ライフサイエンスコーパス: PPAR

1 peroxisome proliferator-activated receptors (PPARs).

2 Peroxisome Proliferator-Activated Receptors (PPARs).

3 eraction with the terminal tyrosine found in PPARs.

4 t that activates PPAR-alpha as well as other PPARs.

5 Pharmacological PPAR activation in vivo reproduces metabolic dysfunction

6 expression of GATA3 and FOXA1 cooperate with PPAR activation to drive transdifferentiation of a basal

7 in vitro, both serum and PPAR agonist induce PPAR activation.

8 nteractions due to upregulation of CYP2C8 by PPAR activators.

9 e antidiabetic drug rosiglitazone, all known PPAR activators.

10 RA substitution allosterically regulates the PPAR AF2 domain via an aromatic interaction with the ter

11 In mouse urothelial organoids, PPAR agonism is sufficient to drive growth-factor-indepe

12 ised as an alternative, notably with the pan-PPAR agonist bezafibrate; clinical trial agents are also

13 In germ-like cells in vitro, both serum and PPAR agonist induce PPAR activation.

14 the efficacy of fenofibrate (Tricor), a pan-PPAR agonist that activates PPAR-alpha as well as other

15 hat the administration of bezafibrate, a pan-PPAR agonist, increases the expression of PGC-1alpha and

16 peroxisome proliferator-activated receptor (PPAR) agonist GW501516 (GW), an agent known to boost FAO

17 peroxisome proliferator-activated receptor (PPAR) agonist, relieves cholestasis-associated itch by a

18 n models of such conditions exceed its known PPAR agonistic profile.

19 The PPAR agonists also activated a 1-kb reporter containing

20 ovel FAAH inhibitors able to directly act as PPAR agonists and their promising utilization as leads f

21 Recent evidence suggests that PPAR agonists are attractive therapeutic agents for trea

22 PPAR agonists have well-documented anti-inflammatory and

23 signature, which raises the possibility that PPAR agonists may be targeting neurons rather than glia

24 The substrates of FAAH are also PPAR agonists, which explains the PPAR-mediated effects

25 , Hdac3 deletion enhances their induction by PPAR-agonists, and pharmacological HDAC3 inhibition indu

26 e tested the hypothesis that saroglitazar, a PPAR alpha/gamma agonist would improve NASH in the diet-

27 peroxisome proliferator-activated receptor (PPAR) alpha and gamma To determine the mechanism respons

28 peroxisome proliferator-activated receptor (PPAR)alpha and under normal conditions accounts for 70%

29 peroxisome proliferator-activated receptor (PPAR)alpha expression.

30 peroxisome proliferator-activated receptor (PPAR)-alpha by the endocannabinoid congener N-palmitoyle

31 peroxisome proliferator-activated receptor (PPAR)-alpha signaling and catabolism of fatty acids (FAs

32 peroxisome proliferator-activated receptor (PPAR)-alpha, carnitine palmitoyl transferase I (CPT1)a,

33 peroxisome proliferator-activated receptor (PPAR)-alpha.

34 y pretreatment with an antagonist for either PPAR-alpha (MK886) or cannabinoid CB1 receptors (rimonab

35 is study demonstrates that the activation of PPAR-alpha action via fenofibrate leads to neuroprotecti

36 We studied the impact of PPAR-alpha activation on emotional behavior in a mouse m

37 receptor alpha (PPAR-alpha)(3), and lowered PPAR-alpha activity increased Notum expression.

38 Palmitoylethanolamide is an agonist of PPAR-alpha and an important regulator of pain and innate

39 , and were prevented by PPAR-alpha deletion, PPAR-alpha antagonists, and neurosteroid-enzyme inhibito

40 ce points to NAAA-regulated PEA signaling at PPAR-alpha as a critical control point for the induction

41 opment of therapeutic strategies to activate PPAR-alpha as well as other PPARs may lead to new therap

42 (Tricor), a pan-PPAR agonist that activates PPAR-alpha as well as other PPARs.

43 enofibrate and GW7647, and were prevented by PPAR-alpha deletion, PPAR-alpha antagonists, and neurost

44 er kinase B1 but fails to normalize impaired PPAR-alpha expression or metabolic abnormalities associa

45 dence supports a previously unknown role for PPAR-alpha in behavior regulation and suggests new strat

46 iptional activation of lipogenesis, FXR-RXR, PPAR-alpha mediated lipid oxidation and oxidative stress

47 However, effects of PPAR-alpha on emotional behavior are poorly understood.

48 ective autophagy, restores SIRT1/FoxO3a/AMPK/PPAR-alpha signaling and rectifies metabolic abnormaliti

49 show that impaired SIRT1, FoxO3a, AMPK, and PPAR-alpha signaling are responsible for autophagy impai

50 iated by downregulation of SIRT1/FoxO3a/AMPK/PPAR-alpha signaling.

51 These effects were mimicked by the PPAR-alpha synthetic agonists, fenofibrate and GW7647, a

52 is required for the induction of PGC-1alpha/PPAR-alpha target genes and oxidative metabolism in resp

53 isome proliferator-activated receptor-alpha (PPAR-alpha) agonist that exerts profound anti-inflammato

54 isome proliferator-activated receptor alpha (PPAR-alpha) stimulation.

55 isome proliferator activated receptor alpha (PPAR-alpha)(3), and lowered PPAR-alpha activity increase

56 isome proliferator-activated receptor-alpha (PPAR-alpha), and mammalian target of rapamycin (mTOR).

57 for the pharmacological target of fibrates (PPAR-alpha), could be used to improve the selection of p

58 caused by dietary treatment with a PPAR-pan (PPAR-alpha, -gamma, and -delta) agonist were profiled by

59 creases the activity of the nuclear receptor PPAR-alpha, a PGC-1alpha binding partner, to promote fat

60 correlated with PEA-induced upregulation of PPAR-alpha, neurosteroidogenic enzyme expression, and no

61 FAS, PPAR-alpha, PPAR-gamma, and CB1-R were markedly altered

62 me proliferator-activated receptors (PPARs), PPAR-alpha, PPAR-gamma, and PPAR-delta.

63 No such effect was seen in PPAR-alpha-deficient mice.

64 inical proof-of-concept for combined FXR and PPAR-alpha/delta agonist-based therapies in NASH.

65 proliferator-activated receptor alpha/delta (PPAR-alpha/delta), respectively.

66 o improvement in insulin sensitivity through PPAR-alpha/gamma agonism, which remains unexplored.

67 Saroglitazar is a dual PPAR-alpha/gamma agonist approved for the treatment of d

68 14,643, besides being valued as agonists for PPAR, also inhibit hAR.

69 mmatory processes, whereas the expression of PPAR and insulin target gene transcripts was increased.

70 s is associated with decreased signaling via PPAR and TGF-beta/Smad.

71 Gastric microbiomes from PPARD and control mice did not differ significantly.

72 identified a positive-feedback loop between PPARD and interferon gamma signaling that sustained gast

73 s illuminate the oncosuppressive function of PPARD and understanding of the pathogenic molecular path

74 PPARD and VGPCs might be therapeutic targets for stomach

75 c molecular determinants driving activity on PPARs and RXRs.

76 peroxisome proliferator-activated receptor (PPAR), and PI3K-Akt-AMPK-mechanistic target of rapamycin

77 peroxisome proliferator-activator receptors [PPARs], and incretins) are modulated by circadian protei

78 ols to characterize the molecular effects of PPARs are indispensable.

79 Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor famil

80 Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-

81 Peroxisome proliferator-activated receptors (PPARs) are targets for the treatment of various diseases

82 e identify lipid-activated nuclear receptors PPARs as potential mediators of the effects from father

83 is reversible by PPAR inhibition, supporting PPARs as targetable drivers of bladder cancer.

84 peroxisome proliferator-activated receptor (PPAR) beta/delta deficiency in hepatic FGF21 regulation.

85 The nuclear receptor PPAR-beta/delta (PPARD) has essential roles in fatty aci

86 imulation of SCFA receptors GPR41, GPR43, or PPAR, but instead were associated with inhibition of his

87 peroxisome proliferator activated receptors (PPARs) chiral ligands have been designed following the a

88 tor-activated receptor alpha (PPARalpha) and PPAR coactivator-1 alpha (PGC1alpha) signaling with redu

89 Although agonists of all three PPARs could activate SULT1C3 transcription, RNA interfer

90 peroxisome proliferator-activated receptor (PPAR) delta as key regulator of osteoblast metabolism.

91 peroxisome proliferator-activated receptor (PPAR) delta have been validated as molecular targets to

92 Peroxisome proliferator-activated receptor (PPAR)-delta is a fatty acid-activated transcription fact

93 PPAR-delta activation also reduced HTT-induced neurotoxi

94 These findings highlight how diet-modulated PPAR-delta activation alters not only the function of in

95 ed from individuals with HD, indicating that PPAR-delta activation may be beneficial in HD and relate

96 those, 13 molecules were found as potential PPAR-delta agonist leads with EC(50) between 4-19 nM and

97 nking model to distinguish between confirmed PPAR-delta agonists and random molecules.

98 PPAR-delta agonists are known to enhance fatty acid meta

99 onists were found to be highly selective for PPAR-delta and are structurally different than agonists

100 ported that mice with a global deficiency of PPAR-delta develop an exacerbated course of experimental

101 These studies revealed a role for PPAR-delta in DC in limiting Th cell priming during EAE.

102 tudy, we studied the specific involvement of PPAR-delta in myeloid cells during EAE using mice that h

103 Expression of dominant-negative PPAR-delta in the central nervous system of mice was suf

104 em cells), and pharmacological activation of PPAR-delta recapitulates the effects of a HFD on these c

105 Notably, HFD- and agonist-activated PPAR-delta signalling endow organoid-initiating capacity

106 iating capacity to progenitors, and enforced PPAR-delta signalling permits these progenitors to form

107 Expression of dominant-negative PPAR-delta specifically in the striatum of medium spiny

108 Subsequent docking to PPAR-delta structures was mainly evaluated by geometric

109 However, the cell-specific contribution of PPAR-delta to the more severe CNS inflammatory response

110 Increased PPAR-delta transactivation ameliorated mitochondrial dys

111 se models of HD, pharmacologic activation of PPAR-delta using the agonist KD3010 improved motor funct

112 isome proliferator-activated receptor delta (PPAR-delta) interacts with HTT and that mutant HTT repre

113 isome proliferator-activated receptor delta (PPAR-delta) signature in intestinal stem cells and proge

114 isome proliferator-activated receptor-delta (PPAR-delta), which is implicated in bile acid homoeostas

115 ewal potential of these organoid bodies in a PPAR-delta-dependent manner.

116 racts with HTT and that mutant HTT represses PPAR-delta-mediated transactivation.

117 ceptors (PPARs), PPAR-alpha, PPAR-gamma, and PPAR-delta.

118 rs to terminate inflammation, down-regulates PPAR-delta.

119 Our results fill critical gaps in PPAR distribution and define novel cell type specificity

120 tory network consisting of GATA3, FOXA1, and PPAR drive luminal cell fate.

121 ice that had Cre-mediated excision of floxed Ppard driven by the lysozyme M (LysM) promoter (LysM (Cr

122 besogen by PPARgamma transactivation assays, PPAR-driven luciferase induction in vivo, PPARgamma bind

123 s gene in vitro and in vivo Mechanistically, PPARD exerted its activity in a DNA binding-dependent an

124 hways, including LPS, members of the TLR and PPAR families, NF-kappaB, and TNF-related weak inducer o

125 ion genes are transcriptional targets of the PPAR family of nuclear receptors, Hdac3 deletion enhance

126 peroxisome proliferator-activated receptor (PPAR) family comprises three subtypes: PPARalpha, PPARga

127 peroxisome proliferative-activated receptor (PPAR) family of transcription factors and are critical f

128 severe course of this disease compared with Ppard (fl/fl) controls.

129 rotein (MOG)-specific Th cells compared with Ppard (fl/fl) counterparts; the effects of DC on Th1 cyt

130 11c(+) dendritic cells (DC) from LysM (Cre) :Ppard (fl/fl) mice had a heightened capacity to prime my

131 ies linked this EAE phenotype in LysM (Cre) :Ppard (fl/fl) mice to heightened Th responses.

132 The more severe EAE in LysM (Cre) :Ppard (fl/fl) mice was associated with an increased accu

133 We observed that LysM (Cre) :Ppard (fl/fl) mice were more susceptible to EAE and deve

134 the lysozyme M (LysM) promoter (LysM (Cre) :Ppard (fl/fl)).

135 We expressed PPARD from a villin promoter to investigate the role of

136 at hyperactive PPAR signaling, either due to PPAR gamma gene amplification or RXRA hot-spot mutation

137 peroxisome proliferator-activated receptor (PPAR) gamma, which regulates its activity in the opposit

138 [peroxisome proliferator-activated receptor (PPAR) gamma-coactivator 1alpha], PPARalpha, and catalase

139 Peroxisome proliferator-activated receptor (PPAR)gamma activation, through rosiglitazone treatment,

140 Peroxisome proliferator-activated receptor (PPAR)-gamma activation leads to suppression of productio

141 peroxisome proliferator-activated receptor (PPAR)-gamma ligands have been focused on agonists.

142 peroxisome proliferator-activated receptor (PPAR)-gamma protein; P < 0.05) compared with NW-MSCs.

143 peroxisome proliferator-activated receptor (PPAR)-gamma proteins.

144 ic epithelium with 5-amino salicylic acid, a PPAR-gamma (peroxisome proliferator-activated receptor g

145 rotein response and suggest that blockade of PPAR-gamma (Ser-273) phosphorylation may prevent type 1

146 eated with pioglitazone showed reductions in PPAR-gamma (Ser-273) phosphorylation.

147 Our results demonstrate that PPAR-gamma activation directly improves beta cell functi

148 Our results suggest that pharmacological PPAR-gamma activation is a potential strategy for preven

149 In vitro, PPAR-gamma activation with pioglitazone switched macroph

150 Our results suggest that pharmacologic PPAR-gamma activation, via its vasoactive properties, ma

151 o-lipotoxicity and possibly directly through PPAR-gamma agonism in patients ofT2DM with hypertriglyce

152 evaluate the effectiveness of the selective PPAR-gamma agonist pioglitazone (PIO) for preventing hyp

153 The PPAR-gamma agonist rosiglitazone elicited similar change

154 Pretreatment with partial or selective PPAR-gamma agonists ameliorate the pathological outcomes

155 PPAR-gamma agonists, like pioglitazone, appear antiprote

156 PPAR-gamma agonists, such as rosiglitazone, may therefor

157 equire the mTORC2/AKT/ACLY pathway to induce PPAR-gamma and establish the epigenetic landscape during

158 Thus, inhibition of PPAR-gamma and GLUT-1 by E. coli K1 is a novel pathogeni

159 The suppression of PPAR-gamma and GLUT-1 by the bacteria in the brain micro

160 ingitis, and pharmacological upregulation of PPAR-gamma and GLUT-1 levels may provide novel therapeut

161 nsitizers that activate the nuclear receptor PPAR-gamma and have been shown to partially ameliorate a

162 rough mechanisms involving downregulation of PPAR-gamma and increased activation of NF-kappaB.

163 This study aims to explore expression of PPAR-gamma and NF-kappaB in placentas of women with peri

164 roups and analyzed to quantify expression of PPAR-gamma and NF-kappaB using real-time polymerase chai

165 n factor known to interact with and activate PPAR-gamma and NF-kappaB, is suppressed in the glomerula

166 Addition of the PPAR-gamma antagonist GW 9662 abrogated the effects of A

167 Rats receiving PPAR-gamma antagonists displayed proteinuria and increas

168 Chromatin immunoprecipitation showed PPAR-gamma binding to the TRPC6 promoter.

169 be partly due to increased expression of the PPAR-gamma co-activator 1-alpha.

170 trating T cells showed a progressive loss of PPAR-gamma coactivator 1alpha (PGC1alpha), which program

171 Myeloid PPAR-gamma deficiency resulted in enhanced host morbidit

172 As such, myeloid PPAR-gamma deficiency resulted in impaired inflammation

173 ion of PPAR-gamma target genes and increased PPAR-gamma DNA-binding activity.

174 down or application of antagonists of PKG or PPAR-gamma enhanced TRPC6 expression in podocytes and co

175 Here we identify that PPAR-gamma expression in AM is crucial to suppress pulmo

176 PPAR-gamma expression in AM was critical for the suppres

177 Our data suggest a critical role of PPAR-gamma expression in lung macrophages in the modulat

178 te recruiting monocytes, we demonstrate that PPAR-gamma expression in resident AM is likely important

179 acental insufficiency, and reduced placental PPAR-gamma expression; PIO prevented approximately half

180 -6, and FIV RNA detection in brain, although PPAR-gamma in glia was increased compared with PBS-treat

181 beta-catenin content and normalized nuclear PPAR-gamma in Ob-MSCs.

182 d RSV infections, suggesting that macrophage PPAR-gamma is vital for restricting severe host disease

183 e TRPC6 expression, as did podocyte-specific PPAR-gamma knockout mice, which were more sensitive to a

184 Our data suggest that targeting macrophage PPAR-gamma may be a promising therapeutic option in the

185 Importantly, inhibition of PPAR-gamma partially prevents the increase in tumorigene

186 Activation of PPAR-gamma partially restored mitochondrial membrane pot

187 d fetal growth restriction reduces placental PPAR-gamma protein expression and placental vascularizat

188 ptor gamma in luciferase reporter assay, and PPAR-gamma selective antagonist completely inhibited MDS

189 Microbiota-induced PPAR-gamma signaling also limits the luminal bioavailabi

190 Therefore, microbiota-activated PPAR-gamma signaling is a homeostatic pathway that preve

191 ide synthase, was elevated in the absence of PPAR-gamma signaling.

192 DP-glucuronic acid altered the expression of PPAR-gamma target genes and increased PPAR-gamma DNA-bin

193 ), a coactivator of the transcription factor PPAR-gamma that controls mitochondrial biogenesis and fu

194 a through cGMP- and PKG-dependent binding of PPAR-gamma to the TRPC6 promoter, which inhibits TRPC6 p

195 Furthermore, we show that PPAR-gamma was critical for the expression of wound heal

196 We found that the transcription factor PPAR-gamma was downregulated following IAV infection in

197 Expression of PPAR-gamma was downregulated in patients with preeclamps

198 GM-CSF and intact GM-CSF receptor signaling, PPAR-gamma was not sufficiently upregulated in developin

199 isome proliferator-activated receptor gamma (PPAR-gamma) and glucose transporter 1 (GLUT-1) levels in

200 isome proliferator-activated receptor-gamma (PPAR-gamma) expression both in vitro and in vivo during

201 isome proliferator-activated receptor gamma (PPAR-gamma) expression.

202 isome proliferator-activated receptor gamma (PPAR-gamma) is a downstream target of sildenafil in the

203 isome proliferator-activated receptor gamma (PPAR-gamma) is an important regulator of uteroplacental

204 isome proliferator-activated receptor gamma (PPAR-gamma) protects against hypoxia-associated fetal gr

205 isome proliferator-activated receptor gamma (PPAR-gamma), a ligand-activated nuclear receptor that pr

206 isome proliferator-activated receptor-gamma (PPAR-gamma), which is induced by exposure to granulocyte

207 isome proliferator-activated receptor gamma (PPAR-gamma), which is suppressed by HIV-1 replication.

208 isome proliferator-activated receptor gamma (PPAR-gamma)-dependent beta-oxidation of microbiota-deriv

209 isome proliferator-activated receptor gamma (PPAR-gamma).

210 isome proliferator-activated receptor-gamma (PPAR-gamma).

211 gulator peroxisome activator receptor-gamma (PPAR-gamma).

212 FAS, PPAR-alpha, PPAR-gamma, and CB1-R were markedly altered in WT-FF.

213 tor-activated receptors (PPARs), PPAR-alpha, PPAR-gamma, and PPAR-delta.

214 ression of lipid metabolism genes, including PPAR-gamma, by directly methylating their promoters.

215 lous bacterial colonization were observed in Ppar-gamma-deficient mice, highlighting the major role o

216 hibits TRPC6 expression in podocytes through PPAR-gamma-dependent mechanisms, thereby counteracting p

217 us carcinomas are sensitive to inhibition of PPAR-gamma.

218 on of ZAG in the liver via the activation of PPAR-gamma.

219 tal Lyme arthritis through the activation of PPAR-gamma.

220 ferator-activated receptor-gamma and -alpha (PPAR-gamma/-alpha) in the NTS and NG in HFD rats were ma

221 peroxisome proliferator-activated receptor (PPAR-gamma/alpha/delta) agonists, sodium glucose cotrans

222 When combined with a PPAR-gammainhibitor GW9662, the effect of DAPA on ZAG wa

223 In murine prostate epithelium, PPARD gene deletion resulted in increased cellularity.

224 The nuclear receptor PPAR-beta/delta (PPARD) has essential roles in fatty acid catabolism and

225 peroxisome proliferator-activated receptors (PPARs), has been generally used to treat hyperlipidemia

226 We found that PPARs have unique cell type specificities that are consi

227 peroxisome proliferator-activated receptors (PPARs) have been identified as part of the cannabinoid s

228 cer/promoter activity in the context of RXRA/PPAR heterodimers in human bladder cancer cells.

229 peroxisome proliferator-activated receptors (PPARs) hold therapeutic potential in neurodegeneration.

230 r to investigate the role of these cells and PPARD in development of gastric cancer.

231 Genetic modulation of PPARD in human prostate cancer cell lines validated the

232 de evidence of tumor suppressive activity of PPARD in prostate cancer through a noncanonical and liga

233 signal-regulated kinase (ERK) activation by PPARD in the testis was observed in Ppard(+/+) mice and

234 ound an inverse correlation between level of PPARD in tumor tissue and patient survival time.

235 Moreover, the cell type specificity of PPARs in mouse and human brain tissue has yet to be inve

236 driven growth of urothelium is reversible by PPAR inhibition, supporting PPARs as targetable drivers

237 00-fold selectivity for PPARalpha over other PPAR isoforms.

238 they share anti-inflammatory activities, the PPAR isotypes distinguish themselves by differential act

239 entary and distinct metabolic effects of the PPAR isotypes together with the underlying cellular and

240 so performed immunohistochemical analysis of PPARD levels in 2 sets of human gastric tissue microarra

241 lecular mechanisms, as well as the synthetic PPAR ligands that are used in the clinic or under develo

242 We highlight the potential of new PPAR ligands with improved efficacy and safety profiles

243 gies to activate PPAR-alpha as well as other PPARs may lead to new therapeutic agents to slow or halt

244 H are also PPAR agonists, which explains the PPAR-mediated effects of FAAH inhibitors.

245 significant upregulation of genes related to PPAR-mediated lipid metabolism and downregulation of gen

246 PRE (at nt -769) was essential for obtaining PPAR-mediated transcriptional activation.

247 a To determine the mechanism responsible for PPAR-mediated upregulation, we prepared reporter plasmid

248 Thirty-eight percent of PPARD mice developed spontaneous, invasive gastric adeno

249 s (VGPCs) as the origin of gastric tumors in PPARD mice.

250 ation by PPARD in the testis was observed in Ppard(+/+) mice and was associated with decreased serum

251 uptake (CAV1, CD36) and lipogenesis (PPARA, PPARD, MLXIPL) genes were enriched in metastatic tumors.

252 uorescence microscopy to determine that both PPAR mRNA and protein are expressed ubiquitously through

253 However, the distribution of PPAR mRNA and protein in brain regions associated with t

254 eceptor alpha (PPARalpha) is a member of the PPAR nuclear hormone receptor superfamily, which can be

255 We found PPARD overexpression in VPGCs to result in inflammation,

256 rat liver caused by dietary treatment with a PPAR-pan (PPAR-alpha, -gamma, and -delta) agonist were p

257 peroxisome proliferator-activated receptors (PPARs), particularly that of PPARalpha, significantly de

258 l the retinoid receptor and particularly the PPAR pathway is involved in progressive hair miniaturiza

259 Peroxisome Proliferator Activated Receptor (PPAR) pathway would be related to brain development.

260 naling (4.47), insulin signaling (3.81), and PPAR pathways (3.75), and downregulated pathways involve

261 lammatory cascades, namely Wnt, Hedgehog and PPAR pathways, were downregulated.

262 peroxisome proliferator-activated receptor (PPAR) pathways in the effects of exposure to the germlin

263 h marked attenuation of phagocytosis-induced PPAR (peroxisome proliferator-activated receptor) expres

264 ng with TGFbeta1 for receptor binding, while PPAR (peroxisome proliferator-activated receptor)-beta/d

265 Activation of the PPAR (peroxisome proliferator-activated receptor)-fatty

266 gnition and may hold implications for TH and PPAR pharmacology.

267 peroxisome proliferator-activated receptors (PPARs), PPAR-alpha, PPAR-gamma, and PPAR-delta.

268 d gastric tissues from mice that express the Ppard (PPARD1 and PPARD2 mice) from a villin promoter, a

269 peroxisome proliferator-activated receptors (PPARs), PPARgamma, is the receptor for the thiazolidined

270 the murine myeloid cell-targeted deletion of Ppard reduces expression in vitro of genes that are acti

271 Peroxisome proliferator-activated receptors (PPARs) regulate both inflammatory and multiple other pat

272 Peroxisome proliferator-activated receptors (PPARs) regulate energy metabolism and hence are therapeu

273 sh a central role for HDAC3 in co-ordinating PPAR-regulated lipid oxidation in the intestinal epithel

274 isome proliferator-activated receptor delta (PPARD) regulates cell metabolism, proliferation, and inf

275 peroxisome proliferator-activated receptor (PPAR), respectively, thereby contributing to healthy lon

276 PPAR response element (PPRE) activity was measured in PP

277 among people, with 1 SNP allele disrupting a PPAR response element and giving less activation by PPAR

278 inding assays, we have mapped the functional PPAR-responsive element to a proximal region from -135 t

279 lism that were associated with IL6, AMPK and PPAR signal pathways.

280 Mus the complement and coagulation cascades, PPAR signaling pathway and ECM-receptor interactions pre

281 and up-regulated gene expression related to PPAR signaling pathways in maternal and fetal livers ([F

282 ons suggest a potential connection of TH and PPAR signaling through overlapping ligand recognition an

283 esponse to EtOH, while defense responses and PPAR signaling were upregulated.

284 TCGA raised the possibility that hyperactive PPAR signaling, either due to PPAR gamma gene amplificat

285 acid metabolism, cholesterol metabolism and PPAR signaling.

286 ociated with fatty acid/lipid metabolism via PPAR signalling pathway.

287 ivers of oxidative metabolism, PGC1alpha and PPARD, suggesting an inverse relationship.

288 Profiling expression of PPAR target genes showed upregulation of several genes i

289 isome proliferator-activated receptor alpha (PPAR) target genes, Cpt1alpha, Pgc1alpha, and Ucp1, and

290 iptomic analysis further confirmed increased PPAR-target expression and an anti-inflammatory effect w

291 identified a novel set of genes repressed by PPARD that failed to respond to ligand-mediated activati

292 ising selective and dual agonism on RXRs and PPARs that may serve as superior pharmacological tools t

293 und to the promoter regions of PGC1alpha and PPARD to counteract their upregulation driven by HDAC1/-

294 However, prolonged PPAR treatment in animal models has led to adverse side

295 In these mice, PPARD up-regulated CCL20 and CXCL1, which increased infi

296 PPARD was downregulated in prostate cancer specimens.

297 peroxisome proliferator-activated receptors (PPARs), we investigated the effects of a PPARgamma antag

298 peroxisome proliferator-activated receptors (PPARs), we sought to assess whether HFPO-DA affects andr

299 mmation, whereas the mRNA levels of UCP2 and PPARD were decreased in peripheral blood mononuclear cel

300 Levels of PPARD were increased in human gastric cancer tissues, co