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 treatment of primary BPDCN cells and BPDCN c

5 LXR agonist treatment was responsible for limiting BPDCN

6 LXR agonists also reduced intracellular trafficking of t

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

8 LXR-cofactor complexes activate the gene expression prog

9 LXR-induced liver toxicity, poor drug aqueous solubility

10 LXR/RXR activation and complement activation pathways we

11 LXRs and their ligands are present in oligodendrocytes.

12 LXRs are highly similar, and despite notable exceptions,

13 LXRs have been of interest as targets for the treatment

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

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

16 rophage response to GM-CSF or IL4, activated LXR repressed IRF4 expression, resulting in subsequent d

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

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

19 ated whether increased cholesterol activates LXRs to maintain cholesterol homeostasis in highly-dense

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

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

22 nia associated with increased survival after LXR agonist treatment.

23 rpesviruses are ubiquitous oncogenic agents, LXRs may represent a targetable host factor for the trea

24 r of DNA 3 (ID3) and liver X receptor-alpha (LXR-alpha).

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

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

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

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

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

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

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

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

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

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

35 hough neutrophils express both LXR-alpha and LXR-beta, the consequences of their activation, particul

36 Both iron chelators and LXR agonists improve the response of P47S mice to bacter

37 scription factors, such as USF1, ChREBP, and LXR, interact with and recruit specific histone modifier

38 here it is rescued by an ACAT1 inhibitor and LXR agonist.

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

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

41 d through concerted action of the SREBPs and LXRs.

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

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

44 fied by Ingenuity Pathways Analysis, such as LXR/RXR, FXR/RXR activation (- log[P-value] = 30-31) and

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

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

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

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

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

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

51 Although neutrophils express both LXR-alpha and LXR-beta, the consequences of their activa

52 viously demonstrated that deficiency of both LXR isoforms (alpha and beta) leads to an increase in fa

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

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

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

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

57 ts the enhanced phagocytic uptake induced by LXR ligation.

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

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

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

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

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

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

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

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

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

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

68 sinusoidal endothelial cells and endogenous LXR ligands were required for the induction and maintena

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

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

71 , as ligand-activated transcription factors, LXRs represent potential targets for the treatment of hy

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

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

74 es lower than those previously described for LXR agents, which may have additional safety benefits.

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

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

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

78 effects of the agonist depends on functional LXR activity in host cells.

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

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

81 However, LXR agonists administration triggers undesirable liver s

82 However, LXR also upregulates the expression of sterol regulatory

83 phologically distinct macrophages identified LXR/RXR as the most enriched pathway in large macrophage

84 Biological pathway analyses implicate LXR/RXR activation, neuroinflammation, atherosclerosis s

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

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

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

88 ibited tumor growth in wild-type, but not in LXR-deficient mice, indicating that the antitumor effect

89 concomitant with a significant reduction in LXR expression and increase in Nox4 expression and activ

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

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

92 duced HO-1, lipid regulatory genes including LXR (lipid X receptor), the growth factor IGF1 (insulin-

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

94 ut microbiota play a role in arsenic-induced LXR/RXR signaling inhibition and the subsequent lipid an

95 a critical factor regulating arsenic-induced LXR/RXR signaling perturbation, suggesting that modulati

96 endothelial cells and stellate cells induced LXR-alpha via a synergistic NOTCH-BMP pathway.

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 We therefore theorized that inhibiting LXR would induce immune-mediated TNBC-tumor clearance.

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

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

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

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

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

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

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

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

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

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

112 addition to their roles in lipid metabolism, LXRs participate in the transcriptional regulation of ma

113 Moreover, LXR target gene products facilitated the efflux of lipid

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

115 Our data suggest that neuronal LXRs may regulate non-neuronal cell function via a Nrg1-

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

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

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

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

120 Moreover, targeted activation of LXR or specific inhibition of Nox4 in vivo and in vitro

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

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

123 and hepatic steatosis through activation of LXR.

124 317 (T7)-induced transcriptional activity of LXR, which functions as a major regulator of lipid metab

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

126 omotes the ubiquitination and degradation of LXR.

127 Deletion of LXR alpha/beta from sensory neurons lead to pain-like be

128 Dysregulation of LXR pathways have been identified in many neuropathic mo

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

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

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

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

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

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

135 betes (T2DM), we revealed the implication of LXR and Nox4 in the pathophysiology of DPN.

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

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

138 e we show that pharmacological inhibition of LXR activity induces tumor destruction primarily through

139 pecific approaches, we observed that loss of LXR from sensory neurons altered genes in non-neuronal c

140 ssenger ribonucleic acid levels (a marker of LXR activation) and impaired chemotactic response toward

141 description of three possible mechanisms of LXR transcriptional activation.

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

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

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

145 nd puncture (CLP) to investigate the role of LXR activation during sepsis.

146 This study reveals unrecognized roles of LXR in the transcriptional control of the tumor microenv

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

148 opulations limit the clinical translation of LXR agonists.

149 ld facilitate future clinical translation of LXR-loaded sHDLs.

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

151 e common and differential genomic actions of LXRs and their impact on biological processes in macroph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 to the antitumoral effects of pharmacologic LXR activation.

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 Liver X nuclear receptor (LXR) agonists are promising anti-atherosclerotic agents

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

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

179 crophages reveal decreased liver X receptor (LXR) activation, inflammation and antibacterial defense

180 we found that insulin and liver X receptor (LXR) activators promote the expression of the intronic m

181 molecules and found that a liver X receptor (LXR) agonist rescued all three phenotypes in HSP neurons

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

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

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

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

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

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 ation product and a potent liver X receptor (LXR) ligand.

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

191 highlights the role of the liver X receptor (LXR) signaling pathway and the cross talk with the react

192 Desmosterol activated liver X receptor (LXR) signaling to resolve inflammation, creating a permi

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

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

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

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

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

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

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

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

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

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

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

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

207 s a novel 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 genic transcription factor liver X receptor (LXR)alpha.

212 nduced liver X receptor/retinoid X receptor (LXR/RXR) signaling inhibition is a potential mechanism u

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

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

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

216 Liver X receptors (LXR) are transcription factors from the nuclear receptor

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 nuclear receptors activated by oxidized lipids

223 itoneal cavity.IMPORTANCE Liver X receptors (LXRs) are nuclear receptors that mediate cholesterol and

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

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

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

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

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

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

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

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

232 ysterols are agonists for Liver X Receptors (LXRs), we investigated whether increased cholesterol act

233 Here, we show that liver X receptors (LXRs)-a class of nuclear receptors and transcription fac

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

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

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

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

238 ere driven by AP-1 and EGR that reprogrammed LXR functions required for Kupffer cell identity and sur

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

240 The cholesterol sensor, LXR alpha/beta, expressed in sensory neurons are necessa

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

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

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

244 oenvironment and suggests use of a synthetic LXR agonist as a novel therapeutic strategy to stimulate

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

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

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

248 assessed the antitumor effects of synthetic LXR agonist TO901317 in a murine model of syngeneic Lewi

249 model expressing equivalent levels of tagged LXRs.

250 thogenesis of DPN and suggest that targeting LXR/Nox4 axis is a promising therapeutic approach.

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

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

253 In this study, we identified that LXR alpha/beta expressed in sensory neurons regulates ne

254 Our results imply that LXR inverse agonists may be a promising new class of TNB

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

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

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

258 Therefore, our findings suggest that LXR activation impairs neutrophil functions, which might

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

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

261 In this study, we verified that LXR activation reduces neutrophil chemotactic and killin

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

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

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

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

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

267 The LXR agonist significantly increased biliary cholesterol

268 The LXR-target genes were affected as well, primarily in act

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

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

271 vation and maintained RCT stimulation by the LXR ligand.

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

273 In the latter, the LXR-transactivated genes (Abca1, Abcg1, Apod, Apoe, Myli

274 ing indicated a broad negative impact of the LXR agonist on other mechanisms used by TAM for the main

275 herogenic strategy for administration of the LXR agonist, T0901317 (T1317), by encapsulating in synth

276 his work reveals the combined actions of the LXR pathway in the control of TAM responses that contrib

277 Pharmacologic activation of the LXR pathway reduced the intratumoral abundance of regula

278 similarly, there was an up-regulation of the LXR-transrepressed genes (Ccl2, Ptgs2, Cxcl1, Il1b, Il6,

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

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

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

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

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

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

285 we demonstrate that LXRalpha, one of the two LXR isoforms, restricts reactivation of latent gammaherp

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

287 anced regression of established plaques upon LXR activation.

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

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

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

291 e expression levels of genes associated with LXR/RXR signaling were quantified by quantitative real-t

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

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

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

295 Mice treated with LXR agonists showed higher sepsis-induced mortality, whi

296 In contrast, septic mice treated with LXR antagonist showed increased number of neutrophils in

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