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1 ad been deleted by homologous recombination (PPAR-alpha(-/-)).
2 isome proliferator-activated receptor alpha (PPAR alpha).
3 isome proliferator-activated receptor-alpha (PPAR-alpha).
4 some proliferators activated receptor-alpha (PPAR-alpha).
5 isome proliferator-activated receptor alpha (PPAR-alpha).
6 isome proliferator-activated receptor alpha (PPAR-alpha).
7 l M2 genes (IL-13, SPHK1, CD163, LYVE-1, and PPAR-alpha).
8 me peptides on PPAR delta and in one case on PPAR alpha.
9 iferation, but not in the genetic absence of PPAR alpha.
10 lta-subtype can compensate for deficiency of PPAR alpha.
11 gonists and abolished in mutant mice lacking PPAR-alpha.
12 s the activation of microglia independent of PPAR-alpha.
13 e from a Th1 to a Th2 profile independent of PPAR-alpha.
14 sses the activity of PPAR-gamma (PPAR-g) and PPAR-alpha.
15  mice but has no effect in mice deficient in PPAR-alpha.
16 which also were dependent on the presence of PPAR-alpha.
17 e its analog OEA, as an endogenous ligand of PPAR-alpha.
18 re that, in the liver, TRB-3 is a target for PPAR-alpha.
19 wild-type mice, but not in mice deficient in PPAR-alpha.
20 re stimulated by pharmacologic activation of PPAR-alpha.
21 alpha, the dominant-negative mutant of human PPAR-alpha.
22 hat gemfibrozil inhibits iNOS independent of PPAR-alpha.
23 cts of 15D-PGJ2 may include 1) activation of PPAR-alpha, 2) activation of PPAR-gamma, 3) expression o
24 isome proliferator activated receptor alpha (PPAR-alpha)(3), and lowered PPAR-alpha activity increase
25 isome proliferator-activated receptor alpha (PPAR alpha), a member of the nuclear receptor family.
26 isome proliferator-activated receptor alpha (PPAR-alpha), a fatty acid binding transcription factor t
27 isome-proliferator-activated receptor-alpha (PPAR-alpha), a nuclear receptor that regulates several a
28 creases the activity of the nuclear receptor PPAR-alpha, a PGC-1alpha binding partner, to promote fat
29 n insulin sensitivity, and direct effects of PPAR-alpha action on the islet itself.
30 is study demonstrates that the activation of PPAR-alpha action via fenofibrate leads to neuroprotecti
31 h LDL(-) alone, LPL-treated LDL(-) increased PPAR alpha activation 20-fold in either cell-based trans
32          These findings suggest LPL-mediated PPAR alpha activation as an alternative catabolic pathwa
33      Although human plasma possesses minimal PPAR alpha activation despite containing abundant free f
34 containing abundant free fatty acids, marked PPAR alpha activation is seen with human plasma after LP
35                                          The PPAR alpha activation seen with LDL, however, was dispro
36                       These findings suggest PPAR-alpha activation as a hepatoprotective adaptive res
37                                              PPAR-alpha activation in the enterocyte on HDL and chylo
38                                              PPAR-alpha activation in vivo led to increased insulin s
39  lipids, the pharmacological consequences of PPAR-alpha activation on cardiac metabolism and function
40                     We studied the impact of PPAR-alpha activation on emotional behavior in a mouse m
41  expressed genes between PPAR-beta/delta and PPAR-alpha activation revealed distinct profiles.
42      Previous studies have demonstrated that PPAR-alpha activation stimulates keratinocyte differenti
43                               In contrast to PPAR-alpha activation, PPAR-beta/deltain vivo did not di
44 nd anti-inflammatory effects exerted through PPAR-alpha activation.
45 AR-gamma activator (troglitazone), but not a PPAR-alpha activator (bezafibrate), strikingly diminishe
46 de that LTB(4) is a physiologically relevant PPAR-alpha activator in cells of the immune system.
47 ydroxy-octadecadienoic acids (HODEs), potent PPAR alpha activators.
48 de an added benefit to patients treated with PPAR-alpha activators for dyslipidemia.
49                                              PPAR-alpha activators, including fibrates, have been use
50 of fibroblasts with ciprofibrate or WY14643, PPAR-alpha activators, led to peroxisome proliferation a
51                            Importantly, both PPAR-alpha activators, such as the fibric acid class of
52 oducts as candidate physiologically relevant PPAR-alpha activators.
53 on of antisteatotic versus anti-inflammatory PPAR-alpha activities in counteracting dietary-induced l
54  receptor alpha (PPAR-alpha)(3), and lowered PPAR-alpha activity increased Notum expression.
55 sion, and this suggests that ATGL influences PPAR-alpha activity independently of ligand-induced acti
56                                     In fact, PPAR-alpha agonism overstimulated mitochondrial TCA cycl
57                                     However, PPAR-alpha agonism was unable to normalize the effects o
58 which were presumably due to the concomitant PPAR-alpha agonism, lower respiratory quotient, and less
59 s that were similar to those elicited by the PPAR alpha agonist GW647.
60                     This novel effect of the PPAR-alpha agonist could provide an added benefit to pat
61  weeks of either placebo (PLA) or 5 mg/kg of PPAR-alpha agonist fenofibrate (FEN) treatment, within 3
62                                          The PPAR-alpha agonist fenofibrate exhibited submicromolar a
63            Treatment of diabetic rats with a PPAR-alpha agonist induced hepatic fat oxidation via ket
64                                  The natural PPAR-alpha agonist oleoylethanolamide (OEA) and the synt
65                                The synthetic PPAR-alpha agonist Wy-14643 produced similar effects, wh
66 patocytes treated with dexamethasone and the PPAR-alpha agonist Wy14,643 induced PPARA and gluconeoge
67 We further demonstrate that treatment with a PPAR-alpha agonist, bezafibrate, is able to reverse the
68   The results indicate that OEA, acting as a PPAR-alpha agonist, facilitates memory consolidation thr
69 y studying the effects of a highly selective PPAR-alpha agonist, GW7647, on [(14)C]oleate metabolism
70                A highly selective and potent PPAR-alpha agonist, GW7647, was administered by mouth fo
71 amine the safety and efficacy of LY518674, a PPAR-alpha agonist.
72 isome proliferator-activated receptor-alpha (PPAR-alpha) agonist that exerts profound anti-inflammato
73 isome proliferator-activated receptor-alpha (PPAR-alpha) agonist WY-14,643 and the glucocorticoid dex
74 the present study, we demonstrate that these PPAR alpha agonists can increase the production of the T
75                   These results suggest that PPAR alpha agonists such as gemfibrozil and fenofibrate,
76                                          The PPAR alpha agonists, gemfibrozil, ciprofibrate, and feno
77           The actions of OEA are mimicked by PPAR-alpha agonists and abolished in mutant mice lacking
78                              Next generation PPAR-alpha agonists are more potent at high-density lipo
79  stress was evident in mice treated with the PPAR-alpha agonists coinciding with increased peroxisoma
80 drazine (PHZ)-induced stress erythropoiesis, PPAR-alpha agonists facilitate recovery of wild-type but
81 activated receptor alpha (PPAR-alpha) by the PPAR-alpha agonists GW7647 and fenofibrate synergizes wi
82 t oleoylethanolamide (OEA) and the synthetic PPAR-alpha agonists GW7647 and Wy-14643 mimic these effe
83                                 Two distinct PPAR-alpha agonists have similar effects that are also c
84                 Our discovery of the role of PPAR-alpha agonists in stimulating self-renewal of early
85 ly explain the sometimes equivocal effect of PPAR-alpha agonists on glycemia.
86 or cells suggests that the clinically tested PPAR-alpha agonists we used may improve the efficacy of
87 y chromatin sites with GR; when activated by PPAR-alpha agonists, additional PPAR-alpha is recruited
88                                  Dissociated PPAR-alpha agonists, selectively modulating PPAR-alpha t
89                            We also show that PPAR-alpha alleviates anaemia in a mouse model of chroni
90                      Interestingly, although PPAR alpha also exhibited high affinity for saturated lo
91 hat human airway smooth muscle cells express PPAR alpha and -gamma subtypes.
92                            It interacts with PPAR alpha and acts as a coactivator by moderately stimu
93  PPAR delta agonist activity, improvement of PPAR alpha and gamma activity required the introduction
94 ha, although only in the genetic presence of PPAR alpha and with intact LPL hydrolysis.
95       Palmitoylethanolamide is an agonist of PPAR-alpha and an important regulator of pain and innate
96 ion downregulated mRNA expression of cardiac PPAR-alpha and FAO enzyme genes, decreased myocardial FA
97 ing effects, and safety profile, of the dual PPAR-alpha and PPAR-gamma agonist aleglitazar.
98 eNOS transgenic mice showed higher levels of PPAR-alpha and PPAR-gamma gene expression, elevated abun
99 ulates fat utilization through activation of PPAR-alpha and that this effect may contribute to its an
100 ss of fat, we infused adenovirus-leptin into PPAR alpha(-/-) and PPAR alpha(+/+) mice.
101 isome proliferator-activated receptor alpha (PPAR-alpha) and its target genes in mice with suppressed
102 isome proliferator-activated receptor-alpha (PPAR-alpha), and liver X receptor-alpha (LXRalpha).
103 isome proliferator-activated receptor-alpha (PPAR-alpha), and mammalian target of rapamycin (mTOR).
104 three nuclear receptor isoforms, PPAR gamma, PPAR alpha, and PPAR delta, encoded by different genes.
105 diated through AMP-activated protein kinase, PPAR-alpha, and PPAR-gamma coactivator alpha, which in t
106 the DNA-binding activities of HNF-4alpha and PPAR-alpha, and reduced HNF-4alpha and PPAR-alpha target
107 c(+) ATMPhis expressing elevated PGC-1alpha, PPAR-alpha, and Ym-1 transcripts were selectively enrich
108 diet-induced hepatic insulin resistance in a PPAR-alpha-and diacylglycerol-dependent manner.
109 cell carcinoma, and support the concept that PPAR-alpha antagonism may be a potential therapeutic app
110 g-induced reinstatement were reversed by the PPAR-alpha antagonist, MK886.
111 , and were prevented by PPAR-alpha deletion, PPAR-alpha antagonists, and neurosteroid-enzyme inhibito
112 uorescence resonance energy transfer between PPAR alpha aromatic amino acids and bound corresponding
113 ce points to NAAA-regulated PEA signaling at PPAR-alpha as a critical control point for the induction
114 These results identify hepatic activation of PPAR-alpha as a mechanism underlying glucocorticoid-indu
115 opment of therapeutic strategies to activate PPAR-alpha as well as other PPARs may lead to new therap
116  (Tricor), a pan-PPAR agonist that activates PPAR-alpha as well as other PPARs.
117 isome proliferator-activated receptor-alpha (PPAR-alpha) as the molecular target responsible for the
118  peroxisome proliferator-activated receptor (PPAR alpha) binds and is activated by a variety of synth
119 eroxyeicosatetrenoic acid (5-HPETE) activate PPAR-alpha but have no significant endogenous effect ind
120 rentiating effects persisted in mice lacking PPAR-alpha, but were decreased in mice deficient in reti
121 teatosis, and reactivation of HNF-4alpha and PPAR-alpha by increasing zinc availability and inhibitin
122 isome proliferator-activated receptor alpha (PPAR-alpha) by the PPAR-alpha agonists GW7647 and fenofi
123 trol and corticosteroid-treated BFU-E cells, PPAR-alpha co-occupies many chromatin sites with GR; whe
124  known how putative endogenous ligands alter PPAR alpha conformation in order to affect transcription
125  for the pharmacological target of fibrates (PPAR-alpha), could be used to improve the selection of p
126  tissue repair in WT-DB mice, but not in the PPAR-alpha-/--DB mice.
127 re absent in endothelial cells isolated from PPAR alpha-deficient mice.
128 idized EPA had no such effect in LPS-treated PPAR alpha-deficient mice.
129                                   Studies in PPAR-alpha-deficient mice demonstrated that cardiomyocyt
130                   No such effect was seen in PPAR-alpha-deficient mice.
131 enofibrate and GW7647, and were prevented by PPAR-alpha deletion, PPAR-alpha antagonists, and neurost
132  mimicked by exogenous PEA, and abolished by PPAR-alpha deletion.
133 Peroxisome proliferator-activated receptors (PPAR alpha, delta, gamma) are nuclear transcription fact
134                 Three subfamilies, including PPAR-alpha, -delta, and -gamma, have been identified wit
135                                     The dual PPAR-alpha/delta agonist, GFT505, is a promising liver-t
136 inical proof-of-concept for combined FXR and PPAR-alpha/delta agonist-based therapies in NASH.
137 proliferator-activated receptor alpha/delta (PPAR-alpha/delta) agonist.
138 proliferator-activated receptor alpha/delta (PPAR-alpha/delta), respectively.
139                          This occurred via a PPAR alpha-dependent mechanism because oxidized EPA had
140  its protective effects are mediated by both PPAR-alpha-dependent and -independent mechanisms.
141 GW7647 and Wy-14643 mimic these effects in a PPAR-alpha-dependent manner.
142                      By co-activating normal PPAR-alpha-dependent metabolism and abnormal PPAR-gamma
143 cement assays showed for the first time that PPAR alpha exhibits high affinity (1-14 nM K(d) values)
144                              Indeed, whereas PPAR-alpha expression is first noted at gestational day
145 er kinase B1 but fails to normalize impaired PPAR-alpha expression or metabolic abnormalities associa
146  similar effects that are also contingent on PPAR-alpha expression, whereas potent and selective agon
147 isome proliferator-activated receptor-alpha (PPAR-alpha) expression, but its function in this tissue
148     In contrast to the similar affinities of PPAR alpha for fatty acyl-CoAs and unsaturated fatty aci
149 nd develop the hypothesis that modulation of PPAR-alpha function may be important for the regulation
150 caused by dietary treatment with a PPAR-pan (PPAR-alpha, -gamma, and -delta) agonist were profiled by
151 e tested the hypothesis that saroglitazar, a PPAR alpha/gamma agonist would improve NASH in the diet-
152 s been identified as a non-thiazolidinedione PPAR alpha/gamma dual agonist that shows potent activity
153 f 4-thiazolyl-phenyl derivatives with potent PPAR alpha/gamma/delta pan agonistic activity.
154 o improvement in insulin sensitivity through PPAR-alpha/gamma agonism, which remains unexplored.
155                       Saroglitazar is a dual PPAR-alpha/gamma agonist approved for the treatment of d
156 substrate (VLDL >> LDL > HDL), PPAR isoform (PPAR alpha >> PPAR delta > PPAR gamma), and among fatty
157 igand binding domain activation in the order PPAR-alpha> >-gamma>-delta.
158 and wild-type mice, but not in mice in which PPAR-alpha had been deleted by homologous recombination
159  in nonhepatoma cells, whereas the RXR alpha-PPAR alpha heterodimer inhibits HNF4-dependent DHBV repl
160 isome proliferator-activated receptor alpha (PPAR alpha) heterodimer.
161  show that OEA induces satiety by activating PPAR-alpha, identify an unexpected role for this nuclear
162 ing or intracellular lipids by activation of PPAR-alpha improved insulin sensitivity and the diabetic
163 ear extracts that interacts with full-length PPAR alpha in the presence of ciprofibrate, a synthetic
164 ically distinct activators of PPAR-gamma and PPAR-alpha in a rat model of acute myocardial infarction
165 sion of wild-type or a DNA-binding-deficient PPAR-alpha in acute and chronic models of inflammation w
166                                  The role of PPAR-alpha in acute ischemia/reperfusion myocardial inju
167 dence supports a previously unknown role for PPAR-alpha in behavior regulation and suggests new strat
168  APAP toxicity, suggesting the importance of PPAR-alpha in diabetes-induced protection.
169 alpha (PPAR-alpha), we were unable to detect PPAR-alpha in either gemfibrozil-treated or untreated hu
170 uced both PPRE binding and nuclear levels of PPAR-alpha in fatty livers but increased those in lean l
171  but not isoform 2) as well as PPAR-beta and PPAR-alpha in freshly isolated cardiac myocytes and card
172 ha (PPAR-alpha), we investigated the role of PPAR-alpha in gemfibrozil-mediated inhibition of iNOS.
173   The results suggest that PEA activation of PPAR-alpha in leukocytes serves as an early stop signal
174                 Adenoviral reconstitution of PPAR-alpha in the livers of nondiabetic, normotensive, d
175                    PEA selectively activates PPAR-alpha in vitro with an EC(50) value of 3.1 +/- 0.4
176 isome proliferator-activated receptor-alpha (PPAR-alpha) in microglial cells and isolating primary mi
177 peroxisome proliferator-activated receptors (PPAR-alpha) in the gut and recruiting local afferents of
178 isome proliferator-activated receptor-alpha (PPAR-alpha), in inhibiting the disease process of adopti
179  We demonstrate that two distinct ligands of PPAR-alpha (including clofibrate and WY 14643) also caus
180 ect the expression of genes independently of PPAR alpha, including the gene for the major inducible d
181                     To determine the role of PPAR-alpha-independent mechanisms, the effect of GFT505
182 d inflammation, indicating a contribution of PPAR-alpha-independent mechanisms.
183 llar bilayers was delayed in animals lacking PPAR-alpha, indicating a transient functional defect.
184 activity and units indicates that clofibrate/PPAR alpha induced expression of retinal-reducing enzyme
185                  Pharmacologically activated PPAR-alpha inhibited hepatic inflammatory responses and
186 ification of such a transcriptionally active PPAR alpha-interacting cofactor (PRIC) complex from rat
187                                Activation of PPAR-alpha is a direct effect of intracellularly generat
188 activated by PPAR-alpha agonists, additional PPAR-alpha is recruited to GR-adjacent sites and presuma
189 isome proliferator-activated receptor alpha (PPAR-alpha) is a potential candidate for this key regula
190 isome proliferator-activated receptor-alpha (PPAR-alpha) is expressed in the heart and regulates gene
191                 In the present study we used PPAR alpha knockout (KO) mice to determine whether this
192 ct of GFT505 was assessed in hApoE2 knock-in/PPAR-alpha knockout mice.
193    These findings suggest that activation of PPAR-alpha leads to increased cardiac fatty acid oxidati
194  a diet containing clofibrate (0.5%, w/w), a PPAR alpha ligand and peroxisome proliferator, increased
195                                          The PPAR-alpha ligand pirinixic acid (WY14643) functionally
196 on of PPAR-alpha receptors using a selective PPAR-alpha ligand results in cardiomyocyte necrosis in m
197 somal proliferator-activated receptor alpha (PPAR alpha) ligand, thus limiting inflammation.
198                                We found that PPAR alpha ligands (clofibrate and WY14643) enhanced IL-
199 han saturated fatty acids, are high affinity PPAR alpha ligands provides a mechanism accounting for s
200  act on circulating lipoproteins to generate PPAR alpha ligands, providing a potentially important li
201 ed fatty acids may both represent endogenous PPAR alpha ligands.
202 ifferent types of lipids serve as endogenous PPAR-alpha ligands, with the relevant ligand varying bet
203 derived from ATGL-catalyzed lipolysis act as PPAR-alpha ligands.
204     We have attempted to analyze the role of PPAR-alpha-linked fatty acid metabolism in islet functio
205  We speculate that ligands of PPAR-gamma and PPAR-alpha may be useful in the therapy of conditions as
206 eptor (PPAR) gamma coactivator-1 (PGC-1) and PPAR-alpha may shift myocytes toward glycolytic metaboli
207 iptional activation of lipogenesis, FXR-RXR, PPAR-alpha mediated lipid oxidation and oxidative stress
208 of omega-3 fatty acids may be explained by a PPAR alpha-mediated anti-inflammatory effect of oxidized
209 s as a coactivator by moderately stimulating PPAR alpha-mediated transcription in transfected cells.
210 inhibitor of beta-oxidation, indicating that PPAR-alpha-mediated TAG depletion does not depend on rec
211                 These findings indicate that PPAR-alpha mediates the anti-inflammatory effects of PEA
212 isome proliferator-activated receptor-alpha (PPAR-alpha) mediates these sequelae, mice deficient in l
213 hogenesis of cardiac dysfunction by crossing PPAR-alpha mice with transgenic mice with cardiac-specif
214 tion in skeletal muscle strips isolated from PPAR-alpha mice.
215 d adenovirus-leptin into PPAR alpha(-/-) and PPAR alpha(+/+) mice.
216                                     Thus, in PPAR alpha(-/-) mice, up-regulation of carnitine palmito
217 reduced in the liver of wild-type but not in PPAR alpha(-/-) mice.
218 liver of wild-type mice but was unchanged in PPAR alpha(-/-) mice.
219 n the wild-type mice but did not increase in PPAR alpha(-/-) mice.
220 ght declined 55% in wild-type but only 6% in PPAR alpha(-/-) mice; liver triacylglycerol fell 39% in
221 se rats and wild-type mice, but not in obese PPAR-alpha(-/-) mice.
222 dendrocytes isolated from both wild type and PPAR-alpha(-/-) mice.
223                                           In PPAR-alpha-/- mice we observed delayed stratum corneum f
224 l cells and isolating primary microglia from PPAR-alpha-/- mice, we have demonstrated that gemfibrozi
225 liferation and cell death appeared normal in PPAR-alpha-/- mice.
226 rformed on livers from non-DB and DB (WT and PPAR-alpha-/-) mice at 0 and 12 h after APAP.
227      In contrast, diabetes in PPAR knockout (PPAR-alpha-/-) mice failed to protect against APAP toxic
228 y pretreatment with an antagonist for either PPAR-alpha (MK886) or cannabinoid CB1 receptors (rimonab
229 +/- 0.4 microM and induces the expression of PPAR-alpha mRNA when applied topically to mouse skin.
230 ng dietary-induced liver fibrosis, we used a PPAR-alpha mutant lacking its DNA-binding-dependent acti
231  correlated with PEA-induced upregulation of PPAR-alpha, neurosteroidogenic enzyme expression, and no
232     To directly test this hypothesis, we fed PPAR-alpha null and wild-type mice for 2 weeks with isoc
233  fed safflower oil), whereas in contrast, in PPAR-alpha null mice failed to counteract hepatic insuli
234                                           In PPAR-alpha null mice fed the fish oil diet, safflower oi
235  hepatic insulin resistance (HGP, P = NS vs. PPAR-alpha null safflower oil-fed mice).
236  In the small intestine of wild-type but not PPAR-alpha-null mice, OEA regulates the expression of se
237 ection by GW7647 was completely abolished in PPAR-alpha-null mice.
238              The transrepression activity of PPAR-alpha on chronic liver inflammation is sufficient t
239                          However, effects of PPAR-alpha on emotional behavior are poorly understood.
240 emphasized the potential for both actions of PPAR-alpha on insulin sensitivity that may be relayed sy
241 lta is severalfold more abundant than either PPAR alpha or PPAR gamma.
242 athic phenotype that occurred as a result of PPAR-alpha overexpression without affecting the metaboli
243 ight gain by activating the nuclear receptor PPAR-alpha (peroxisome proliferator-activated receptor a
244       These data relate retinoid metabolism, PPAR alpha, peroxisomes, and RRD, and are consistent wit
245                  These results indicate that PPAR-alpha plays a physiologic role during fetal stratum
246      This study was designed to test whether PPAR-alpha plays a physiologic role in epidermal differe
247 isome proliferator-activated receptor alpha (PPAR alpha) plays a central role in the cell-specific pl
248 ave a subfamily of three different isoforms: PPAR alpha, PPAR gamma, and PPAR beta/delta.
249 ome proliferator-activated receptors (PPARs; PPAR-alpha, PPAR-delta, and PPAR-gamma) comprise a famil
250 peroxisome proliferator-activated receptors (PPAR-alpha, PPAR-gamma and PPAR-delta) exemplify this co
251                                         FAS, PPAR-alpha, PPAR-gamma, and CB1-R were markedly altered
252                     Treatments that activate PPAR-alpha, PPAR-gamma, and PPAR-delta alone or in combi
253 me proliferator-activated receptors (PPARs), PPAR-alpha, PPAR-gamma, and PPAR-delta.
254  than currently available fibrates, and dual PPAR-alpha/PPAR-gamma agonists are under investigation t
255                                 The liganded PPAR alpha-PRIC complex enhanced transcription from a pe
256                                Activation of PPAR-alpha protected the heart from reperfusion injury.
257                          Robust induction of PPAR-alpha protein expression occurred during muscle cel
258 ntrast, hepatic levels of the PPAR-gamma and PPAR-alpha proteins were significantly lower in the Acc2
259                   In contrast, activators of PPAR-alpha, RAR, RXR, or vitamin D receptor did not alte
260        Therefore, we evaluated the role that PPAR-alpha receptors play in the heart.
261   Our studies demonstrate that activation of PPAR-alpha receptors using a selective PPAR-alpha ligand
262 crosis is a consequence of the activation of PPAR-alpha receptors.
263 lpha-type peroxisome proliferator-activated (PPAR-alpha) receptors; (2) shifted nicotine self-adminis
264                    We conclude that liganded PPAR alpha recruits a distinctive multiprotein complex f
265                                Activation of PPAR-alpha reduces secretion of LTB(4) by stimulating de
266          Fasting increased expression of all PPAR-alpha -regulated genes in lean Zucker rat hearts, w
267      During fasting, a microbiota-dependent, Ppar alpha-regulated increase in hepatic ketogenesis occ
268 with the nuclear hormone receptors HNF-4 and PPAR-alpha, respectively.
269 fier of PGC-1alpha, a nuclear coactivator of PPAR-alpha responsive gene transcription.
270 ic models of inflammation were used to study PPAR-alpha's anti-inflammatory versus metabolic activiti
271 ective autophagy, restores SIRT1/FoxO3a/AMPK/PPAR-alpha signaling and rectifies metabolic abnormaliti
272 tion that 5-lipoxygenase stimulation induces PPAR-alpha signaling and that this results specifically
273  show that impaired SIRT1, FoxO3a, AMPK, and PPAR-alpha signaling are responsible for autophagy impai
274          This miR-27b-mediated repression of PPAR-alpha signaling represents a novel mechanism of HCV
275 iated by downregulation of SIRT1/FoxO3a/AMPK/PPAR-alpha signaling.
276 de an alternate mechanism that links ATGL to PPAR-alpha signaling.
277 isome proliferator-activated receptor alpha (PPAR-alpha) stimulation.
278 y acids), elicited conformational changes in PPAR alpha structure, a hallmark of ligand-activated nuc
279           These effects were mimicked by the PPAR-alpha synthetic agonists, fenofibrate and GW7647, a
280 P-1 activation, increasing expression of the PPAR alpha target gene I kappa B alpha, although only in
281 ein 3, two classical and robustly responsive PPAR alpha target genes, were similar between WT and KO
282 pe controls, despite comparable induction of PPAR alpha target genes.
283 r homogenates; and hepatic expression of key PPAR-alpha target (MCAD, mitochondrial HMG CoA synthase,
284 naling on SIRT1 activity, and PGC-1alpha and PPAR-alpha target gene expression independent of changes
285 o normalize the effects of ATGL knockdown on PPAR-alpha target gene expression, and this suggests tha
286  is required for the induction of PGC-1alpha/PPAR-alpha target genes and oxidative metabolism in resp
287 ice, OEA regulates the expression of several PPAR-alpha target genes: it initiates the transcription
288 a and PPAR-alpha, and reduced HNF-4alpha and PPAR-alpha target proteins.
289                Fatty acids bind and activate PPAR-alpha; therefore, it has been presumed that fatty a
290          We show here that MUT LDL activates PPAR alpha to an extent proportional to its LDL(-) conte
291 es were established that overexpressed human PPAR alpha to levels between 6- and 26-fold over normal
292 nk between lipoprotein metabolism and distal PPAR alpha transcriptional effects.
293                                              PPAR-alpha transgenic mice develop spontaneous cardiac h
294  PPAR-alpha agonists, selectively modulating PPAR-alpha transrepression activity, could thus be an op
295                                              PPAR-alpha was investigated further by immunohistochemis
296 isome proliferator-activated receptor-alpha (PPAR-alpha), we investigated the role of PPAR-alpha in g
297 isome proliferator-activated receptor-alpha (PPAR-alpha), we were unable to detect PPAR-alpha in eith
298 isome proliferator-activated receptor-alpha (PPAR-alpha) were examined as a model of diabetic cardiom
299 r-/-), with (Ppara+/+) or without (Ppara-/-) PPAR-alpha, were treated chronically with dexamethasone.
300 rug was equally effective in treating EAE in PPAR-alpha wild-type as well as knockout mice.

 
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