ライフサイエンスコーパス: ABCA1

1 RDX5), and metabolism (SLC2A3, SLC2A5, GHRL, ABCA1).

2 t (LXRE) of SREBP-1c, but not to the LXRE of ABCA1.

3 omotes the transcription of SREBP-1c but not ABCA1.

4 /Apoa1 double deletion as well as by lack of ABCA1.

5 ell surface, and enhanced internalization of ABCA1.

6 rs associated with the upregulation of their Abca1.

7 its interaction with gp160 at the expense of ABCA1.

8 known to interact with cathepsin D, NPC1 and ABCA1.

9 DL production and interaction with beta-cell ABCA1.

10 dent of the ATP binding cassette transporter ABCA1.

11 when mice were also deficient in intestinal ABCA1.

12 eted in the intestine alone or together with ABCA1.

13 phenotype and likely functions downstream of ABCA1.

14 , and LDL receptor, and increasing Acox1 and ABCA1.

15 in HDL biogenesis, and mice lacking hepatic ABCA1 (ABCA1(-l/-l)) have very low plasma HDL concentrat

16 ABCA1, ABCA7, and ABCA4 are members of the ABCA subfamil

17 We have purified and reconstituted ABCA1, ABCA7, and ABCA4 into liposomes for fluorescent-l

18 3 cellular miRNAs were confirmed that target ABCA1, ABCC1, ABCC5, ABCC10, and ABCE1 genes and mediate

19 l levels are increased in Aibp-deficient and Abca1 Abcg1-deficient embryos.

20 s involved in reverse cholesterol transport (ABCA1, ABCG1 and 27-hydroxylase) and scavenger receptors

21 enes involved in cholesterol efflux, such as Abca1, Abcg1, and Apoe, in a macrophage cell line.

22 a and LXRbeta, resulting in the induction of ABCA1, ABCG1, and apolipoprotein E expression.

23 id of Ager (RAGE) displayed higher levels of Abca1, Abcg1, and Pparg mRNA transcripts versus Ager-exp

24 on is lipidation of apoE4, then induction of ABCA1/ABCG1 may be beneficial.

25 mouse apolipoprotein E (apoE) or increasing ABCA1/ABCG1-induced apoE lipoprotein association/lipidat

26 1), cholesterol transport or uptake (SCARB1, ABCA1, ABCG5, and LIPC), long-chain omega-3 fatty acid s

27 e changes were accompanied by a reduction of ABCA1 abundance in the liver, but not in the vessels.

28 exit from the endoplasmic reticulum, reduced ABCA1 abundance, and inhibited cholesterol efflux; the s

29 the cholesterol efflux deficit by restoring ABCA1 activation in response to cholesterol loading.

30 ABCA1 actively exported or flipped phosphatidylcholine,

31 candidate biomarkers for in-vivo whole-body ABCA1 activity: the absolute concentration and the % lip

32 ment of ATP-binding cassette transporter A1 (ABCA1) activity by the HIV-1 protein Nef.

33 loci for POAG (primary-open-angle glaucoma) (ABCA1, AFAP1, GMDS, PMM2, TGFBR3, FNDC3B, ARHGEF12, GAS7

34 In the present study, we demonstrate that ABCA1 also promotes the secretion of IL-10, an anti-infl

35 Dysregulated angiogenesis is phenocopied in Abca1 (also known as Abca1a) Abcg1-deficient embryos, an

36 The transport and ATPase activities of ABCA1 and ABCA4 were reduced by 25% in the presence of 2

37 tudies provide the first direct evidence for ABCA1 and ABCA7 functioning as phospholipid transporters

38 Combined deficiency of ABCA1 and ABCG1 also resulted in significant islet infla

39 ient macrophages had decreased expression of ABCA1 and ABCG1 and reduced lipid efflux.

40 ABCA1 and ABCG1 control the proliferation of hematopoiet

41 that RXR activation and increased levels of ABCA1 and ABCG1 could be useful in the treatment of huma

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

43 ABCA1 and ABCG1 facilitate the efflux of cholesterol fro

44 ene increases the mRNA and protein levels of ABCA1 and ABCG1 in hippocampal neurons, but has no effec

45 ulates degradation of endogenously expressed ABCA1 and ABCG1 in human THP-1 macrophages.

46 Turnover of ABCA1 and ABCG1 is strongly inhibited by proteasomal inh

47 cholesterol in post-translational control of ABCA1 and ABCG1 protein expression.

48 rol-dependent, post-translational control of ABCA1 and ABCG1 protein levels, mediated through a speci

49 ATP-binding cassette transporters A1 and G1 (ABCA1 and ABCG1) in macrophages (MAC-ABC(DKO) mice) but

50 lation of ATP-binding cassette transporters (ABCA1 and ABCG1) that mediate cellular cholesterol efflu

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

52 on of the ATP-binding cassette transporters, ABCA1 and ABCG1, in beta-cells (beta-DKO mice).

53 ATP-binding cassette transporters A1 and G1 (ABCA1 and ABCG1, respectively) are the most important ap

54 the ATP-binding cassette (ABC) transporters ABCA1 and ABCG1, which are membrane lipid translocases.

55 d with the ATP-binding cassette transporters ABCA1 and ABCG1, which are responsible for initiating re

56 , MC1-R activation upregulated the levels of ABCA1 and ABCG1.

57 osphate-binding cassette (ABC) transporters, ABCA1 and ABCG1.

58 olesterol loading inhibits ubiquitination of ABCA1 and ABCG1.

59 d the mechanisms by which RAGE downregulates ABCA1 and ABCG1.

60 optic nerve and trabecular meshwork and that ABCA1 and AFAP1 are also expressed in retinal ganglion c

61 , enhances LXR:RXR target gene expression of Abca1 and ApoE, reduces soluble forms of Abeta, and abro

62 ittle importance for the interaction between ABCA1 and calnexin.

63 mechanism for Nef-dependent inactivation of ABCA1 and dysregulation of cholesterol metabolism.

64 Furthermore, it binds to ABCA1 and links the ABCA1, CAV1/CAV2 and GAS7 pathway to

65 l analyses indicate that signals observed at ABCA1 and LIPC for HDL cholesterol and NCAN/MAU2 for tri

66 key enzymes involved in cholesterol efflux (ABCA1 and NPC1), fatty acid metabolism (CROT and CPT1a),

67 = 2.79 x 10(-19) for rs2487032 representing ABCA1 and P = 5.77 x 10(-10) for rs3785176 representing

68 ome 9 (P = 2.80 x 10(-11) for rs2472493 near ABCA1 and P = 6.39 x 10(-11) for rs8176693 within ABO) a

69 miR-144 in mice increases the expression of ABCA1 and plasma HDL levels.

70 els of miR-144, which in turn lowers hepatic ABCA1 and plasma HDL levels.

71 Both ABCA1 and PMM2 are expressed in the trabecular meshwork,

72 We and others have previously reported that Abca1(-/-) and Abcg1(-/-) macrophages have increased TLR

73 porters ATP binding cassette transporter A1 (ABCA1) and ABCG1.

74 g ATP-binding cassette subfamily A member 1 (ABCA1) and ABCG1.

75 riphosphate-binding cassette transporter A1 (ABCA1) and adenosine triphosphate-binding cassette trans

76 ATP-binding cassette, subfamily A, member 1 (ABCA1) and circulating high-density lipoprotein choleste

77 tion (Socs3, Il10, Crem, Stat3, Thbd, Thbs1, Abca1) and genes involved in host defense (Gja1, Csf3, T

78 sion of ATP binding cassette transporter A1 (ABCA1) and of neutral cholesterol ester hydrolase (NCEH1

79 targets, including ATP-binding cassette A1 (ABCA1) and sterol response element binding protein 1c.

80 ), CD36, ATP-binding cassette transporter 1 (ABCA1), and ABCG8 levels on the membrane, thus significa

81 midin decreased scavenger receptor AI, CD36, ABCA1, and ABCG1 expression which led to suppression of

82 uding Lxr and downstream transporters, Apoe, Abca1, and Abcg1 genes in vitro.

83 xarotene on mRNA and protein levels of apoE, ABCA1, and ABCG1 in young, naive apoE3- and apoE4-target

84 DL metabolism, such as the ATP transporters, ABCA1, and ABCG1, and the scavenger receptor, SRB1.

85 of the cholesterol efflux regulatory protein ABCA1, and enhanced cholesterol efflux activity in macro

86 orption was reduced by 28% in the absence of ABCA1, and it was reduced by 92-95% when MTP was deleted

87 er receptors, the membrane lipid transporter ABCA1, and its upstream regulator Liver X receptor (LXR)

88 tyrosine kinase and the phagocytosis-related ABCA1, and that of retinaldehyde dehydrogenases leading

89 This occurs through an ABCA1- and ABCG1-dependent mechanism and is reversible b

90 esterol uptake while concomitantly promoting ABCA1- and ABCG1-mediated reverse cholesterol transport.

91 rapib with statins also increased total, non-ABCA1-, and ABCA1-specific CEC by 21%, 27%, and 15%, res

92 ent changes from baseline in CEC (total, non-ABCA1-, and ABCA1-specific) and HDL subpopulations were

93 10(-4) to 4.62x10(-18)), whereas LPL, TRIB1, ABCA1, APOA1-C3-A4-A5, CETP, and APOE displayed signific

94 ly pathogenic variants in known lipid genes (ABCA1, APOB, APOE, LDLR, LIPA, and PCSK9); however, we w

95 t (Bex or LG100268; 5.75-6 months) increased ABCA1, apoE4 lipoprotein-association/lipidation, and apo

96 These studies show that intestinal MTP and ABCA1 are critical for lipid absorption and are the main

97 elovl and fads2) and cholesterol metabolism (abca1) are regulated by Lxr and Srebp TFs in salmon, ind

98 , we identify the putative lipid transporter Abca1 as a critical mediator of LXR's anti-inflammatory

99 T0901317 (T09) showed reduced expression of ABCA1 as compared with stimulation with T0901317 alone,

100 calnexin was essential for functionality of ABCA1, as knockdown of calnexin blocked the ABCA1 exit f

101 ignificant association at multiple SNPs near ABCA1 at 9q31.1 (rs2487032; P = 1.66 x 10(-8)) and sugge

102 The results show that lack of Abca1 augments dissemination of exogenous amyloid signif

103 f disrupted interaction between calnexin and ABCA1 but increased affinity and enhanced interaction of

104 ty increases Abeta deposition only in APP/E4/Abca1(-/+) but not in APP/E3/Abca1(-/+) mice.

105 Mutations in ABCA1 cause Tangier disease characterized by defective c

106 Furthermore, it binds to ABCA1 and links the ABCA1, CAV1/CAV2 and GAS7 pathway to Mendelian POAG gene

107 und to date associated with IOP and POAG are ABCA1, CAV1/CAV2, GAS7 and TMCO1.

108 hift to larger particles was observed in BHK-ABCA1 cells when the available cell lipid:apoAI ratio wa

109 Higher ABCA1 cg14019050 methylation was correlated with lower A

110 ic oxidation of apolipoprotein A-I and HDL's ABCA1 cholesterol efflux capacity in control subjects an

111 ptor (LDLR) and the ATP-binding cassette A1 (ABCA1) cholesterol transporter.

112 to accept cholesterol from cells expressing ABCA1 compared with HDL from control subjects.

113 Intestinal deletions of Mttp and Abca1 decreased plasma cholesterol concentrations by 45

114 as aggravated in mice with podocyte-specific ABCA1 deficiency and was partially prevented by choleste

115 ABCA1 deficiency did not affect cellular lipids, but Mtt

116 ly reduced triglyceride absorption, although ABCA1 deficiency had no effect.

117 Reportedly, Abca1 deficiency in mice expressing human APP accelerate

118 oid precursor protein (APP) transgenic mice, Abca1 deficiency increased amyloid deposition in the bra

119 We tested the effect of Apoe, Apoa1 or Abca1 deficiency on spreading of exogenous amyloid-beta

120 ecause microparticle release is abolished in ABCA1-deficient cells.

121 erminant of circulating HDL-c, by increasing ABCA1 degradation, with compensatory upregulation of ABC

122 of the ATP-binding cassette transporter A1 (ABCA1)-dependent cholesterol acceptor activity of apoA1

123 s PS flip and promotes cholesterol efflux in ABCA1-dependent and -independent manners.

124 higher cholesterol efflux from cells by both ABCA1-dependent and ABCA1-independent mechanisms.

125 nstream NF-kappaB and MAPK effectors through Abca1-dependent changes in membrane lipid organization t

126 tion is transported in a lipidated state and ABCA1-dependent efflux to individual HDL subfractions ha

127 Our data implicate an NFATc1/ABCA1-dependent mechanism in which local TNF is sufficie

128 o enhance ATP-binding cassette A1-dependent (ABCA1-dependent) reverse cholesterol transport (RCT), li

129 ABCA1 does not simply suppress inflammatory response.

130 Remarkably, ABCA1 downregulation is evident in all prostate cancers

131 man lymphocytes secreted calpains through an ABCA1-driven process.

132 xidized methionine associated inversely with ABCA1 efflux capacity and positively with atheroscleroti

133 eneration of dysfunctional HDL with impaired ABCA1 efflux capacity in humans with atherosclerosis.

134 ABCA1, as knockdown of calnexin blocked the ABCA1 exit from the endoplasmic reticulum, reduced ABCA1

135 Expression of apoM(Q22A) in ABCA1-expressing HEK293 cells resulted in the formation

136 ApoM overexpression in ABCA1-expressing HEK293 cells stimulated larger nascent

137 019050 methylation was correlated with lower ABCA1 expression (r = -0.61, P = 0.009) in the ENCODE co

138 Overexpression of miR-144 reduces ABCA1 expression and attenuates cholesterol efflux to ap

139 -sensing machinery that is known to regulate ABCA1 expression and cholesterol efflux.

140 lates cholesterol metabolism via suppressing ABCA1 expression and modulation of miRNAs may represent

141 EMP release in a NO-dependent regulation of ABCA1 expression and of cytoskeletal reorganization.

142 ABCA1 expression by intimal SMCs was significantly reduc

143 ced atherosclerotic lesions, with no loss in ABCA1 expression by myeloid lineage cells.

144 Downregulation of ABCA1 expression correlated with decreased cholesterol e

145 miR-144 oligonucleotides to mice attenuates ABCA1 expression in the liver, reducing HDL levels.

146 PARP-1 activity augmented LXR ligand-induced ABCA1 expression in the RAW 264.7 macrophage line and pr

147 In vivo, increased monocyte ABCA1 expression in untreated HIV-infected patients and

148 ll clearance process is linked to macrophage ABCA1 expression is not known.

149 Upregulation of ABCA1 expression may therefore be beneficial for the mai

150 Stimulation of ABCA1 expression with liver X receptor agonist or overex

151 d HIV-infected patients and normalization of ABCA1 expression with virological suppression by ART sup

152 ABCA1 expression, which was greater under low SS than un

153 duction, which in conjunction with increased ABCA1 expression, works to promote macrophage cholestero

154 and demonstrate they differentially control Abca1 expression.

155 functions as an LXR corepressor to attenuate Abca1 expression.

156 levated ATP-binding cassette transporter A1 (ABCA1) expression and activity or raised cell density (i

157 erocyte ATP-binding cassette transporter A1 (Abca1) expression and increased LXR protein without chan

158 tion of ATP-binding cassette transporter A1 (ABCA1) expression, which, in turn, contributed to reduce

159 The ATP binding cassette transporter A1 (ABCA1) facilitates cholesterol efflux to lipid-free apol

160 led at the promoter of the lipid transporter Abca1 following downregulation of its expression.

161 P(Sc) accumulation in rafts, displacement of ABCA1 from rafts and the cell surface, and enhanced inte

162 e of (3)H-cholesterol efflux and to increase ABCA1/G1 and LXRalpha expressions in RAW264.7 macrophage

163 e studies show that macrophage deficiency of ABCA1/G1 is proatherogenic likely by promoting plaque in

164 ABCA1/G1-deficient macrophages in lesions showed increas

165 rophage RCT through the PPARalpha- LXRalpha- ABCA1/G1pathway in vitro and in vivo.

166 X6, an intergenic region on chromosome 8q22, ABCA1, GAS7, AFAP1, GMDS, PMM2, and TGFBR3-CDC7) identif

167 LXR response element in the promoter of the ABCA1 gene.

168 ABCA1 has PIP2 floppase activity, which increases cell s

169 Mice lacking beta-cell ABCA1 have increased islet expression of ABCG1, another

170 nsoluble amyloid-beta (Abeta) also show that Abca1 hemizygosity increases Abeta deposition only in AP

171 secretory capacity that was also greater in ABCA1 heterozygous subjects than in control subjects, wi

172 Our results suggest that cancer-specific ABCA1 hypermethylation and loss of protein expression di

173 g cassette transporter subfamily A member 1 (ABCA1) impair cellular cholesterol efflux and are associ

174 We conclude that hepatic ABCA1 improves glucose tolerance by improving beta-cell

175 foam cell population and their expression of ABCA1 in comparison with intimal monocyte-derived macrop

176 inability to release excess cholesterol via ABCA1 in comparison with myeloid lineage cells.

177 To investigate the role of hepatic ABCA1 in glucose tolerance and beta-cell function, we us

178 Increased abundance of ABCA1 in prion disease was confirmed in prion-infected m

179 lity to activate the cholesterol transporter ABCA1 in response to cholesterol loading.

180 indicate that loss-of-function mutations in ABCA1 in young adults may be associated with enhanced be

181 xporter ATP-binding cassette transporter A1 (ABCA1) in comparison with medial arterial SMCs.

182 TP) and ATP-binding cassette transporter A1 (ABCA1) in these pathways.

183 jor cellular cholesterol efflux transporter, ABCA1, in LNCaP prostate cancer cells.

184 fflux from cells by both ABCA1-dependent and ABCA1-independent mechanisms.

185 athways, we generated mice that lack MTP and ABCA1, individually and in combination, in the intestine

186 ransgenic BAI1 overexpression showed greater ABCA1 induction in response to apoptotic cells compared

187 ulfment cell motility 1 (ELMO1) and Rac1, as ABCA1 induction was attenuated in primary macrophages fr

188 d cardiometabolic and stress-response genes (ABCA1, INS-IGF2, LEP, HSD11B2, and NR3C1).

189 Interestingly, gp160 and ABCA1 interacted with calnexin differently; although gp1

190 bind to calnexin did not affect the calnexin-ABCA1 interaction.

191 The membrane transporter ABCA1 is a key player in cholesterol efflux from macroph

192 The beneficial effect of hepatic ABCA1 is decreased under metabolic stress.

193 holesterol to apolipoprotein A-I promoted by ABCA1 is essential for HDL biogenesis.

194 In addition, ABCA1 is highly expressed in the ganglion cell layer of

195 We show that ABCA1 is the major mediator of macrophage cholesterol ef

196 Hepatic ABCA1 is the rate-limiting protein in HDL biogenesis, an

197 ATP binding cassette transporter A1 (ABCA1) is a major determinant of plasma high-density lip

198 expressing the Tangier disease W590S mutant ABCA1 isoform rescued the defect in PS exposure and rest

199 d ABCA1 overexpression in beta-cell-specific ABCA1 knockout islets rescued normal insulin secretion a

200 In Abca1 knockout mice (Abca1(ko)), high density lipoprotei

201 m cleared at a rate twice faster compared to Abca1 knockout mice.

202 formance was undistinguishable from those of Abca1 knockout mice.

203 935S) with an ABCA1 mutation with functional ABCA1 knockout that was associated with severe atheroscl

204 ockout mice would mimic the phenotype of APP/Abca1(ko) mice in regards to amyloid plaques and cogniti

205 er in Apoe/Apoa1 double-knockout then in APP/Abca1(ko) mice.

206 In Abca1 knockout mice (Abca1(ko)), high density lipoproteins and ApoA-I are vir

207 a1 double-knockout mice were compared to APP/Abca1(ko), APP/PS1dE9, and single Apoa1 and Apoe knockou

208 the lowest level of plasma lipoproteins, APP/Abca1(ko), have the lowest level of peripheral amyloid-b

209 lipoproteins compared to APP/PS1dE9 and APP/Abca1(ko).

210 lerance or insulin secretion, and serum from ABCA1(-l/-l) and WT mice fed a high-fat diet did not aff

211 After high-fat feeding, WT and ABCA1(-l/-l) mice showed no difference in glucose tolera

212 tion from beta-cells from wild-type (WT) and ABCA1(-l/-l) mice was similar.

213 se tolerance and beta-cell function, we used ABCA1(-l/-l) mice, which showed impaired glucose toleran

214 -cell ABCA1 were not affected differently by ABCA1(-l/-l) or WT serum.

215 etion was, however, reduced upon addition of ABCA1(-l/-l) serum to the medium compared with WT serum,

216 biogenesis, and mice lacking hepatic ABCA1 (ABCA1(-l/-l)) have very low plasma HDL concentrations.

217 sociations: ZFHX3 (cardioembolic stroke) and ABCA1 (large-vessel stroke).

218 floppase activity (outward translocation) of ABCA1 leads to plasma membrane remodeling that plays a r

219 P2 reporter-binding assays demonstrated that ABCA1 led to PIP2 redistribution from the inner to the o

220 models, where we found decreased ApoA-I and Abca1 levels in hepatic tissues.

221 on by enhancing CD36 expression and reducing ABCA1 localization in the cell surface.

222 ABCA1 may also be important in regulating beta-cell chol

223 Increasing hepatic ABCA1 may represent a novel therapeutic strategy for imp

224 hibitor 3-aminobenzamide enhanced macrophage ABCA1-mediated cholesterol efflux to the lipid-poor apol

225 red fully functional mitochondria to enhance ABCA1-mediated cholesterol efflux.

226 ger receptor-mediated cholesterol uptake and ABCA1-mediated cholesterol efflux.

227 ggests potential mechanisms by which hepatic ABCA1-mediated nascent HDL formation regulates VLDL-trig

228 TP-binding cassette transporter A1-mediated (ABCA1-mediated) cholesterol efflux and reduced cholester

229 ficient mediators of cholesterol efflux, and ABCA1 mediates cholesterol efflux to small dense HDL and

230 y which ATP-binding cassette transporter A1 (ABCA1) mediates cellular binding of apolipoprotein A-I (

231 gradation, with compensatory upregulation of ABCA1 messenger RNA (mRNA).

232 only in APP/E4/Abca1(-/+) but not in APP/E3/Abca1(-/+) mice.

233 eelin or human apoE3 significantly increased ABCA1 mRNA and protein levels, and apoAI-mediated choles

234 pathway that drives a rapid upregulation of ABCA1 mRNA and protein.

235 to miR-144 in the 3' untranslated region of ABCA1 mRNA that are necessary for miR-144-dependent regu

236 HDL-c was lower and expression of ABCA1 mRNA was higher in ART-Naive subjects than in both

237 The Tangier disease W590S ABCA1 mutation has defective PS floppase activity and di

238 We compared the consequences of an ABCA1 mutation that produced an apparent lack of atheros

239 osclerosis (Tangier family 1, N935S) with an ABCA1 mutation with functional ABCA1 knockout that was a

240 inine tests in three subjects homozygous for ABCA1 mutations (age 25 +/- 11 years), eight heterozygou

241 ine subjects with isolated low HDL-C with no ABCA1 mutations (age 26 +/- 6 years) and nine pair-match

242 sought to determine whether loss-of-function ABCA1 mutations affect beta-cell secretory capacity in h

243 Homozygotes for ABCA1 mutations exhibited enhanced oral glucose toleranc

244 etory capacity but in contrast to those with ABCA1 mutations, exhibited impaired insulin sensitivity,

245 ts with large effects (within ANGPTL3, APOB, ABCA1, NR1H3, APOA1, LIPC, CETP, LDLR, and APOC1) and re

246 gulation of ATP-binding cassette transporter ABCA1 occurs in normal human podocytes exposed to the se

247 nd both mouse and human macrophages in which ABCA1 or ABCG1 expression was deleted.

248 man plasma HDL, cell lines stably expressing ABCA1 or ABCG1, and both mouse and human macrophages in

249 Using CHO cell lines stably expressing human ABCA1 or ABCG1, we observed that the abundance of these

250 sion in apolipoprotein E knockout islets and ABCA1 overexpression in beta-cell-specific ABCA1 knockou

251 ABCA1 overexpression or cholesterol depletion was suffic

252 s, including cholesterol homeostasis, ApoA-I/ABCA1 pathway, and fatty acid biosynthesis/triglyceride

253 a implied that HLP up-regulated the LXRalpha/ABCA1 pathway, which in turn led to stimulation of chole

254 Ralpha)/ATP-binding cassette transporter A1 (ABCA1) pathway, as demonstrated by the transfection of L

255 by the ATP-binding cassette transporter A1 (ABCA1) pathway.

256 afts by statins MCD, and filipin recuperates ABCA1 phenotype and likely functions downstream of ABCA1

257 erol flux, as the cholesterol efflux channel ABCA1 potentiated metastatic behaviors in vitro and in v

258 - and binding-dependent association with the Abca1 promoter and demonstrate they differentially contr

259 wledge of regulatory inputs impinging on the Abca1 promoter and indicate a central role for NCOA5 in

260 wering Drugs and Diet Network) study, higher ABCA1 promoter cg14019050 methylation was associated wit

261 ABCA1 promoter hypermethylation is enriched in intermedi

262 ABCA1 promoter hypermethylation renders the promoter unr

263 In vitro, RAGE ligands suppressed ABCG1 and ABCA1 promoter luciferase activity and transcription of

264 osstalk promotes recruitment of NCOA5 to the Abca1 promoter together with loss of RNA polymerase II a

265 d the inhibitory actions of IFN-gamma on the Abca1 promoter, suggesting that competition for CREB-bin

266 of miR-144 in vitro decreased both cellular ABCA1 protein and cholesterol efflux to lipid-poor apoli

267 silencing miR-144 in mice increased hepatic ABCA1 protein and HDL-cholesterol.

268 ereas overexpression in vivo reduced hepatic ABCA1 protein and plasma HDL-cholesterol.

269 monomeric and dimeric protein forms, however ABCA1 protein expression was unaffected.

270 heterogeneity of nascent HDL produced by BHK-ABCA1, RAW 264.7, J774, and HepG2 cells under different

271 or agonist or overexpression of heterologous ABCA1 reduced the conversion of prion protein into the p

272 binding cassette transporter A1 (encoded by ABCA1) regulates cholesterol efflux from cells to apolip

273 k factor for late-onset Alzheimer's disease, ABCA1 role as a modifier of APOE lipidation is of signif

274 t ATP-binding cassette subfamily A member 1 (ABCA1) rs2246293 (beta = -0.6 mg/dL, P = 0.015) and high

275 These loci are located upstream of ABCA1 (rs2472493[G], odds ratio (OR) = 1.31, P = 2.1 x 1

276 ing site-directed mutagenesis, we found that ABCA1's PIP2 and phosphatidylserine translocase activiti

277 ms by which potent CETP inhibition increases ABCA1-specific CEC and pre-beta-1 HDL require further st

278 only increased total CEC, but also increased ABCA1-specific CEC and pre-beta-1 HDL.

279 tatins also increased total, non-ABCA1-, and ABCA1-specific CEC by 21%, 27%, and 15%, respectively.

280 Evacetrapib monotherapy also increased ABCA1-specific CEC up to 26%.

281 erapy increased dose-dependent total and non-ABCA1-specific CEC up to 34% and 47%, respectively.

282 Consistent with ABCA1-specific CEC, evacetrapib monotherapy and evacetra

283 simvastatin significantly reduced total and ABCA1-specific CEC, whereas atorvastatin had no signific

284 from baseline in CEC (total, non-ABCA1-, and ABCA1-specific) and HDL subpopulations were evaluated af

285 Nine ABCA1 Tangier mutants and the corresponding ABCA4 Starga

286 a novel pathway involving FXR, miR-144, and ABCA1 that together regulate plasma HDL-cholesterol.

287 and protein expression of Mertk, Tyro3, and Abca1, three proteins that promote macrophage efferocyto

288 rase activity and transcription of ABCG1 and ABCA1 through peroxisome proliferator-activated receptor

289 ATP-binding cassette transporter A1 (ABCA1) transporter regulates cholesterol efflux and is a

290 n would not result in an increased RCT rate, ABCA1 up-regulation should increase both HDL-C and RCT r

291 d ATP-binding cassette transporter member 1 (ABCA1) up-regulation.

292 Glomerular downregulation of ABCA1 was confirmed in biopsies from patients with early

293 y the finding in breast cancer patients that ABCA1 was overexpressed in 41% of metastatic tumors, red

294 In addition, ZFHX3 and ABCA1 were discovered to have protein-coding variants as

295 h WT serum, whereas islets lacking beta-cell ABCA1 were not affected differently by ABCA1(-l/-l) or W

296 Cholesterol efflux genes (APOE and ABCA1) were identified as risk factors for AMD, although

297 lux pump ATP-binding cassette transporter 1 (ABCA1), which is regulated by activation of the liver X

298 tors, by strongly inducing the expression of ABCA1, while poorly or not activating the lipogenic gene

299 t is triggered by apoptotic cells to enhance ABCA1 within engulfing phagocytes and with functional co

300 K6 and NCAN/MAU2 for total cholesterol, LPL, ABCA1, ZNF259/APOA5, LIPC and CETP for HDL cholesterol,