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1 ssed cyclooxygenase 1/2 and basally secreted prostaglandin E2.
2 key modulator of inflammation and immunity, prostaglandin E2.
3 oduction/release of TNF-alpha, IL-1beta, and prostaglandin E2.
4 inflammatory factors, including TGF-beta and prostaglandin E2.
5 mpaired levels of cysteinyl-leukotrienes and prostaglandin E2.
6 ction of proinflammatory effectors including prostaglandin E2.
7 h cyclooxygenase (COX)-2 in the synthesis of prostaglandin E2.
8 ajor histocompatibility complex class II and prostaglandin E2.
9 rleukin-1ra, keratinocyte growth factor, and prostaglandin E2.
10 were observed for IL-1alpha, MIP-1alpha, and prostaglandin E2.
11 rly induces the beta-catenin pathway through prostaglandin E2.
12 the biosynthesis of prostacyclin (PGI2) and prostaglandin E2.
13 nd the cyclooxygenase-associated metabolites prostaglandin E2, 11-hydroxyeicosatetraenoic acid, and t
14 (HCC) growth by 15-PGDH through the 15-keto-prostaglandin E2 (15-keto-PGE2)/peroxisome proliferator-
16 PPARgamma) activator rosiglitazone (Rosi) or prostaglandin E2 analog (16,16-dimethyl PGE2) to adipose
19 n were performed and included measurement of prostaglandin E2 and cytosolic phospholipase A2 activity
20 isruption of the protein's ability to induce prostaglandin E2 and cytosolic phospholipase A2 synthesi
21 sident peritoneal macrophages, prostacyclin, prostaglandin E2 and leukotriene C4 were produced within
22 portantly, we discovered that Galphaq-linked prostaglandin E2 and leukotriene D4 receptors also regul
24 tantly, MKO(GFAP) mice exhibit reduced brain prostaglandin E2 and pro-inflammatory cytokine levels up
25 tion initiating mediators leukotriene B4 and prostaglandin E2 and pro-resolving mediators resolvin D1
26 1 sensitization to the inflammatory mediator prostaglandin E2 and the chemotherapeutic drug oxaliplat
28 nalogues, and the cyclooxygenase metabolites prostaglandin E2 and thromboxane B2 differed at baseline
30 ammatory lipid mediators, Leukotriene B4 and Prostaglandin E2, and a concomitant decrease of resolvin
31 n explants were stimulated with IL-1beta and prostaglandin E2, and their effects on the release of CO
32 lammatory lipid mediators leukotriene B4 and prostaglandin E2 are elevated in the chronic spinal cord
35 accelerate thrombogenesis, while suppressing prostaglandin E2, but increasing biosynthesis of PGI2.
37 ia-synapse cross talk requires production of prostaglandin E2 by microglia, leading to the activation
39 inhibited mechanical hyperalgesia induced by prostaglandin E2, carrageenan-induced hyperalgesia, and
41 e with the loss of the antifibrotic mediator prostaglandin E2 contributes to the fibrotic process in
44 otriene B4 , 11-dehydro-thromboxane B2 , and prostaglandins E2 , D2 , and F2alpha and their metabolit
47 pressed biosynthesis of prostaglandin I2 and prostaglandin E2, elevated blood pressure, and accelerat
48 izes prostanoid prostaglandin D2 (DP)1, DP2, prostaglandin E2 (EP)1, EP4, prostaglandin F2alpha, and
50 with cardiomyocyte-selective knockout of the prostaglandin E2 EP4 receptor sub-type (EP4 KO) exhibit
52 induced by diverse pronociceptive mediators, prostaglandin E2, epinephrine, TNFalpha, and interleukin
53 eased medullary COX-2 expression and urinary prostaglandin E2 excretion and developed salt-sensitive
54 , increased free water reabsorption, urinary prostaglandin E2 excretion, and reduced excretion of ser
61 Elevation of baseline urinary metabolite of prostaglandin E2, indicating activation of the COX-2 pat
62 monstrate that paracrine signaling involving prostaglandin E2-induced cAMP generation has the potenti
64 obesity-associated and tumor-derived factor prostaglandin E2, inhibits p53 in the breast adipose str
65 on of cultured small-diameter DRG neurons by prostaglandin E2 is also prevented and reversed by HMWH.
69 with clinically approved drugs that augment prostaglandin E2 levels in these settings prevented acut
72 phorylation of PREX1 after isoproterenol and prostaglandin E2-mediated GPCR activation is partially P
74 oncentrations counterregulated adenosine and prostaglandin E2-mediated inhibition of ERK1/2 activatio
75 omponents, the enantioselective synthesis of prostaglandin E2 methyl ester has been achieved through
78 h and bone density (P <0.01), enhanced 7-day prostaglandin E2 (P <0.01), and reduced 28-day inflammat
79 and elevated levels of its enzymatic product prostaglandin E2 (PGE(2)) occur in the majority of color
80 tion of the Galphas-coupled EP2 receptor for prostaglandin E2 (PGE(2)) promotes cell survival in seve
82 h increased levels of interleukin (IL)-6 and prostaglandin E2 (PGE(2)), 2 inflammatory mediators know
83 Decreased COX-2 was accompanied by reduced prostaglandin E2 (PGE(2)), a major prostanoid produced d
86 flammatory mediators including cytokines and prostaglandin E2 (PGE(2)), with limited side effects ass
90 enase-2 (COX-2) and its prostanoid products, prostaglandin E2 (PGE2 ) in particular, are key contribu
91 89 +/- 17.47 pg/mg protein; P <0.05); and 3) prostaglandin E2 (PGE2) (LPS: 159.20 +/- 38.70 pg/mg wet
93 The two synthetic pathways are connected by prostaglandin E2 (PGE2) activation of the aromatase enzy
97 nhanced biosynthesis of eicosanoids, such as prostaglandin E2 (PGE2) and PGF2alpha, precedes the onse
106 Proinflammatory lipid mediators including prostaglandin E2 (PGE2) contribute to the establishment
107 actor A (VEGF-A), interleukin 10 (IL-10) and prostaglandin E2 (PGE2) cooperatively induced FasL expre
108 the cyclooxygenase (COX)-derived eicosanoid prostaglandin E2 (PGE2) drives cirrhosis-associated immu
109 cell activation via producing high level of prostaglandin E2 (PGE2) due to their thousands-fold high
112 ase (mPGES)-1 is responsible for the massive prostaglandin E2 (PGE2) formation during inflammation.
113 cible enzyme that catalyzes the formation of prostaglandin E2 (PGE2) from prostaglandin H2 (PGH2).
118 ical hyperalgesia and marked prolongation of prostaglandin E2 (PGE2) hyperalgesia, a key feature of h
120 vestigated the contribution of COX-2-derived prostaglandin E2 (PGE2) in the formation of a premetasta
122 induced a large increase in the excretion of prostaglandin E2 (PGE2) in urine, which was suppressed i
123 ntestine with 5-hydroxytryptamine (5-HT) and prostaglandin E2 (PGE2) induced goblet cell exocytosis f
124 we report that the proinflammatory cytokine prostaglandin E2 (PGE2) induces the malignant SN12C, but
132 n strongly linked to adhesion formation, and Prostaglandin E2 (PGE2) is associated with both adhesion
135 ly induced priming is detected not only when prostaglandin E2 (PGE2) is presented to the peripheral n
138 strated that the immunomodulatory eicosanoid prostaglandin E2 (PGE2) is synergistically increased dur
139 lls with defective PKA regulation, increased prostaglandin E2 (PGE2) led to increased cAMP levels and
140 effect of MSK1/2 knockout was seen on plasma prostaglandin E2 (PGE2) levels following intraperitoneal
141 cholamines induce inflammation by increasing prostaglandin E2 (PGE2) levels in ovarian cancer cells.
142 X-1 and PGIS protein expression and PGI2 and prostaglandin E2 (PGE2) levels in the kidney and renal v
143 Local and systemic interleukin-6 (IL-6) and prostaglandin E2 (PGE2) levels were significantly elevat
144 ted the effects of the inflammatory mediator prostaglandin E2 (PGE2) on colorectal CSC development an
149 vate, via Tpl2, the cyclooxygenase-2 (Cox-2)-prostaglandin E2 (PGE2) pathway, which we show here to b
152 We tested the hypothesis that astrocytic prostaglandin E2 (PgE2) plays a key role for cerebrovasc
153 ntent, total antioxidant capacity, effect on prostaglandin E2 (PGE2) production and anticancer cell p
154 f iPSC-MSCs and BM-MSCs were associated with prostaglandin E2 (PGE2) production and cell-cell contact
155 endothelial cells, we demonstrate that local prostaglandin E2 (PGE2) production in deep brain areas,
160 py effectively induces apoptosis, associated prostaglandin E2 (PGE2) release paradoxically promotes n
161 ge (0.57-fold Nrf-2 and 0.34-fold HO-1), and prostaglandin E2 (PGE2) release was increased in samples
164 ion of infected apoptotic cells (IACs) drive prostaglandin E2 (PGE2) secretion to generate Th17 cells
166 e results from LPS-induced the production of prostaglandin E2 (PGE2) show that, esculetin, curcumin a
167 pithelial cell culture system, we found that prostaglandin E2 (PGE2) signaling through one of its rec
171 is in mouse neonates through upregulation of prostaglandin E2 (PGE2) synthesis pathway consisting of
173 eurological conditions, mainly via producing prostaglandin E2 (PGE2) that activates four membrane rec
174 TLR4 ligand, induces macrophages to generate prostaglandin E2 (PGE2) through inducible COX-2 and micr
176 le cyclooxygenase-2 (COX-2) and its mediator prostaglandin E2 (PGE2) to inhibit transforming growth f
179 dent manner for their enhanced production of prostaglandin E2 (PGE2) via a calcium-dependent cytosoli
181 In a targeted embryonic chemical screen, prostaglandin E2 (PGE2) was identified as a potential th
182 nsforming growth factor beta (TGF-beta), and prostaglandin E2 (PGE2) were higher in patients with DCL
184 hanges in the PR pathway on the secretion of prostaglandin E2 (PGE2), a key factor for promoting cell
186 aim of this study was to analyze the role of prostaglandin E2 (PGE2), a prostaglandin known to be inc
187 lones, with a focus on modulatory effects of prostaglandin E2 (PGE2), and evaluate progeny for p53 mu
188 ls overexpress cyclooxygenase-2, overproduce prostaglandin E2 (PGE2), and exhibit defective intracell
189 Although immunoregulatory factors, such as Prostaglandin E2 (PGE2), and their mechanisms of action
190 looxygenases (COXs) and their final product, prostaglandin E2 (PGE2), are known to play important rol
191 macrophages, resulting in enhanced levels of prostaglandin E2 (PGE2), autocrine activation of the mac
192 s: estradiol-17-beta-glucuronide (E17betaG), prostaglandin E2 (PGE2), cholecystokinin 8 (CCK8), and v
193 vs. patient 0.1 ng/ml) and leukocytes [e.g., prostaglandin E2 (PGE2), control 21.9 +/- 7.4 ng/ml vs.
195 scued by the addition of arachidonic acid or prostaglandin E2 (PGE2), indicating a phospholipase-depe
196 a-intercalated cells, via release of ATP and prostaglandin E2 (PGE2), influence the activity of trans
197 valuate levels of four major labor triggers, prostaglandin E2 (PGE2), interleukin (IL)-1beta, IL-6, a
199 rs, such as vasoactive intestinal peptide or prostaglandin E2 (PGE2), regulate intestinal anion/fluid
201 at the key products of NOS2 and COX2, NO and prostaglandin E2 (PGE2), respectively, promote feed-forw
203 this enzyme, the proinflammatory eicosanoid prostaglandin E2 (PGE2), stimulates adipose tissue aroma
204 al cells with M27 increases the secretion of prostaglandin E2 (PGE2), the enzymatic product of Ptges,
205 nd were treated with vehicle, diclofenac, or prostaglandin E2 (PGE2), the most important COX-2 produc
207 Cyclooxygenase-2 (COX-2) and its metabolite prostaglandin E2 (PGE2), two pivotal proinflammatory/onc
208 ce the synthesis of the small lipid mediator prostaglandin E2 (PGE2), which alters the host T cell re
209 ry enzyme responsible for the degradation of prostaglandin E2 (PGE2), which is known to promote tumor
211 similar to that of intraplantar injection of prostaglandin E2 (PGE2), which was significantly attenua
212 gene-7 (MIG-7) protein as critical for COX-2/prostaglandin E2 (PGE2)- and Akt/GSK-3beta-dependent tum
213 volves calcium efflux and stimulation of the prostaglandin E2 (PGE2)-cyclic adenosine monophosphate (
214 ted macrophages and expressed high levels of prostaglandin E2 (PGE2)-forming enzymes microsomal PGE2
215 saccharide-, parathyroid hormone (PTH)-, and prostaglandin E2 (PGE2)-induced expression of MMP-13 in
216 al of this study was to functionally compare prostaglandin E2 (PGE2)-sensitive receptors in human pri
233 nhancing ability of a short-term exposure of prostaglandin E2 (PGE2); this strategy has now progresse
235 Here we report that signaling through the prostaglandin-E2 (PGE2) EP4 receptor potently suppresses
236 protocol with bone morphogenetic protein 4, prostaglandin-E2 (PGE2), and StemRegenin 1 (SR1) for hem
238 synaptic inhibition occur partially through prostaglandin E2- (PGE2-) and PKA-dependent phosphorylat
240 njunctiva (CNJ) of the mice was cultured for prostaglandin E2 production induced by sPLA2-IIa with va
241 e, gedunin (10 microM) inhibited LPS-induced prostaglandin E2 production, cyclooxygenase-2 expression
246 Plasma levels of histamine, leukotriene B4, prostaglandin E2, prostaglandin F2, pH, and HCO3 were me
247 essenger RNA expression of cyclooxygenase-2, prostaglandin E2, prostanoid receptor-1, tumour necrosis
248 ked whether cyclooxygenase-2, its derivative prostaglandin E2, prostanoid receptors and pro-inflammat
249 sphatidylcholine, lysophosphatidic acid, and prostaglandin E2) recapitulated M1 phenotype in iPLA2bet
251 els of acquired AI resistance indicated that prostaglandin E2 receptor 4 (PTGER4) is upregulated afte
252 of noscapine in HLFs were blocked by the EP2 prostaglandin E2 receptor antagonist, PF-04418948, but n
256 nd first intron of the PTGER4 gene (encoding prostaglandin E2 receptor subtype 4; all P < 5 x 10(-5))
257 ed a potent and selective antagonist for the prostaglandin E2 receptor subtype EP2, TG6-10-1, with a
258 el mechanism of noscapine action through EP2 prostaglandin E2 receptor-mediated activation of PKA in
259 n D2 receptors (DPs) DP1 (49) and DP2 (558), prostaglandin E2 receptors (EPs) EP1 (266) and EP4 (117)
260 resistance protein 4, and G-protein-coupled prostaglandin E2 receptors 1 and 2), abolished P-glycopr
261 Increased cyclooxygenase-2 expression and prostaglandin E2 release could be abrogated in metastati
263 s activators of PKA, including adenosine and prostaglandin E2, results in a profound delay of neutrop
264 ated cyclooxygenase-2 (COX-2) expression and prostaglandin E2 secretion, indicating a proinflammatory
266 g components in the cyclooxygenase-2 (COX-2)/prostaglandin E2 signaling cascade (phospholipase A2, CO
268 Immunity, Coulombe et al. (2014) report that prostaglandin E2 suppresses innate and adaptive immune r
269 e been extensively investigated, identifying prostaglandin E2 synthase (mPGES)-1 and 5-lipoxygenase (
271 S) 2, and fibronectin expression by HLFs and prostaglandin E2 synthase (PGE2S) expression by AECs wer
272 e were a coding variant in the gene encoding prostaglandin E2 synthase (PTGES2; P = 9.3 x 10(-5)) res
275 also been linked to asthma, where deficient prostaglandin E2 synthesis has been associated with airw
278 into the role played by genetic variation in prostaglandin E2 synthetic and signaling pathways in PGD
279 sion induced by inflammatory pain depends on prostaglandin E2 that is synthesized by cyclooxygenase 2
280 t of diffusible signaling molecules, such as prostaglandin E2 The capability of human or murine CAFs
281 erinatal lethal with reduced brain levels of prostaglandin E2 The non-functional phospholipase A2-act
282 reversed hyperalgesia induced by intrathecal prostaglandin E2 To distinguish between a peripheral/spi
287 r the formation of the potent lipid mediator prostaglandin E2 under proinflammatory conditions, and t
288 rometry revealed the very specific nature of prostaglandin E2 up-regulation as the other analyzed AA
290 Cyclooxygenase and lipoxygenase metabolites prostaglandin E2 (vasodilator) and 12-hydroxyeicosatetra
291 eukin-6, chemokine (C-C motif) ligand 5, and prostaglandin E2 was assessed by enzyme-linked immunosor
294 ls pulsed in vitro for 2 hours with dimethyl prostaglandin E2 were functionally similar to those from
295 e metabolites 11-hydroxyeicosatetraenoic and prostaglandin E2 were reduced by 80% to 90% in septic pa
296 ecursor self-renewal also was obtained using prostaglandin E2, which is downstream of cyclooxygenase
298 DUSP2 led to overproduction of COX-2-derived prostaglandin E2, which promoted cancer stemness via the
299 ocompetent host requires their production of prostaglandin E2, which suppresses immunity and fuels tu
300 induced increase in hippocampal and thalamic prostaglandin E2, while the COX-2-specific inhibitor NS-
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