by which 12/15LO regulates ABCG1.

233 Furthermore, T cell-specific ABCG1 deficiency led to a 30% increase in Treg percentag

234 fed a high-cholesterol diet, T cell-specific ABCG1 deficiency protected against atherosclerotic lesio

235 In vitro, RAGE ligands suppressed ABCG1 and ABCA1 promoter luciferase activity and transcr

236 ne genes (SREBF1, SREBF2, PHOSPHO1, SYNGAP1, ABCG1, CPT1A, MYLIP, TXNIP and SLC7A11) and 2 intergenic

237 In mouse macrophages, miR-33 also targets ABCG1, reducing cholesterol efflux to nascent high-densi

238 Our data demonstrate that ABCG1 is an intracellular sterol transporter that locali

239 These observations demonstrate that ABCG1 plays a major role in macrophage cholesterol efflu

240 These results demonstrate that ABCG1 plays critical roles in pulmonary homeostasis, bal

241 In summary, our results demonstrate that ABCG1 plays essential roles in pulmonary lipid homeostas

242 In this study, we demonstrate that ABCG1 regulates iNKT cell development and functions in a

243 Recent studies have also demonstrated that ABCG1 functions as an intracellular lipid transporter, l

244 ssed in adipose tissue, we hypothesized that ABCG1 is implicated in adipocyte TG storage and therefor

245 These studies indicate that ABCG1 and ABCG4 promote cholesterol efflux from cells to

246 Early studies with Abcg1 mice indicated that ABCG1 was crucial for tissue lipid homeostasis, especial

247 More detailed analysis indicated that ABCG1 was expressed primarily in ECs, and that these cel

248 Our study indicates that ABCG1 regulates T cell differentiation into Tregs, highl

249 Previous studies reported that ABCG1 is ubiquitinated and degraded via the ubiquitin pr

250 Further analyses revealed that ABCG1 is expressed in roots and tuber periderm, as well

251 Other studies show that ABCG1 expression is induced following activation of the

252 Here we show that ABCG1 function is dependent on localization to intracell

253 These studies show that ABCG1 redistributes cholesterol to cell-surface domains

254 In conclusion, we have shown that ABCG1 deletion in macrophages causes a striking inflamma

255 These findings suggest that ABCG1 acts primarily to regulate subcellular cholesterol

256 Our data suggest that ABCG1 and HDL maintain EC function in HCD-fed mice by pr

257 in neuronal tissues and the eye suggest that ABCG1-dependent cholesterol efflux may be critical for n

258 (25 mM glucose for 7 days), suggesting that ABCG1 expression in diabetic macrophages is regulated by

259 of RNA interference plants, suggesting that ABCG1 is required for the export of suberin components.

260 The ABCG1 transporter plays a key role in regulating cellula

261 cant reduction in protein levels of both the ABCG1 monomeric and dimeric forms.

262 ediating free cholesterol efflux to HDL, the ABCG1 transporter equally promotes lipid accumulation in

263 ABCG1 significantly increased levels of the ABCG1 monomeric and dimeric protein forms, however ABCA1

264 r morphology, whereas the aerial part of the ABCG1-RNAi plants appear normal.

265 f a diet high in both fat and cholesterol to ABCG1 mice results in massive cholesterol accumulation i

266 as fully functional and of a similar size to ABCG1 expressed by cholesterol-loaded human monocyte-der

267 Transgenic ABCG1-RNAi potato plants with downregulated expression o

268 decreased expression of the ABC transporter ABCG1 and increased expression of the scavenger receptor

269 The ATP-binding cassette transporter ABCG1 has an essential role in cellular cholesterol home

270 The ATP-binding cassette transporter ABCG1 was recently shown to promote efflux of cholestero

271 cently, the ATP-binding cassette transporter ABCG1, a macrophage liver X receptor (LXR) target, has b

272 Inactivation of the sterol transporter ABCG1 uncouples LXR signaling from proliferation, direct

273 P-binding cassette transmembrane transporter ABCG1 show progressive and age-dependent severe pulmonar

274 ession of a reverse cholesterol transporter (ABCG1; P=7.2E-28) and incident cardiovascular disease ev

275 e levels of another cholesterol transporter, ABCG1.

276 ng to three well-characterized genes (TXNIP, ABCG1 and SAMD12) independently explained 7.8% of the he

277 t significantly different between wild-type, ABCG1, and hABCG1 transgenic mice.

278 In other cell types, ABCG1 expression is downregulated in diabetes and upregu

279 Strategies to upregulate ABCG1 expression and function in type 2 diabetes mellitu

280 involved in macrophage RCT in vivo, we used ABCG1-overexpressing, -knockdown, and -knockout macropha

281 effects by promoting cholesterol efflux via ABCG1 and ABCA1 with consequent attenuation of signaling

282 and for synthesis of an intact pollen wall (ABCG1 and ABCG16).

283 creased cholesterol efflux to CETP-D HDL was ABCG1 dependent.

284 Whether ABCG1 regulates adaptive immune responses to the environ

285 Elucidation of the mechanisms by which ABCG1 affects intracellular sterol flux/movement should

286 cidation of the molecular mechanism by which ABCG1 controls sterol flux should provide critical infor

287 d two HECT domain E3 ligases associated with ABCG1, named HUWE1 (HECT, UBA, and WWE domain containing

288 These observations are consistent with ABCG1 controlling cellular sterol metabolism.

289 uggest that methylation of a CpG site within ABCG1 is associated with fasting insulin and merits furt