ライフサイエンスコーパス: FXR

1 FXR activity is regulated by glucose fluxes in hepatocyt

2 FXR agonists are currently being evaluated as therapeuti

3 FXR agonists were found to promote liver regeneration in

4 FXR also regulates postprandial lipid and glucose metabo

5 FXR and GP-BAR1, two bile acid-activated receptors, have

6 FXR and MYC were also discovered in our analysis as two

7 FXR deficiency enriched Desulfovibrionaceae, Deferribact

8 FXR expression and involved intrahepatic vasoactive path

9 FXR is also essential for maintaining bile acid homeosta

10 FXR KO also had reduced Firmicutes and increased Proteob

11 FXR proteins drive the assembly of vRCs of Venezuelan eq

12 1, and ileum ASBT and decreased liver IL-10, FXR, CAR, VDR, BSEP, MRP2, MRP3, MRP4 was also observed

13 SIRT1 regulated HNF-1alpha/FXR signaling partially through dimerization cofactor of

14 hanism of metabolic regulation of HNF-1alpha/FXR signaling.

15 Protein levels of FGF19, FGF receptor 4, FXR and short heterodimer partner were increased in cirr

16 gene expression and improves glycaemia in a FXR-dependent manner.

17 of pyruvate dehydrogenate kinase 4 (PDK4), a FXR target gene.

18 However, little is known about FXR-associated proteins that contribute to metabolic reg

19 novel series of highly potent non-bile acid FXR agonists that introduce a bicyclic nortropine-substi

20 The bile acid-FXR interaction regulates bile acid synthesis, transport

21 Recently, bile acid-FXR regulation has been reported to play an integral rol

22 Elevated bile acids activate FXR, which in turn switches off bile acid synthesis by r

23 onic liver diseases; compounds that activate FXR might promote ammonium clearance in these patients.

24 SUMOylation of agonist-activated FXR increased its interaction with NF-kappaB but blocked

25 composition, but does so without activating FXR target genes in the liver.

26 After feeding or pharmacological activation, FXR trans-repressed these genes by disrupting the functi

27 with re-expression of constitutively active FXR in enterocytes (FXR(-/-)iVP16FXR) and corresponding

28 pressed inflammatory genes without affecting FXR/RXRalpha target genes.

29 The high-affinity FXR agonist GW4064 blocks Gly-MCA action in the gut, and

30 Gly-MCA is a selective high-affinity FXR inhibitor that can be administered orally and preven

31 ment and characterization of a high-affinity FXR modulator not comprising an acidic residue.

32 and predicted microbiota functions were all FXR-dependent.

33 ed effects of obeticholic acid (INT-747), an FXR agonist, on gut permeability, inflammation, and BTL.

34 ly conjugated tauro-beta-muricholic acid, an FXR antagonist.

35 tified the RNA-binding protein Zfp36l1 as an FXR target gene and determined that gain and loss of fun

36 esoid X receptor (FXR), mice that express an FXR transgene specifically in the intestine, and ABCG8-k

37 We identified an FXR-responsive element on the Tgr5 gene promoter.

38 ximal tubular cells with free fatty acid and FXR agonists showed that FXR activation protected cells

39 These results point to bile acids and FXR signalling as an important molecular underpinning fo

40 oth gain and loss of function approaches and FXR promoter activity studies, we identified caudal-rela

41 cids are poorly selective toward GP-BAR1 and FXR.

42 After CCl4 treatments, TERT, C/EBPalpha and FXR are repressed by different mechanisms.

43 s (PPARalpha, PPARgamma, PPARdelta, LXR, and FXR).

44 idence that hepatic targets of PPARalpha and FXR are dysregulated in chronic undernutrition.

45 We conclude that PPARalpha and FXR function coordinately to integrate liver energy bala

46 Here we show that both PPARalpha and FXR regulate hepatic autophagy in mice.

47 In particular, the synthesis and FXR/TGR5 activity of novel bile acids bearing different

48 changes in expression of BA transporters and FXR in the intestine.

49 Wild-type and FXR KO mice were on a control (CD) or Western diet (WD)

50 ydrate, were used to feed wild type (WT) and FXR knockout (KO) mice followed by phenotyping character

51 t the SAR of anthranilic acid derivatives as FXR modulators and development, synthesis, and character

52 oviding the molecular basis for dual GP-BAR1/FXR agonism.

53 erlapping metabolic functions; thus, GP-BAR1/FXR dual agonists, by enhancing the biological response,

54 ncreased in the frontal cortex, and blocking FXR signaling delayed AOM-induced neurological decline.

55 Both FXR and SHP inhibit hepatic autophagy interdependently,

56 Activation of both FXR and TGR5 may therefore represent an effective therap

57 liver neoplasm has been associated with both FXR gene deletion and BA-mediated metabolic abnormalitie

58 expression, which was markedly attenuated by FXR antagonist.

59 ilicity of the bile salt pool, controlled by FXR and FGF15/19, is an important determinant of cholest

60 ed in glutathione metabolism were induced by FXR activation in the remnant kidney, which was consiste

61 ctly suppressed by PPARalpha, but induced by FXR.

62 fy the renal signaling pathways regulated by FXR and TGR5, which may be promising targets for the tre

63 lts suggest that WD increases cancer risk by FXR inactivation, leading to BA deregulation and increas

64 ch is induced by PPARalpha but suppressed by FXR.

65 In experimental cholestasis, FXR agonism improved ileal barrier function by attenuati

66 itation and high-throughput sequencing data, FXR and CREB binding peaks were detected at 178 and 112

67 d bile duct-ligated rats exhibited decreased FXR pathway expression in both jejunum and ileum, in ass

68 conditions associated with increased direct FXR target gene expression and decreased liver bile acid

69 hat intestinal PPARalpha-UGTs and downstream FXR-FGF15 signalling play vital roles in control of bile

70 Here, we studied the effects of the dual FXR and TGR5 agonist INT-767 on hepatic bile acid synthe

71 diabetic DBA/2J and db/db mice with the dual FXR/TGR5 agonist INT-767 improved proteinuria and preven

72 IP, and subsequent repression of C/EBPalpha, FXR, and TERT promoters.

73 A lack of interaction with either FXRs or G3BPs does not affect vRC formation; however, re

74 of constitutively active FXR in enterocytes (FXR(-/-)iVP16FXR) and corresponding control mice (FXR(-/

75 r1h4, which encodes the transcription factor FXR that is required for maximal urinary concentration.

76 T mice harboring simple steatosis and CD-fed FXR KO mice, in which the steatosis had a potential to d

77 In addition, both CD- and WD-fed FXR KO male mice, which had hepatic lymphocyte and neutr

78 cteria and Bacteroidetes persisted in WD-fed FXR KO mice even after Abx treatment.

79 Male WD-fed FXR KO mice had the most severe steatohepatitis.

80 Our data revealed that male WD-fed FXR KO mice had the most severe steatosis and highest he

81 B could reduce hepatic lymphocytes in WD-fed FXR KO mice.

82 s and lymphocytes in CD-fed, but not WD-fed, FXR KO mice.

83 findings demonstrate a pivotal function for FXR in bile acid homeostasis and liver protection.

84 n-23-ol (NorECDCOH, 30) as novel ligands for FXR and GP-BAR1 that might hold utility in the treatment

85 demonstrating a crucial protective role for FXR in the gut-liver axis.

86 11beta position affords high selectivity for FXR.

87 We found FXR to bind to regulatory sites of genes encoding these

88 Liver tissues from FXR-knockout mice had reduced expression of urea cycle p

89 Furthermore, FXR activation induced expression of FXR target genes, i

90 To this end, we generated FXR-null mice with re-expression of constitutively activ

91 Mice fed CA diet also demonstrated hepatic FXR hyperacetylation and induction of the Janus kinase/p

92 ort (RCT) dependent on activation of hepatic FXR.

93 damage to HCC even in the absence of hepatic FXR.

94 Targeting hepatic FXR and/or bile acids may be useful for boosting RCT and

95 Activity of the hepatic FXR/FGF15 signalling axis is reduced and associated with

96 However, FXR activation has little effect on the glycolytic metab

97 In FXR-null mice, intestinal selective FXR reactivation nor

98 asting state, and this response is absent in FXR knockout (Fxr(-/-), also known as Nr1h4(-/-)) mice,

99 hibition of macroautophagy was attenuated in FXR-knockout mice.

100 crobiota that affect hepatic inflammation in FXR knockout (KO) mice.

101 ulation, leading to considerable interest in FXR as a therapeutic target for the treatment of cholest

102 Expression of genes involved in FXR signaling in the liver and intestine was significant

103 us hepatocarcinogenesis has been observed in FXR-null mice.

104 and-dependent manner with FXR, and increased FXR binding to chromatin.

105 High glucose concentrations increased FXR O-GlcNAcylation, hence its protein stability and tra

106 tic cholestasis, metformin treatment induced FXR phosphorylation, perturbed bile acid homeostasis, an

107 antidiabetic biguanide metformin, inhibited FXR agonist induction of FXR target genes in mouse liver

108 cine-beta-muricholic acid (Gly-MCA) inhibits FXR signalling exclusively in intestine, and improves me

109 Intestinal FXR is sufficient to restore BA homeostasis through the

110 ring a meal selectively activates intestinal FXR.

111 At 16 months of age, intestinal FXR reactivation protected FXR-null mice from spontaneou

112 demonstrate that inhibition of an intestinal FXR/ceramide axis mediates gut microbiota-associated NAF

113 we found TICE to be regulated by intestinal FXR via induction of its target gene Fgf15 (FGF19 in rat

114 the intestinal lumen and decrease intestinal FXR activity.

115 Activation of intestinal FXR conferred hepatoprotection by restoring hepatic home

116 work suggests that inhibition of intestinal FXR is a potential therapeutic target for NAFLD treatmen

117 ation along with up-regulation of intestinal FXR transcriptome and reduction of hepatic BA synthesis.

118 We studied potential intestinal FXR dysfunction in a rat model of cholestatic liver inju

119 h transcriptional activation of lipogenesis, FXR-RXR, PPAR-alpha mediated lipid oxidation and oxidati

120 In addition, liver FXR-knockout mice had reduced hepatic expression of enzy

121 In liver FXR-knockout mice on a high-protein diet, the plasma con

122 th liver-specific disruption of Nr1h4 (liver FXR-knockout mice) were re-fed with a high-protein diet

123 /-)iVP16FXR) and corresponding control mice (FXR(-/-)iVP16).

124 In livers of mice, FXR regulates amino acid catabolism and detoxification o

125 In both cirrhotic models, FXR expression was decreased.

126 d that with RXRalpha, so that SUMO2-modified FXR was selectively recruited to and trans-repressed inf

127 ve hexosamine biosynthetic pathway modulates FXR activity.

128 provide a putative novel tool for modulating FXR expression against bile acid-related colorectal canc

129 established EAE with 6-ECDCA, or the natural FXR ligand chenodeoxycholic acid (CDCA), clinical diseas

130 This study identifies the new FXR-CREB axis as a key physiological switch regulating a

131 er, we used mice with a disruption of Nr1h4 (FXR-knockout mice) and compared them with floxed control

132 ulatory activities of the hepatic TR, NR1H4 (FXR; farnesoid X receptor), as our model system to tackl

133 SIRT1, which correlated with the absence of FXR, suggesting its oncogenic potential.

134 Moreover, in the absence of FXR, the ability of VSG to reduce body weight and improv

135 rapamycin (mTOR) activation, acetylation of FXR and histones, leading to an overall lower BA product

136 Mechanistically, acetylation of FXR blocked its interaction with the SUMO ligase PIASy a

137 vel mechanism in which INT-767 activation of FXR induces Tgr5 gene expression and increases Ca(2+) le

138 Activation of FXR inhibits bile acid synthesis and increases bile acid

139 Activation of FXR inhibits intestinal cholesterol absorption by modula

140 Pharmacological activation of FXR repressed many autophagy genes and inhibited autopha

141 Therefore, pharmacological activation of FXR seems a valuable therapeutic approach for several co

142 Activation of FXR suppressed kidney fibrosis and downregulated Smad3 e

143 e and primary rat hepatocytes, activation of FXR with obeticholic acid increased expression of protei

144 and their conjugates resulting in agonism of FXR in intestine and liver resulting in a smaller, uncon

145 JN452), a novel and highly potent agonist of FXR.

146 UDCA, a clinically used bile acid devoid of FXR agonist activity, to develop a large family of side

147 d obesity and targeted genetic disruption of FXR.

148 This study also revealed a dysregulation of FXR signaling in the liver and intestine of NAFLD mice t

149 TGR5 that demonstrated beneficial effects of FXR and TGR5 activation in the kidney, we reasoned that

150 and caloric restriction on the expression of FXR and TGR5 in the kidney.

151 nalysis revealed downregulated expression of FXR in HNF-1beta mutant kidneys.

152 Indeed, reduced expression of FXR in the intestine increases colorectal cancer suscept

153 ermore, FXR activation induced expression of FXR target genes, including fibroblast growth factor 15,

154 etabolic abnormalities after inactivation of FXR transcriptional activity.

155 etformin, inhibited FXR agonist induction of FXR target genes in mouse liver and intestine.

156 dent PD models by measuring the induction of FXR target genes in various tissues.

157 ome mice with intestine-specific knockout of FXR were given daily injections of fibroblast growth fac

158 In this study, we found that the level of FXR was negatively correlated with that of Smad3 and fib

159 ver regeneration and metabolic regulation of FXR was elusive.

160 nscription factor as a positive regulator of FXR expression in the enterocytes.

161 Here, we investigated the protective role of FXR against kidney damage induced by obesity in mice tha

162 epatocytes were used to validate the role of FXR in amino acid catabolism by gene expression and meta

163 To study the role of FXR in mouse liver, we used mice with a disruption of Nr

164 The role of FXR in regulation of bile acid synthesis and hepatic met

165 A dysregulated acetyl/SUMO switch of FXR in obesity may serve as a general mechanism for dimi

166 strogen receptor (ER) alpha, but not that of FXR, to Shp promoter, suggesting a predominant role of E

167 that might hold utility in the treatment of FXR and GP-BAR1 mediated disorders.

168 their roles are not as critical as those of FXRs and G3BPs.

169 e small intestine, while it had no effect on FXR target genes in the liver.

170 s HCC development that occurred in otherwise FXR-null mice.

171 tors of liver proliferation C/EBPalpha, p53, FXR, SIRT1, PGC1alpha, and TERT by C/EBPbeta-HDAC1 compl

172 oncept, we developed agents exerting partial FXR agonism and sEH inhibitory activity.

173 Hence, partial FXR activators are required for long-term treatment of m

174 ompound 51, which is a highly potent partial FXR agonist in a reporter gene assay with an EC50 value

175 ysregulation of BA homeostasis by persistent FXR deacetylation.

176 To date, potent FXR agonists share a negatively ionizable function that

177 erosis, we have developed a series of potent FXR agonists that robustly lower plasma LDL and vLDL in

178 f age, intestinal FXR reactivation protected FXR-null mice from spontaneous HCC development that occu

179 logical activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in th

180 affinity for the nuclear bile acid receptor FXR, is effective in treating primary biliary cholangiti

181 reduced activity of the nuclear BA receptor FXR.

182 The nuclear receptor FXR (farnesoid X receptor), a multiple functional transc

183 etabolism by binding to the nuclear receptor FXR (farsenoid-X receptor, also known as NR1H4).

184 ecules interacting with the nuclear receptor FXR and the G-protein coupled receptor 1 (GP-BAR1/TGR5).

185 elevated acetylation of the nuclear receptor FXR as a model.

186 brane receptor TGR5 and the nuclear receptor FXR.

187 Farnesoid X-activated receptor (FXR) is a key transcription regulator in hepatic and int

188 In particular, farnesoid X receptor (FXR) activation that revealed antisteatotic and antifibr

189 clear hormone receptor farnesoid X receptor (FXR) and G protein-coupled membrane receptor TGR5 that d

190 Nuclear receptors farnesoid X receptor (FXR) and small heterodimer partner (SHP) are important r

191 tes bile acid receptor farnesoid X receptor (FXR) and subsequently enhances hepatic expression of sma

192 r biology: C/EBPalpha, Farnesoid X Receptor (FXR) and telomere reverse transcriptase (TERT).

193 clear hormone receptor farnesoid X receptor (FXR) and the G protein-coupled receptor TGR5.

194 ted receptors, nuclear farnesoid X receptor (FXR) and the membrane Takeda G-protein receptor 5 (TGR5)

195 mation via the nuclear farnesoid X receptor (FXR) and the Takeda G protein-coupled receptor 5 (TGR5).

196 is induced by diet and farnesoid X receptor (FXR) deficiency in both genders.

197 h factor 19 (FGF19) or farnesoid X receptor (FXR) dependent signaling are involved in the regulation

198 Activation of the farnesoid X receptor (FXR) has indicated a therapeutic potential for this nucl

199 bile acid (BA) sensor farnesoid X receptor (FXR) has led to promising new therapies targeting choles

200 feedback antagonism of farnesoid X receptor (FXR) in intestine and liver.

201 The farnesoid X receptor (FXR) is a member of the "metabolic" subfamily of nuclear

202 The farnesoid X receptor (FXR) is a nuclear bile acid receptor involved in bile ac

203 The farnesoid X receptor (FXR) is a nuclear receptor that acts as a master regulat

204 ear bile acid receptor farnesoid X receptor (FXR) is an important transcriptional regulator of bile a

205 Farnesoid X receptor (FXR) is the master regulator of bile acid (BA) homeostas

206 Activation of farnesoid X receptor (FXR) markedly attenuates development of atherosclerosis

207 ular bile acid sensor, farnesoid X receptor (FXR) participates in regulation of bile acid, lipid and

208 The nuclear receptor farnesoid X receptor (FXR) plays a major role in the enterohepatic cycling of

209 Farnesoid X receptor (FXR) plays a pivotal role in the regulation of various m

210 crease of BA-activated farnesoid X receptor (FXR) protein levels were seen in ascending and sigmoid c

211 The farnesoid X receptor (FXR) regulates bile acid, lipid and glucose metabolism.

212 n of genes involved in farnesoid X receptor (FXR) signaling in the liver and intestine was analyzed.

213 ary TCDF inhibited the farnesoid X receptor (FXR) signaling pathway, triggered significant inflammati

214 had reduced intestinal farnesoid X receptor (FXR) signaling via hepatocyte nuclear factor 1alpha (HNF

215 t inhibited intestinal farnesoid X receptor (FXR) signaling.

216 entricular infusion of farnesoid X receptor (FXR) Vivo-morpholino before AOM injection.

217 1H4, which encodes the farnesoid X receptor (FXR), a bile acid-activated nuclear hormone receptor tha

218 ecific knockout of the farnesoid X receptor (FXR), mice that express an FXR transgene specifically in

219 egulated expression of Farnesoid X receptor (FXR), small heterodimer partner (SHP) and bile salt expo

220 e the nuclear receptor farnesoid X receptor (FXR).

221 lear hormone receptor, farnesoid X receptor (FXR).

222 ed by nuclear receptor farnesoid X receptor (FXR).

223 receptors (LXRs), and farnesoid X receptor (FXR).

224 ncer also have reduced farnesoid X receptor (FXR).

225 (encoded by NR1C1) and farnesoid X receptor (FXR, encoded by NR1H4) are activated in the liver in the

226 Farnesoid X receptor (FXR, NR1H4) is a bile acid-activated transcription facto

227 nd membrane receptors, farnesoid X receptor (FXR-alpha) and TGR5 (G-protein-coupled bile acid recepto

228 ne receptors including farnesoid X receptor (FXR; also known as NR1H4).

229 p H member 4 (NR1H4 or farnesoid X receptor [FXR]) regulates bile acid synthesis, transport, and cata

230 eal opposing roles for the nuclear receptors FXR and CAR in disease progression from non-alcoholic fa

231 d decreased binding of the nuclear receptors FXR, RXR, HNF4alpha, and LRH-1 to promoter response elem

232 Despite increased hepatic nuclear receptors (FXR, CAR, SHP), and FGF19, neither CYP7A1 suppression no

233 ct ability to specifically bind and regulate FXR activity in vivo, thus providing a bona fide novel t

234 t AMPK directly phosphorylates and regulates FXR transcriptional activity to precipitate liver injury

235 ctivity, the molecular mechanisms regulating FXR expression in the intestine are still unknown.

236 ontain one or more of the Fragile X related (FXR) proteins (FMRP, FXR2P, and FXR1P) along with mRNA a

237 tingly, in long-lived Ames dwarf mice, renal FXR and TGR5 expression levels were also increased.

238 tissue-selective effect, the gut-restricted FXR agonist fexaramine (Fex) robustly induces enteric fi

239 bolic improvements suggest tissue-restricted FXR activation as a new approach in the treatment of obe

240 Together, the presented data revealed FXR-dependent concomitant relationships between gut micr

241 This molecule is a potent and selective FXR agonist in vitro and has robust lipid modulating pro

242 In FXR-null mice, intestinal selective FXR reactivation normalized BA enterohepatic circulation

243 sed the hypothesis that intestinal selective FXR reactivation would be sufficient to restore the fibr

244 Intestinal-selective FXR modulators could stand as potential therapeutic inte

245 eticholic acid (INT-747), a potent selective FXR agonist, on intrahepatic hemodynamic dysfunction and

246 ined the individual effects of the selective FXR agonist obeticholic acid (OCA) and the TGR5 agonist

247 Several FXR agonists have been reported in the literature to hav

248 patic malignancy, even if carrying a somatic FXR mutation.

249 efficiently utilizes both the VEEV-specific FXR protein family and the Old World alphavirus-specific

250 In summary, FXR activation maintains endogenous glutathione homeosta

251 chenodeoxycholic acid, 6-ECDCA), a synthetic FXR agonist, is an orally available drug that is current

252 Therefore, we conclude that FXR may promote the proliferation of tumor cells and the

253 In this study, we found that FXR activation significantly promotes HepG2 cell prolife

254 We found that FXR and TGR5 expression levels are decreased in the agin

255 In this study, we found that FXR knockout mice had more disease severity in experimen

256 r in neuroinflammation and we highlight that FXR agonists represent a potential previously unidentifi

257 In summary, our results indicate that FXR and TGR5 may play an important role in modulation of

258 5 activation in the kidney, we reasoned that FXR and TGR5 could be excellent candidates.

259 and gene expression profiling revealed that FXR acetylation increased proinflammatory gene expressio

260 Luciferase reporter assay revealed that FXR activation inhibited the transcriptional activity of

261 Here, we show that FXR activation in L cells decreases proglucagon expressi

262 Here, we show that FXR activation triggers a rapid posttranscriptional mech

263 Thus, we show that FXR functions as a negative regulator in neuroinflammati

264 We further show that FXR signalling in ileum biopsies of humans positively co

265 vivo fasting-refeeding experiments show that FXR undergoes O-GlcNAcylation in fed conditions associat

266 free fatty acid and FXR agonists showed that FXR activation protected cells from free fatty acid-indu

267 The in vivo experiments showed that FXR agonist protected against renal fibrosis and downreg

268 We have shown that FXR and TGR5 have renoprotective roles in diabetes- and

269 These results suggested that FXR may serve as an important negative regulator for man

270 The FXR agonist OCA and the TGR5 agonist INT-777 modulated d

271 We administered the FXR/TGR5 dual agonist INT-767 to DBA/2J mice with strept

272 r for manipulating Smad3 expression, and the FXR/Smad3 pathway may be a novel target for the treatmen

273 tly represented HVD-binding proteins are the FXR and G3BP family members.

274 Proteomic studies identified K217 as the FXR acetylation site in diet-induced obese mice.

275 wed with high potency and selectivity at the FXR receptor, 3alpha,7alpha,11beta-trihydroxy-6alpha-eth

276 ucose and lipid metabolism more than did the FXR-selective obeticholic acid and TGR5-selective INT-77

277 These findings identify the FXR/GLP-1 pathway as a new mechanism of BA control of gl

278 Moreover, the FXR-mediated repression of fibrosis was significantly al

279 ein interacts with all of the members of the FXR and G3BP protein families, and only a lack of intera

280 Notably, despite the broad knowledge of the FXR enterohepatic transcriptional activity, the molecula

281 Here we performed a systematic survey of the FXR protein composition and mRNA association of FXGs in

282 with INT-747 in TAA and BDL reactivated the FXR downstream signaling pathway and decreased portal pr

283 Here, we show that the FXR agonist, obeticholic acid (OCA), increases fecal cho

284 Mice were gavaged with the FXR agonist obeticholic acid or vehicle for 11 days.

285 In mice treated with the FXR agonist obeticholic acid, renal injury, renal lipid

286 control diet or a diet supplemented with the FXR agonist PX20606, with or without the cholesterol abs

287 tment of 22-month-old C57BL/6J mice with the FXR-TGR5 dual agonist INT-767 induced caloric restrictio

288 types that can be categorized based on their FXR protein complement.

289 This FXR-induced metabolic switch was found dependent on an u

290 ical sodium-dependent bile acid transporter, FXR, and small heterodimer partner increased in the fron

291 Clinical results have validated FXR as therapeutic target in hepatic and metabolic disea

292 In vivo, FXR deficiency increases GLP-1 gene expression and secre

293 Whether FXR is expressed in L cells and controls GLP-1 productio

294 uate these functions and investigate whether FXR regulates amino acid metabolism.

295 However, it remains unclear whether FXR plays direct anti-fibrotic effect in renal fibrosis

296 epatic autophagy interdependently, but while FXR acts early, SHP acts relatively late after feeding,

297 tivation induces fatty acid oxidation, while FXR controls bile acid homeostasis, but both nuclear rec

298 trated that ERalpha directly interacted with FXR in living cells and in vivo in mice.

299 epressive pathway, directly interacting with FXR.

300 associate in a ligand-dependent manner with FXR, and increased FXR binding to chromatin.