ライフサイエンスコーパス: LXR

1 LXR activation in BPDCN cells was shown to interfere wit

2 LXR activation promoted the direct binding of LXRbeta to

3 LXR activation resulted in reduced STAT1 recruitment to

4 LXR agonist TO901317 potentiates LPS-induced C3 gene exp

5 LXR agonist TO901317 stimulates C3 gene expression in hu

6 LXR agonist treatment of primary BPDCN cells and BPDCN c

7 LXR agonist treatment was responsible for limiting BPDCN

8 LXR agonists also reduced intracellular trafficking of t

9 LXR agonists therefore might be developed as therapeutic

10 LXR reduced levels of SR-B1 in Caco-2/TC7 cells via a po

11 LXR stimulation by GW3965 up-regulated genes involved in

12 LXR-cofactor complexes activate the gene expression prog

13 LXRs also mediated inhibitory effects on selected IFN-ga

14 LXRs and their ligands are present in oligodendrocytes.

15 LXRs have been extensively studied in both human and rod

16 LXRs have been of interest as targets for the treatment

17 LXRs interact/cooperate with RXRs and result in the acti

18 Manipulation of the miR-155/LXR pathway may have therapeutic potential for IPF.

19 with T0901317 alone, indicating that Seco A-LXR protein adduct formation inhibits LXR activation by

20 ere MafB mediates the oxidized LDL-activated LXR/RXR-induced expression of apoptosis inhibitor of mac

21 In the absence of MafB, activated LXR/RXR fails to induce the expression of AIM, a protein

22 investigated whether expression of activated LXR protects against intestinal tumorigenesis in mice.

23 arrow-derived macrophages but did not affect LXR-dependent expression of other target genes, ABCG1 an

24 owever, the coregulatory factors that affect LXR-dependent gene activation in macrophages remain to b

25 nia associated with increased survival after LXR agonist treatment.

26 ing and establish that NCOA5 functions as an LXR corepressor to attenuate Abca1 expression.

27 poly(ADP-ribose) polymerase-1 (PARP-1) as an LXR-associated factor.

28 hallenges that need to be overcome before an LXR modulator can reach clinical use.

29 Consistent with this being an LXR-mediated process, inhibition is abolished in the pre

30 oted GSL expression, which was blocked by an LXR antagonist.

31 ncogenic metabolism pathways, we designed an LXR inverse agonist SR9243 that induces LXR-corepressor

32 ation by both microglia and astrocytes in an LXR and apoE-dependent manner.

33 -diHCA) promoted motor neuron survival in an LXR-dependent manner, 3beta-hydroxy-7-oxocholest-5-en-26

34 Conversely, in cultured RGC an LXR agonist led to increased differentiation into OPCs.

35 Treatment of cells with an LXR agonist prevented the cAMP-dependent decrease in GLU

36 gene as a novel LXR-regulated gene, with an LXR response element within its promoter.

37 derstanding the interplay between PARP-1 and LXR may provide insights into developing novel therapeut

38 ppressed by knockdown of ATF-1, and HO-1 and LXR-beta were induced by ATF-1 transfection.

39 Heme-induced HO-1 and LXR-beta were suppressed by knockdown of ATF-1, and HO-1

40 to the reciprocal actions of the SREBP-2 and LXR pathways.

41 R) ligand, increases ER-dependent growth and LXR-dependent metastasis in mouse models of breast cance

42 cholesterol accumulation to inflammation and LXR-dependent response pathways are poorly understood.

43 over the last decade indicates that PPAR and LXR signaling also influence multiple facets of inflamma

44 ries highlighting the importance of PPAR and LXR signaling in the modulation of normal and pathologic

45 targeting the interaction between TRAP80 and LXR should facilitate the development of potential LXR a

46 vel, is important in lung tumorigenesis, and LXR activation might partly contribute to the inhibitory

47 ileum into the proximal jejunum, on FXR and LXRs in rats.

48 d through concerted action of the SREBPs and LXRs.

49 ative cross-talk between IFN-gamma/STAT1 and LXRs with implications both in the control of IFN-gamma-

50 nd the development of autoantibodies in ApoE/LXR-beta-deficient mice was reversed by ApoA-I expressio

51 Fourth, potentially atheroprotective LXR-dependent SREBP1c signaling was normal in TT1, but w

52 and inhibition of PARP-1 activity augmented LXR ligand-induced ABCA1 expression in the RAW 264.7 mac

53 evidence for the development of sterol-based LXR agonists as novel therapeutics for chronic inflammat

54 e show that oral treatment with sterol-based LXR agonists in mice significantly reduces dextran sulfa

55 lore the ability of a series of sterol-based LXR agonists to alleviate inflammatory conditions in mic

56 terestingly, 13, 19, 20, and 25 showed to be LXR target gene-selective modulators, by strongly induci

57 xygenase-1 (HO-1) and Liver X receptor beta (LXR-beta).

58 gate whether a combination therapy with both LXR and PPARgamma agonists results in increased benefits

59 This novel regulation of IL-18 by LXR could be applied to modulate the severity of IL-18 d

60 r activity were enhanced (up to 2.5-fold) by LXR activation using 24(S)-hydroxycholesterol (a cerebra

61 teatosis and hypertriglyceridemia induced by LXR activation and maintained RCT stimulation by the LXR

62 ts the enhanced phagocytic uptake induced by LXR ligation.

63 form to its bioactive state is inhibited by LXR through negative regulation of both pro-caspase 1 ex

64 ly regulates de novo lipogenesis mediated by LXR and SREBP1c in a cell-autonomous manner.

65 ges in iron handling, a process regulated by LXR activation.

66 ced transcriptional response is repressed by LXR activation in macrophages.

67 is of cerebrospinal fluid may be targeted by LXR agonists to facilitate CSF production, turnover and

68 the regulation of SMPDL3A gene expression by LXRs across several human and mouse cell types.

69 In Caco-2/TC7 cells, LXR agonists reduced SR-B1-dependent lipidic-micelle-ind

70 Under conditions of excess cholesterol, LXR activation induces the expression of several genes i

71 These results suggest that combined LXR/PPARgamma agonist treatment merits further investiga

72 In conclusion, LXR activation inhibits IL-18 production through regulat

73 r, the adverse effects of these conventional LXR agonists in elevating liver lipids have impeded expl

74 Agonist-dependent LXR activity or LXR overexpression in the absence of lig

75 used a whole-genome screen to detect direct LXR target genes in THP-1 cells treated with two widely

76 healthy donors with synthetic and endogenous LXR agonists promoted GSL expression, which was blocked

77 The preservation of endogenous LXR protein activates a beneficial profile of gene expre

78 A), in combination with bexarotene, enhances LXR:RXR target gene expression of Abca1 and ApoE, reduce

79 d blunted the lipogenic response to feeding, LXR agonist treatment, or obesity-linked insulin resista

80 Finally, LXR ligands further modulate IL-18 levels by inducing th

81 of an endogenous sterol ligand required for LXR activity and SREBP-1c expression.

82 r of hepatic lipogenesis and is required for LXR-dependent SREBP-1c activation.

83 These studies support a key role for LXR in retinal and bone marrow progenitor dysfunction as

84 We found that mice invalidated for LXRs exhibit altered motor coordination and spatial lear

85 uncovering an important function for hepatic LXR activity in limiting cardiovascular disease.

86 ecific T39 deficiency show increased hepatic LXR protein and target gene expression, and unexpectedly

87 Upregulation of hepatic LXR and Cyp7a1 led to higher bile acid synthesis, which

88 lipogenesis has led to the idea that hepatic LXR activity is undesirable from a therapeutic perspecti

89 However, LXR also upregulates the expression of sterol regulatory

90 presence of a specific LXR antagonist and in LXR-deficient macrophages.

91 and increased LXR protein without change in LXR messenger RNA.

92 orylated LXRalpha S198, and this was lost in LXR-deficient BMDMs.

93 Conversely, cells deficient in LXRs exhibited decreased HSL responsiveness.

94 R correlated with the capacity to inactivate LXR-mediated transcription and to modulate lipid metabol

95 elopment." The top enriched pathways include LXR/RXR Activation and Atherosclerosis Signaling, etc.

96 nsporter A1 (Abca1) expression and increased LXR protein without change in LXR messenger RNA.

97 interacts with LXR and represses T7-induced LXR transcriptional activity by competing with coactivat

98 d an LXR inverse agonist SR9243 that induces LXR-corepressor interaction.

99 tential mechanism by which PARP-1 influences LXR function.

100 us-mediated expression of shTRAP80 inhibited LXR-dependent SREBP-1c expression and RNA polymerase II

101 Seco A-LXR protein adduct formation inhibits LXR activation by traditional agonists.

102 ays revealed that NeoB specifically inhibits LXR-mediated transcription.

103 y which ursodeoxycholic acid (UDCA) inhibits LXR-induced lipogenic gene expression.

104 ver, the molecular mechanisms that integrate LXRs with other lipid metabolic pathways are incompletel

105 We aimed to determine whether intestinal LXRs regulate triglyceride absorption.

106 on of steroidogenesis predominantly involves LXR signaling.

107 tors, induction of IDOL by DUB inhibition is LXR-independent and occurs in Lxralphabeta(-/-) MEFs.

108 es indicate that the induction of SMPDL3A is LXR-dependent and is restricted to human blood cells wit

109 In mice and in the Caco-2/TC7 cell line, LXR agonists caused localization of intestinal SR-B1 fro

110 lowed by O3 exposure causes observable lipid-LXR adduct formation.

111 Moreover, in iron-loaded M2 macrophages, LXR activation induces nuclear factor erythroid 2-like 2

112 asis of increased energy expenditure in male LXR knockout mice and provided support for targeting LXR

113 ion of NOS caused relaxation, while in mice, LXR activation stimulated carotid artery reendothelializ

114 Oral administration of multiple LXR agonists suppressed melanoma invasion, angiogenesis,

115 To date, no LXR modulator has successfully progressed beyond phase I

116 or IRF8, thus identifying IL-18BP as a novel LXR and IRF8 target gene.

117 data strongly suggested that NeoB is a novel LXR antagonist.

118 erase acid-like 3A (SMPDL3A) gene as a novel LXR-regulated gene, with an LXR response element within

119 Furthermore, activation of LXR by engulfed neutrophils directly repressed the IL-23

120 Activation of LXR inhibits signaling from TLRs 2, 4 and 9 to their dow

121 l cancer cells, ligand-induced activation of LXR or transfection with Ad VP16hLXRalpha blocked the G1

122 TC7 cells and mice, intestinal activation of LXR reduces the production of chylomicrons by a mechanis

123 This suggests that activation of LXR signaling can prevent loss of GLUT4 expression in di

124 meostatic responses, including activation of LXR target genes, inhibition of SREBP target genes, sele

125 Activation of LXR-mediated transcription by synthetic agonists, such a

126 317 (T7)-induced transcriptional activity of LXR, which functions as a major regulator of lipid metab

127 xysterols, our data demonstrate adduction of LXR with Seco A.

128 Small molecule agonists of LXR activity are therefore of great therapeutic interest

129 signaling did not involve reduced binding of LXR/retinoid X receptor heterodimers to target gene prom

130 omotes the ubiquitination and degradation of LXR.

131 tribute to STAT1-dependent downregulation of LXR targets.

132 lasma triglycerides that is a side effect of LXR agonist treatment.

133 The protective effect of LXR agonists against TGF-beta-induced pro-fibrotic activ

134 ate the favorable and unfavorable effects of LXR by exploiting the specificity of the coactivator thy

135 y could dissociate the beneficial effects of LXR on cholesterol efflux, inflammation, and ER stress f

136 ells exposed to O3 Additionally, exposure of LXR knock-out mice to O3 enhanced pro-inflammatory cytok

137 lesser extent, and induces the expression of LXR target genes in vitro and in vivo.

138 In this study we have explored the impact of LXR activation on the macrophage response to the endogen

139 Inactivation of LXR alpha and beta in mice leads to autoimmunity; howeve

140 NeoB inhibited the induction of LXR-regulated genes and altered lipid metabolism.

141 transporter Abca1 as a critical mediator of LXR's anti-inflammatory effects.

142 To identify novel regulators of LXR that modulate its activity, we used affinity purific

143 hosphorylation, which leads to repression of LXR-mediated hepatic lipogenic enzyme gene expression.

144 Our data indicate that stimulation of LXR enhances the engulfment of apoptotic cells via regul

145 Here we demonstrate that the ability of LXRs to repress inflammatory gene expression in cells an

146 Interestingly, activation of LXRs also promotes oligodendroglial cell maturation and

147 Conversely, activation of LXRs by either 25-hydroxycholesterol or synthetic TO9013

148 Here we show that ligand activation of LXRs in mouse liver not only promotes cholesterol efflux

149 Agonists of LXRs have been demonstrated previously to reduce Abeta l

150 Depletion of LXRs activated thyroid-stimulating hormone (TSH)-releasi

151 We present evidence that derepression of LXRs contributes to this paradoxical anti-inflammatory p

152 n-underlies the dual biological functions of LXRs in metabolism and inflammation.

153 Significantly, inhibition of LXRs by NeoB enhanced the activity of all known classes

154 xpression and strongly support a new role of LXRs as positive modulators in central (re)myelination p

155 However, the role of LXRs in myelin generation and maintenance is poorly unde

156 s and indicate the potent regulatory role of LXRs in preventing renal damage in diabetes.

157 e present study, we investigated the role of LXRs in vascular endothelial cells (ECs) and discovered

158 o the mechanism revealed that SUMOylation of LXRs, but not the presence of nuclear receptor corepress

159 roposed to involve the indirect tethering of LXRs to inflammatory gene promoters.

160 homeostasis and advance our understanding of LXRs as integrators of phagocyte function, lipid metabol

161 hed light on the important role of PARP-1 on LXR-regulated lipid homeostasis.

162 clear increase in sEng that was dependent on LXR.

163 gamma signaling exerts reciprocal effects on LXR targets.

164 The inhibitory effects of IFN-gamma on LXR signaling did not involve reduced binding of LXR/ret

165 ies was to dissect the effects of insulin on LXR action.

166 Agonist-dependent LXR activity or LXR overexpression in the absence of ligand counteracted

167 Liver X receptors or LXRs are key modulators of macrophage cholesterol homeos

168 n fat and cholesterol) or to pharmacological LXR activation.

169 ould facilitate the development of potential LXR agonists that effectively prevent atherosclerosis.

170 receptors (PPARalpha, PPARgamma, PPARdelta, LXR, and FXR).

171 the nuclear receptors PPARgamma, PPARdelta, LXR, and RXR stimulated microglial phagocytosis in vitro

172 hibited low levels of the survival-promoting LXR ligand 3beta,7alpha-diHCA.

173 The nuclear receptor LXR is necessary for Srebf-1c transcription.

174 ar cholesterol homeostasis, nuclear receptor LXR-alpha was up-regulated significantly in the urethane

175 ishing the liver-X nuclear hormone receptor (LXR) as a therapeutic target in melanoma.

176 zyme LPCAT3 in response to liver X receptor (LXR) activation promoted SREBP-1c processing by driving

177 We reported earlier that liver X receptor (LXR) activation promotes cellular cholesterol efflux and

178 holesterol, treated with a liver X receptor (LXR) agonist, or injected intravenously with [(3) H]sito

179 these tumors sensitive to Liver X receptor (LXR) agonist-dependent cell death.

180 were designed as potential liver X receptor (LXR) agonists.

181 ding protein (CEBP) alpha, liver X receptor (LXR) and H3K4me3 and microRNA target identification for

182 pression mainly depends on liver X receptor (LXR) and partly on Toll-like receptor 4 (TLR4), whereas

183 pha, beta/delta, gamma and liver X receptor (LXR) are members of the nuclear receptor superfamily tha

184 c subset of NRs, including liver X receptor (LXR) beta and peroxisome proliferator-activated receptor

185 ue to the formation of RXR/liver X receptor (LXR) heterodimers, which induced expression of sterol re

186 and its upstream regulator Liver X receptor (LXR) in the macrophages exposed to oxLDL.

187 olesterol transport (RCT), liver X receptor (LXR) is an attractive target for the treatment of athero

188 e nuclear hormone receptor liver X receptor (LXR) is induced by insulin and is a key regulator of lip

189 cholesterol and an ER and liver X receptor (LXR) ligand, increases ER-dependent growth and LXR-depen

190 increased the efficacy of liver X receptor (LXR) ligands on StAR expression and steroid synthesis, s

191 ioned independently of the liver X receptor (LXR) sterol-sensing machinery that is known to regulate

192 retinoid X receptor (RXR)-liver X receptor (LXR) system.

193 stasis, some of them being liver X receptor (LXR) target genes.

194 ts induce fatty liver, the liver X receptor (LXR) transcription factor remains a target of interest b

195 L by the sterol-responsive liver X receptor (LXR) transcription factors, induction of IDOL by DUB inh

196 Liver X receptor (LXR), a nuclear hormone receptor, is an essential regula

197 hormone receptor (TR) and liver X receptor (LXR), both of which control hepatic cholesterol metaboli

198 pression is induced by the liver X receptor (LXR), but CA-FoxO1 did not block the activation of SREBP

199 Of the two isoforms of Liver X receptor (LXR), LXRbeta has been shown to have major effects in th

200 lated by activation of the liver X receptor (LXR), was suppressed in epithelial cells exposed to O3 A

201 the lipid-sensing receptor liver X receptor (LXR), which in response upregulates the expression of th

202 eneficial effects, in both liver x receptor (LXR)-dependent and independent manners.

203 protumor neutrophils in a liver X receptor (LXR)-independent, CXCR2-dependent manner, thus favoring

204 lerotic plaques in part by liver X receptor (LXR)-mediated induction of the chemokine receptor CCR7.

205 lation of nuclear receptor liver X receptor (LXR)-mediated sterol regulatory element binding protein-

206 s a novel inhibitor of the liver X receptor (LXR).

207 nd, as an inhibitor of the liver X receptor (LXR).

208 We observed enrichment for liver X receptor (LXR)/retinoid X receptor (RXR) and farnesoid X receptor/

209 tors (NRs), especially the liver X receptor (LXR)/retinoid X receptor heterodimer, as an important ev

210 he miR-155 target gene the liver X receptor (LXR)alpha in lung fibroblasts and macrophages.

211 The nuclear receptor liver-X-receptor (LXR) directly regulates expression of key glycolytic and

212 Agonists of nuclear receptors LXR:RXR and PPAR:RXR act to ameliorate AD-related cognit

213 olog of mammalian sterol-regulated receptors LXR and FXR.

214 Liver X receptors (LXR) are oxysterol-activated nuclear receptors that play

215 Liver X receptors (LXR) are stimulated by cholesterol-derived oxysterols an

216 Liver X nuclear receptors (LXRs) regulate the expression of the adenosine triphosph

217 Liver X receptors (LXRs) alpha and beta are nuclear receptors activated by

218 receptors, including the liver X receptors (LXRs) and peroxisome-proliferator receptor gamma (PPARga

219 X receptor (FXR) and the liver x receptors (LXRs) are bile acid-activated receptors that are highly

220 Liver X receptors (LXRs) are determinants of hepatic stellate cell (HSC) ac

221 Liver X receptors (LXRs) are involved in maintaining normal myelin in the c

222 Liver X receptors (LXRs) are one class of nuclear receptors, which play a v

223 Liver X receptors (LXRs) are regulators of cholesterol metabolism that also

224 Liver X receptors (LXRs) are transcriptional regulators of cellular and sys

225 Liver X receptors (LXRs) are transcriptional regulators of cholesterol meta

226 The liver X receptors (LXRs) are transcriptional regulators of lipid homeostasi

227 Liver X receptors (LXRs) exert key functions in lipid homeostasis and in co

228 pled metabolic cycle with Liver X Receptors (LXRs) to increase brain apolipoprotein E (apoE) levels.

229 d receptor (PPAR) family, liver X receptors (LXRs), and farnesoid X receptor (FXR).

230 tenoic acids activate the liver X receptors (LXRs), enhance islet-1 expression in zebrafish, and incr

231 roxysterol agonist of the liver X receptors (LXRs), members of the nuclear receptor transcription fac

232 ption factors such as the liver X receptors (LXRs), sterol regulatory element-binding proteins (SREBP

233 ar receptors, such as the liver X receptors (LXRs).

234 rs 2 and 3 (also known as liver X receptors [LXRs]) regulate genes involved in cholesterol and fatty

235 critical to the process of HCV replication: LXR inactivation by NeoB disrupted double-membrane vesic

236 revealed that LXRs support HCV replication: LXR inactivation resulted in dispersion of double-membra

237 ry BPDCN cells and BPDCN cell lines restored LXR target gene expression and increased cholesterol eff

238 In isolated aortic rings, LXR activation of NOS caused relaxation, while in mice,

239 We identify a subset of proteins that show LXR ligand- and binding-dependent association with the A

240 n is abolished in the presence of a specific LXR antagonist and in LXR-deficient macrophages.

241 effects of systemic and macrophage-specific LXR activation were analyzed on renal damage in hyperlip

242 cytokine production in the lung, suggesting LXR inhibits O3-induced inflammation.

243 esterol metabolite) or TO901317 (a synthetic LXR agonist).

244 Endogenous and synthetic LXR agonists tested in diverse cell models blocked alpha

245 cholesterol-enriched diet or given synthetic LXR agonists (GW3965 or T0901317).

246 kout mice and provided support for targeting LXRs in treatment of obesity.

247 We conclude that LXR agonists may have beneficial effects in treatment of

248 Further, we demonstrated that LXR is poly(ADP-ribosyl)ated by PARP-1, a potential mech

249 - and loss-of-function models, we found that LXR signaling regulated the efficient clearance of senes

250 We hypothesized that LXR activation with a synthetic ligand would correct dia

251 We report that LXR ligands increase miR-144 expression in macrophages a

252 The data show that LXR is a regulator of cerebrospinal fluid (CSF) both at

253 Here we show that LXR ligands negatively regulate LPS-induced mRNA and pro

254 We show that LXR-623, a clinically viable, highly brain-penetrant LXR

255 Our results suggest that LXR inverse agonists may be an effective cancer treatmen

256 Together, our data suggest that LXR-mediated transcription regulates the formation of vi

257 Here, we demonstrate that LXRs contribute to the control of neutrophil homeostasis

258 Following our previous finding that LXRs serve as repressors of uncoupling protein-1 (UCP1)

259 adipose tissue in female mice, we found that LXRs, especially LXRbeta, also repress the browning proc

260 Intriguingly, our results indicated that LXRs are critical to the process of HCV replication: LXR

261 lysis using NeoB as a bioprobe revealed that LXRs support HCV replication: LXR inactivation resulted

262 Here, we show that LXRs are involved in myelination and remyelination proce

263 The LXR agonist (GW3965) in WT mice elicited an increase in

264 The LXR agonist significantly increased biliary cholesterol

265 The LXR genome landscape has been investigated in murine mac

266 Experiments using Seco A and the LXR agonist T0901317 (T09) showed reduced expression of

267 eriments confirmed PARP-1 recruitment at the LXR response element in the promoter of the ABCA1 gene.

268 not block the activation of SREBP-1c by the LXR agonist TO9.

269 vation and maintained RCT stimulation by the LXR ligand.

270 r of IDOL, distinct from that containing the LXR-responsive element, which mediates the response to D

271 A loss of function mutation in the LXR response element was required for cAMP-dependent dow

272 inhibited, in a STAT1-dependent manner, the LXR-dependent upregulation of selective targets, includi

273 We found that the LXR agonist GW3965 and the PPARgamma agonist pioglitazon

274 ion and RNA polymerase II recruitment to the LXR responsive element (LXRE) of SREBP-1c, but not to th

275 stern diet (DBA/STZ/WD) and treated with the LXR agonist GW3965 and in LXRalpha(-/-), LXRbeta(-/-), a

276 Treating Atp7b(-/-) mice with the LXR agonist, T0901317, ameliorated disease manifestation

277 HT29 cells also were incubated with the LXR ligand GW3965.

278 , an increase in HSL was correlated with the LXR target genes, steroid receptor element-binding prote

279 These LXR agonists induced an increased matrix metalloproteina

280 Importantly, TLR3-LXR signal crosstalk promotes recruitment of NCOA5 to th

281 Herein, we provide a brief introduction to LXR and PPAR biology and review recent discoveries highl

282 RNF145 expression is induced in response to LXR activation and high-cholesterol diet feeding.

283 ts with SPG5 revealed an excess of the toxic LXR ligand, 3beta-HCA, while patients with CTX and SPG5

284 ration was markedly enhanced (1.9-fold) upon LXR activation.

285 anced regression of established plaques upon LXR activation.

286 in THP-1 cells treated with two widely used LXR ligands [N-(2,2,2-trifluoroethyl)-N-[4-[2,2,2-triflu

287 acids selectively work on motor neurons, via LXR, to regulate the balance between survival and death.

288 Our aim was to determine whether LXRs link cholesterol to retinoid storage in HSCs and ho

289 unctions and form lipid-protein adducts with LXR, thus leading to suppressed cholesterol regulatory g

290 e studied in Caco-2/TC7 cells incubated with LXR agonists.

291 strated that SMILE physically interacts with LXR and represses T7-induced LXR transcriptional activit

292 that the molecular interaction of NeoB with LXR correlated with the capacity to inactivate LXR-media

293 ion signature of macrophages stimulated with LXR agonists, we performed an miRNA profiling microarray

294 ol metabolism in macrophages stimulated with LXR agonists.

295 mouse peritoneal macrophages stimulated with LXR ligands.

296 In addition, mice treated with LXR agonists underwent an increase in the plasma sEng le

297 In addition, treatment with LXR agonists dramatically suppresses inflammatory cytoki

298 PDCN and can be normalized by treatment with LXR agonists which can be proposed as a new therapeutic

299 eoB was also shown to interact directly with LXRs.

300 In recent years, LXR modulators have also garnered interest for potential