ライフサイエンスコーパス: ABCA1

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

2 the activity of the ATP binding cassette A1 (ABCA1).

3 protein ATP-binding cassette transporter A1 (ABCA1).

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

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

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

7 ell surface, and enhanced internalization of ABCA1.

8 rs associated with the upregulation of their Abca1.

9 its interaction with gp160 at the expense of ABCA1.

10 DL production and interaction with beta-cell ABCA1.

11 erols, which activated LXRbeta to upregulate ABCA1.

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

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

14 mutations in the miR-33 binding sites of the Abca1 3'untranslated region, which prevents targeting by

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

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

19 In the latter, the LXR-transactivated genes (Abca1, Abcg1, Apod, Apoe, Mylip, and Arg2) were up-regul

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

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

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

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

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

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

26 Thus, impaired ABCA1 activity of small HDL particles deficient in SERPI

27 Enhancing ABCA1 activity rescued impaired Abeta degradation in Apo

28 Importantly, enhancing ABCA1 activity to lipidate ApoE reduced ApoE and ABCA1 a

29 , and underscores the promise of stabilizing ABCA1 activity to prevent ApoE-driven aggregation pathol

30 Enhancing ABCA1 activity to reduce ApoE and ABCA1 aggregation is a

31 ipoproteins to bind phospholipid and promote ABCA1 activity.

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

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

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

35 at aggregated and lipid-poor ApoE4 increases ABCA1 aggregation and decreases ABCA1 cell membrane recy

36 poE4-treated cells and reduced both ApoE and ABCA1 aggregation in the hippocampus of male ApoE4-targe

37 Enhancing ABCA1 activity to reduce ApoE and ABCA1 aggregation is a potential therapeutic strategy fo

38 1 activity to lipidate ApoE reduced ApoE and ABCA1 aggregation.

39 Data from human cell lines indicate that the ABCA1 AMD risk-conferring allele decreases ABCA1 express

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

41 nce that, along with other ABC transporters (ABCA1 and ABCA7), they might be cornerstones to tackle n

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

43 ABCA1 and ABCG1 control the proliferation of hematopoiet

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

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

46 ABCA1 and ABCG1 facilitate the efflux of cholesterol fro

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

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

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

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

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

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

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

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

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

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

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

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

59 olesterol loading inhibits ubiquitination of ABCA1 and ABCG1.

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

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

62 ning to emerge, with published structures of ABCA1 and ABCG5/G8; these two proteins function in the r

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

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

65 Despite the upregulation of ABCA1 and apoE, the absence of PMP22 resulted in reduced

66 ittle importance for the interaction between ABCA1 and calnexin.

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

68 f similarly resulted in reduced abundance of ABCA1 and elevated abundance of APP in brain tissue.

69 the RPE by generating a mouse model lacking ABCA1 and its partner ABCG1 specifically in this layer.

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

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

72 = 2.79 x 10(-19) for rs2487032 representing ABCA1 and P = 5.77 x 10(-10) for rs3785176 representing

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

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

75 bind to the 3' untranslated region (UTR) of ABCA1 and repress its posttranscriptional gene expressio

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

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

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

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

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

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

82 educing the abundance of ABC transporter A1 (ABCA1) and thus cholesterol efflux and increasing the ab

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

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

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

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

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

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

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

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

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

92 10(-4) to 4.62x10(-18)), whereas LPL, TRIB1, ABCA1, APOA1-C3-A4-A5, CETP, and APOE displayed signific

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

94 ritical insights into the interactions among ABCA1, ApoE lipidation and aggregation, and underscores

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

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

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

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

101 tified overlapping distribution of PMP22 and ABCA1 at the Schwann cell plasma membrane and the two pr

102 6), including locus-specific associations at ABCA1 (ATP Binding Cassette Subfamily A Member 1), APOE-

103 age cholesterol efflux, through targeting of Abca1 (ATP-binding cassette subfamily A member 1).

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

105 oE) and ATP-binding cassette transporter A1 (ABCA1) being highly upregulated.

106 Abca1 binding site mutant ( Abca1(BSM)) mice had increas

107 Macrophages from Abca1(BSM) mice also had increased ABCA1 expression, as

108 t animals transplanted with bone marrow from Abca1(BSM) mice had reduced atherosclerotic plaque forma

109 Abca1 binding site mutant ( Abca1(BSM)) mice had increased hepatic ABCA1 expression

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

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

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

113 Small HDL accounted for almost all of ABCA1 CEC activity of HDL.

114 Then we assessed the ABCA1 CEC of equimolar concentrations of particles.

115 The ABCA1 CEC of small HDL is selectively impaired in type 2

116 ecific cellular cholesterol efflux capacity (ABCA1 CEC) of HDL strongly and negatively associates wit

117 ABCA1 CEC-but not ABCG1 CEC-of small HDL was lower in th

118 Enriching small HDL with SERPINA1 enhanced ABCA1 CEC.

119 E4 increases ABCA1 aggregation and decreases ABCA1 cell membrane recycling.

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

121 or near genes involved in lipid metabolism (ABCA1, CETP, APOE, and LIPC) with metabolites belonging

122 Higher ABCA1 cg14019050 methylation was correlated with lower A

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

124 s pathway, by transcriptionally inducing the ABCA1 cholesterol transporter gene.

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

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

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

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

129 Reportedly, Abca1 deficiency in mice expressing human APP accelerate

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

131 exhibited reduced ABC subfamily A member 1 (ABCA1)-dependent cholesterol acceptor activity in vitro

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

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

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

135 he deficiency in PM cholesterol also reduced ABCA1-dependent cholesterol efflux and LDL receptor acti

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

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

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

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

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

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

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

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

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

145 019050 methylation was correlated with lower ABCA1 expression (r = -0.61, P = 0.009) in the ENCODE co

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

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

148 ant ( Abca1(BSM)) mice had increased hepatic ABCA1 expression but did not show any differences in bod

149 ABCA1 expression by intimal SMCs was significantly reduc

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

151 port, we show that high cell density induces ABCA1 expression in glioblastoma cells, enabling them to

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

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

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

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

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

157 lipid homeostasis through its modulation of ABCA1 expression, as its overexpression or loss leads to

158 ages from Abca1(BSM) mice also had increased ABCA1 expression, as well as enhanced cholesterol efflux

159 e ABCA1 AMD risk-conferring allele decreases ABCA1 expression, identifying the potential molecular ca

160 overexpressing human IGF2BP2 have decreased ABCA1 expression, increased low-density lipoprotein-chol

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

162 and demonstrate they differentially control Abca1 expression.

163 functions as an LXR corepressor to attenuate Abca1 expression.

164 cued PPARgamma binding and rosi induction of ABCA1 expression.

165 works together with miR-33a/b in repressing ABCA1 expression.

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

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

168 binds to miR-33a/b, AGO2, and the 3' UTR of ABCA1 Finally, we show that mice overexpressing human IG

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

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

171 suggest a pathogenic contribution of reduced ABCA1 function to AMD.

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

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

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

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

176 RISPR-mediated knockdown of LXRbeta, but not ABCA1, had decreased cell cycle progression and cell sur

177 ABCA1 has PIP2 floppase activity, which increases cell s

178 Individuals with mutational ablation of ABCA1 have Tangier disease, which is characterized by a

179 ing the ATP-binding cassette transporter A1 (ABCA1), have been associated with AMD risk.

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

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

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

183 The abundance of ABCA1 in brain tissue of HIV-infected human subjects dia

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

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

186 Rbeta gene expression poorly correlates with ABCA1 in glioblastoma patients, and expression of each g

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

188 ession of ARF6 compared with ApoE3, trapping ABCA1 in late-endosomes and impairing its recycling to t

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

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

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

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

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

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

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

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

197 ease in cancer cell membrane polarity due to ABCA1 inhibition and subsequent dysregulation of cholest

198 The ATPase binding cassette protein ABCA1 initiates nascent high-density apolipoprotein (HDL

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

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

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

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

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

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

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

206 data clearly demonstrate that repression of ABCA1 is primarily responsible for the proatherogenic ef

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

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

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

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

211 formance was undistinguishable from those of Abca1 knockout mice.

212 In nerves from ABCA1 KO mice, the expression of PMP22 was significantly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 abolism proteins, including Scp2/x, Abcg5/8, Abca1, Ldlr, Srebf1, and Scd-1 Untargeted lipidomic prof

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

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

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

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

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

233 ely, our data shows that Miltefosine induced ABCA1 mediated cholesterol release, induced AMPK phospho

234 n4 carriers showed a lower ability to induce ABCA1-mediated cholesterol efflux activity and greater p

235 This was associated with lower ABCA1-mediated cholesterol efflux activity, a greater pe

236 The absence of PMP22 also impaired ABCA1-mediated cholesterol efflux capacity.

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

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

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

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

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

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

243 y of lipid-poor ApoE4 to aggregate decreased ABCA1 membrane recycling and its ability to lipidate Apo

244 ophils from septic patients showed increased ABCA1 messenger ribonucleic acid levels (a marker of LXR

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

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

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

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

249 Homozygotes for ABCA1 mutations exhibited enhanced oral glucose toleranc

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

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

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

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

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

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

256 ABCA1 overexpression or cholesterol depletion was suffic

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

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

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

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

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

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

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 Like p53 loss, ablation of ABCA1 promotes murine liver tumorigenesis and is associa

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

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

268 ABCA1 recycling and degradation is regulated by ADP-ribo

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

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

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

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

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

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

275 th the cholesterol efflux regulatory protein ABCA1.SIGNIFICANCE STATEMENT Understanding the subcellul

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

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

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

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

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

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

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

283 The ABCA1-specific cellular cholesterol efflux capacity (ABC

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

285 ught to determine how specific disruption of Abca1 targeting by miR-33 impacts macrophage cholesterol

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

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

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

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

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

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

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

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

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

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

296 ndance of the cholesterol efflux transporter ABCA1, which in turn promoted lipid accumulation and ind

297 Rosi induction of ABCA1, which regulates cholesterol metabolism, was depen

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,