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1                                              PGI has been used to map a total of 3858 BAC clones cove
2                                              PGI is a multifunctional dimeric protein that extracellu
3                                              PGI is a multifunctional dimeric protein that extracellu
4                                              PGI is a multifunctional dimeric protein that extracellu
5                                              PGI phosphorylation by CK2 also led to down-regulation o
6                                              PGI(2) (prostacyclin) is a lipid mediator with vasodilat
7                                              PGI(2) is also increasingly believed to have anti-inflam
8                                              PGI(2) plays a key role in limiting Th2-mediated airway
9                                              PGI-02776 was also readily hydrolyzed to both the mono-e
10                                              PGI-LysAP hydrolyzed bradykinin, Lys-bradykinin, Lys-(de
11                                              PGI/AMF cellular expression in HT1080 human fibrosarcoma
12                                              PGI/AMF has been correlated significantly with breast ca
13 mbination of PGI/II-HpAb (0.786, P < 0.001), PGI/II-OPN (0.787, P < 0.001), and OPN-HpAb (0.801, P =
14 shold (P = 0.002), CGI-Severity (P = 0.048), PGI-Improvement (P = 0.033), and several quality-of-life
15 ese results suggest that activation of COX-1/PGI(2)/PPARdelta pathway is an important mechanism under
16                                      PARP-14-PGI/AMF interaction was confirmed by coimmunoprecipitati
17 -M), and PGI2, 2,3-dinor 6-keto PGF(1alpha) (PGI-M), only PGI-M was depressed by the COX-2 inhibitor.
18  B2 (Tx-M) and 2'3-donor-6-keto-PGF(1alpha) (PGI-M).
19 elease and production of prostaglandin I(2) (PGI(2)) and platelet-activating factor (PAF).
20                          Prostaglandin I(2) (PGI(2)) stimulated VEGF-dependent angiogenesis to preven
21 such as nitric oxide and prostaglandin I(2) (PGI(2)), considerably less is known about intrinsic mech
22 tabolism via stimulation of cyclooxygenase-2/PGI(2) synthase pathway.
23 muM) to the reference drug nitazoxanide (50% PGI release at c = 1.2 muM).
24 , Ph) with comparable in vitro toxicity (50% PGI release at c = 1.4 - 4.7 muM) to the reference drug
25 oprostol (a PGE(1/2) analog) or beraprost (a PGI(2) analog) significantly decreased ConA-induced live
26 gh-salt diet (HSD); this was attenuated by a PGI(2) receptor agonist.
27 t AAMvarphi-derived eicosanoid and propose a PGI(2)-PPARdelta axis maintains AAMvarphi during B malay
28 cident with TP-cAMP generation, promoting a "PGI(2)-like" cellular response to TP activation.
29          Furthermore, unlike the activators (PGI(2) and forskolin) of the cAMP pathway, 2MeSAMP and C
30 latory properties of clinically administered PGI(2) analogs.
31  decreased the synthesis of anti-aggregatory PGI(2) and PGD(2) at non-platelet sites leading to predi
32 ucose isomerase with a lysyl aminopeptidase (PGI-LysAP) activity was identified in Vibrio vulnificus.
33 d protein expression of cyclooxygenase-2 and PGI(2) in adventitia, media, and endothelium.
34 also caused increase in cyclooxygenase-2 and PGI(2) synthase protein expression associated with eleva
35 Ang2 and the hypoxic induction of PGE(2) and PGI(2) in a dose-dependent manner.
36 d against severity; 9alpha,11beta-PGF(2) and PGI(2) metabolites were measured for control purposes.
37 whereas it augmented excretion of PGD(2) and PGI(2) metabolites, reflecting rediversion of the accumu
38 S-stimulated COX-2 expression and PGE(2) and PGI(2) production.
39 I, whereas celecoxib blocked both PGE(2) and PGI(2) production.
40 eased expression of mRNA encoding PGE(2) and PGI(2) synthases.
41                Finally, exogenous PGE(2) and PGI(2) were able to stimulate Ang2 under normoxic condit
42 ed increases in the production of PGE(2) and PGI(2) were associated with increased expression of mRNA
43             Prostaglandins (PGs), PGE(2) and PGI(2), also accumulate in the interstitium during exerc
44 ediated through the production of PGE(2) and PGI(2), which exert anti-inflammatory functions.
45 h contrasting effects of PGD(2), PGE(2), and PGI(2) on ILC2 responses have been previously reported,
46                 Measured PLA(2) activity and PGI(2) production by iPLA(2)beta-KO cells were suppresse
47 were tested for H. pylori IgG antibodies and PGI and PGII levels using enzyme linked immunosorbent as
48  high levels of COX-1 protein expression and PGI(2) biosynthesis in human EPCs outgrown from blood mo
49  that PGE(2) released from muscle fibres and PGI(2) released from capillaries and venular endothelium
50 otogenic, and differentiation functions, and PGI has been implicated in tumor progression and metasta
51 of PDO (Protected Designation of Origin) and PGI (Protected Geographical Indications) characterizatio
52 gnificant associations between PGI, PGII and PGI:PGII levels and vibriocidal seroconversion.
53 n both angiotensin II-induced relaxation and PGI(2) release but also abolished high-glucose-enhanced
54                 Arachidonic acid release and PGI(2) production by stimulated iPLA(2)beta-KO endotheli
55 nt difference was found between sham-TBI and PGI-02776 treated groups in either analysis indicating a
56                                           As PGI(2) is unstable, we sought to define the effects of v
57 a), but not by other prostaglandins, such as PGI(2), TxB(2), or PGD(2).
58 GES-1 depressed PGE(2) expression, augmented PGI(2) expression, and had no effect on thromboxane bios
59 ic procedures, SIMCA achieved to be the best PGI-model with 93.3% of sensitivity and 100% of specific
60 ere were no significant associations between PGI, PGII and PGI:PGII levels and vibriocidal seroconver
61         Intron position is conserved between PGIs of Colias and the silkmoth, but no intron sequence
62                Augmented expressions of both PGI/AMF and AMFR have been implicated in tumor progressi
63 olytic cleavage of human-derived peptides by PGI-LysAP of V. vulnificus using three approaches: (i) a
64 gulates the expression level of tumor cells' PGI/AMF.
65 as associated with up-regulation of cellular PGI enzymatic activity.
66  on the Patient Global Impression of Change (PGI-C) was the key secondary endpoint.
67 and the Patient Global Impression of Change (PGI-C).
68 t are the hallmark of the well characterized PGI family.
69                                  Like Colias PGI's coding sequences, the introns evolve reticulately
70 on of the housekeeping gene product/cytokine PGI/AMF, and the results depicted here suggest a novel t
71 vestigated the impact of disrupted cytosolic PGI (cPGI) function on plant viability and metabolism.
72 2, arachidonic acid release, COX-2-dependent PGI(2) synthesis, and IP receptor-linked elevation of cA
73 regulated expression of the COX-2 dependent, PGI(2) biosynthesis/response pathway in the renal inner
74  NSAID-mediated suppression of COX-2-derived PGI(2) has negative cardiovascular consequences, yet lit
75  deletion of the receptor for PGHS-2-derived PGI(2), was shown to accelerate thrombogenesis and eleva
76       In contrast, the structurally distinct PGIs of eukaryotic or bacterial origin are thought to ca
77                                 The elevated PGI-M in smokers (189+/-25, median 174, range 85 to 390
78  human PGI/AMF down-regulated the endogenous PGI/AMF expression and completely extinguished the secre
79 PII inhibitor ZJ-43 and its prodrug di-ester PGI-02776 reduce the deleterious effects of excessive ex
80 n uninjured animals found that the di-ester (PGI-02776) crossed the blood-brain barrier.
81 ile the mono-ester (PGI-02749) and di-ester (PGI-02776) prodrug compounds exhibited moderate and weak
82 nt inhibitory activity while the mono-ester (PGI-02749) and di-ester (PGI-02776) prodrug compounds ex
83 o readily hydrolyzed to both the mono-ester (PGI-02749) and the parent compound (ZJ-43) in both blood
84 enzyme, compared to bacterial and eukaryotic PGIs.
85 se of equivalent complexes of the eukaryotic PGIs reveals similarities at the active site in the disp
86 ally high levels of endogenous and exogenous PGI/AMF, were stably transfected with PGI/AMF small inte
87 ect studies of the significance of exogenous PGI/AMF on tumor progression have been reported.
88 s in endothelial cells, and VSMCs expressing PGI synthase were enriched in mPGES-1(-/-) LDLR(-/-) les
89 glucose isomerase/autocrine motility factor (PGI/AMF) is a housekeeping gene product present in all c
90 glucose isomerase/autocrine motility factor (PGI/AMF) is a housekeeping gene product/cytokine that ca
91 glucose isomerase/autocrine motility factor (PGI/AMF) plays an important role in glycolysis and gluco
92 ntrast, the percentage of 18:0 was lower for PGI veal, and that of 18:1 c9 was higher in PDO veal, wh
93 terial content of cAMP, second messenger for PGI(2), were significantly augmented after transplantati
94 eural networks) to derive diverse models for PGI-honey class with the objective of detecting possible
95 nal medullary expression of the receptor for PGI(2), but not for other prostanoids, was depressed by
96 xamined the interaction of the receptors for PGI(2) (IP) and TxA(2) (TPalpha).
97 c inflammation, implying a critical role for PGI(2) in the programming of "natural" gammadelta-17 cel
98 od in order to differentiate between genuine PGI-Galician honey samples and other commercial honey sa
99 d as substrates for falsification of genuine PGI ones.
100                      Overexpression of GndA, PGI, or yeast Pho13 suppresses glucose intoxication of D
101                    The siRNA targeting human PGI/AMF down-regulated the endogenous PGI/AMF expression
102  activities, although it is known that human PGI/AMF is phosphorylated at Ser(185) by protein kinase
103                         Our results identify PGI(2)-IP as an important pathway for inhibiting allergi
104                                 Importantly, PGI(2) and its receptor IP, which downregulated airway e
105 he Patient Global Impression of Improvement (PGI-I) scale, which is a patient-reported interpretation
106 e, Patient Global Impression of Improvement (PGI-Improvement) scale, Brief Pain Inventory (short form
107 abolites and potential genotoxic impurities (PGIs).
108  these results suggest a role of miR-200s in PGI/AMF-induced EMT and thus approaches for upregulation
109 requires a rotation of its C2-C3 bond but in PGI this is sterically blocked by Gln511.
110  A proline residue (in place of a glycine in PGI) may also promote PMI activity by positioning the C1
111               Histamine-induced increases in PGI(2) and PGE(2) production were due to increased expre
112  that the expression of miR-200s was lost in PGI/AMF overexpressing MCF-10A cells and in highly invas
113  increased superoxide and 3-nitrotyrosine in PGI(2) synthase (PGIS).
114 pendent kinase inhibitor was up-regulated in PGI/AMF knockdown cells and that superoxide dismutase is
115                                           In PGIs from bacterial and eukaryotic sources, which cannot
116  research supports a role for PGs, including PGI(2), in the regulation of both innate and acquired im
117 and macrophages with bacterial LPS increased PGI(2) and thromboxane A(2) to varied extents.
118 f EPCs promotes vasoprotection by increasing PGI(2) production and intracellular concentration of cAM
119                     Pooled genomic indexing (PGI) is a method for mapping collections of bacterial ar
120 's Mountain Protected Geographic Indication (PGI).
121 neys with protected geographical indication (PGI) "Mel de Galicia" was processed by means of differen
122  (PDO) or Protected Geographical Indication (PGI) product has also been discussed.
123 re administered the NAAG peptidase inhibitor PGI-02776 (10mg/kg) 30 min following TBI combined with a
124 e experiments revealed that PARP-14 inhibits PGI/AMF ubiquitination, thus contributing to its stabili
125 1-selective inhibitor, dramatically inhibits PGI(2) production.
126         Over the two weeks following injury, PGI-02776-treated rats had significantly improved motor
127          Furthermore, two weeks post-injury, PGI-02776-treated animals had a significant decrease in
128  depletion of glucose-6-phosphate isomerase (PGI) in the glucose-depleted Deltamec/Deltamec null back
129 thway and the glucose-6-phosphate isomerase (PGI) reaction.
130 on is dependent on phosphoglucose isomerase (PGI) activity.
131  through action of phosphoglucose isomerase (PGI) and phosphoglucose mutase interconverting glucose 6
132                    Phosphoglucose isomerase (PGI) is an enzyme of glycolysis that interconverts gluco
133                    Phosphoglucose isomerase (PGI) is one of the glycolytic enzymes and is a multifunc
134 To pursue this for phosphoglucose isomerase (PGI) of Colias butterflies, whose polymorphism is mainta
135 ) by baker's yeast phosphoglucose isomerase (PGI) with regard to k(cat) and K(m) were determined from
136 otent inhibitor of phosphoglucose isomerase (PGI).
137 a dual specificity phosphoglucose isomerase (PGI)/phosphomannose isomerase from Pyrobaculum aerophilu
138                    Phosphoglucose isomerase (PGI; EC 5.3.1.9) is a cytosolic housekeeping enzyme of t
139                    Phosphoglucose isomerase (PGI; EC 5.3.1.9) is a housekeeping cytosolic enzyme of t
140                    Phosphoglucose isomerase (PGI; EC 5.3.1.9) is a ubiquitous cytosolic enzyme essent
141                    Phosphoglucose isomerase, PGI, of Colias butterflies offers such a case.
142  commonly seen in phosphoglucose isomerases (PGIs) that are found in bacteria, eukaryotes and some ar
143 s at 24 h post injury revealed that 10 mg/kg PGI-02776 significantly decreased the number of degenera
144            Along with elevated COX-2 levels, PGI(2) and PGE(2) levels were also increased.
145           We identified the PPARdelta ligand PGI(2) as the most abundant AAMvarphi-derived eicosanoid
146                           Thus, PGD(2), like PGI(2), may function as a homeostatic response to thromb
147 e excretion, with the exception of the major PGI(2) metabolite that was suppressed on regular chow an
148 rotected by the European Union with the mark PGI (i.e., Protected Geographical Indication), and culti
149 consequences associated with PGHS-2-mediated PGI(2) suppression.
150 TB) and seven balsamic vinegars from Modena (PGI) were determined by gas chromatography-olfactometry
151 use ventricular cardiomyocytes by modulating PGI activity using erythrose 4-phosphate.
152 eats (n=68), "Vitela Tradicional do Montado"-PGI veal, Mertolenga-PDO veal and Mertolenga-PDO beef we
153  muscle cells generated less PGE(2) but more PGI(2) and expressed reduced tenascin-C compared with wi
154                                    Moreover, PGI(2) pretreatment of Th2 cells suppressed the ability
155 enzymatic activity, whereas the S185A mutant PGI protein retained full enzymatic activity.
156 /mg creatinine (P=0.002), and in nonsmokers, PGI-M at baseline (115+/-10, median 107, range 67 to 198
157 s2 and microsomal type PGE synthases but not PGI synthases are co-expressed.
158 nhibited prostaglandin E(2) (PGE(2)) but not PGI(2) production in response to Ang II, whereas celecox
159 wever, here we have shown that activation of PGI(2) receptor (IP) upregulated the expression of sever
160 rylation modulates the enzymatic activity of PGI thus has an important implication for the understand
161                              The addition of PGI 2 alone also induced the expression of VEGF.
162                            Administration of PGI-02776 immediately following the cessation of hypoxia
163     Conversely, iloprost, a stable analog of PGI(2), augmented IL-17 production by gammadelta T cells
164 madelta-17 cell responses, stable analogs of PGI(2) may be exploited in the development of new immuno
165 th suppression of PGE(2) and augmentation of PGI(2) attenuate tenascin-C expression and vascular smoo
166 801, P = 0.006), as well as one-biomarker of PGI/II (0.735, P < 0.001), HpAb (0.737, P < 0.001) and O
167 of a divergent impact on the biosynthesis of PGI(2).
168 ies are the first to explore the capacity of PGI(2) to regulate bacterial killing and phagocytosis in
169 y higher than two-dimensional combination of PGI/II-HpAb (0.786, P < 0.001), PGI/II-OPN (0.787, P < 0
170 er ROC from three-dimensional combination of PGI/II-HpAb-OPN (0.826) was significantly higher than tw
171                           The combination of PGI/II-HpAb-OPN, yielded a sensitivity of 70.2% and spec
172 hanisms involved in the counterregulation of PGI(2)/TxA(2) signaling are unclear.
173      We show here that ectopic expression of PGI/AMF induced epithelial-to-mesenchymal transition (EM
174 t under hypoxic conditions the expression of PGI/AMF is regulated in part by the HIF pathway, which i
175 e enzyme, resulting in a less active form of PGI, whereas non-phosphorylated protein species retain c
176 cells and again the increase in formation of PGI(2) observed in WTs was suppressed in cells derived f
177 f accumulated PGH(2) to augment formation of PGI(2).
178 at mediate the anti-inflammatory function of PGI(2.) In this study, we determined that PGI(2) analogs
179 lating platelets by maximizing the impact of PGI(2).
180        In addition, the hypoxia induction of PGI/AMF expression was suppressed by inhibitors of vascu
181 ed proteins and confirmed that inhibition of PGI increases protein synthesis.
182 r benefit, despite concomitant inhibition of PGI(2).
183 robic energy generation; thus, inhibition of PGI/AMF expression and activities may provide a new ther
184 n breast epithelial cells, and inhibition of PGI/AMF expression triggered mesenchymal-to-epithelial t
185 e a new therapeutic target for inhibition of PGI/AMF inducing tumor cell migration and invasion durin
186                      A specific inhibitor of PGI/AMF induced cellular senescence and p21 expression i
187 ogether, the results show the involvement of PGI/AMF in both EMT and MET: overexpression of PGI/AMF i
188  tumor cells, we examined the involvement of PGI/AMF in overcoming cellular senescence in cancer cell
189 nhibition of glycolytic flux at the level of PGI caused G6P accumulation, which correlated with incre
190 mice, notably significantly higher levels of PGI(2) metabolite.
191                   Homology-based modeling of PGI's structure shows that these regions are related spa
192 I/AMF in both EMT and MET: overexpression of PGI/AMF induces EMT in normal breast epithelial cells an
193 sis, and an intracellular binding partner of PGI/AMF is expected to regulate in part its diverse biol
194 mino acid variants occur in diverse parts of PGI's sequence.
195                  The increased production of PGI(2) and arterial content of cAMP were inhibited only
196                   Furthermore, production of PGI(2) and arterial content of cAMP, second messenger fo
197 d arachidonic acid release and production of PGI(2) and PAF.
198 in the expression of COX-2 and production of PGI(2) and PGE(2) with no significant change in the expr
199                            The production of PGI(2) leads to an increase in the level of the pro-angi
200 ible Ha-Ras(V12) increases the production of PGI(2) through the coordinate up-regulation of cPLA(2),
201  that the phosphorylation mutant proteins of PGI exhibited decreased enzymatic activity, whereas the
202                             The reduction of PGI activity directly affects myocyte growth by regulati
203 mal breast epithelial cells and reduction of PGI/AMF expression led to MET in aggressive breast cance
204 le is known of the biochemical regulation of PGI/AMF activities, although it is known that human PGI/
205 1, which in turn led to the up-regulation of PGI/AMF expression and was specifically inhibited by inh
206 ld assist in understanding the regulation of PGI/AMF intracellular function(s) and may provide a new
207 ormal fibroblasts whereas down-regulation of PGI/AMF leads to mesenchymal-to-epithelial transition in
208 and completely extinguished the secretion of PGI/AMF in a human fibrosarcoma HT1080, whereas the cont
209                                 Silencing of PGI/AMF expression by RNA interference in MDA-MB-231 cel
210                       Moreover, silencing of PGI/AMF expression in MDA-MB-231 cells led to overexpres
211 ther reexpression of miR-200 or silencing of PGI/AMF suppressed pulmonary metastases of MDA-MB-231 ce
212                               Suppression of PGI/AMF led to a contact-dependent inhibition of cell gr
213                 Furthermore, transfection of PGI(2) synthase siRNA, COX-1 siRNA, or PPARdelta siRNA i
214 f its fold, with the inner core structure of PGIs from eubacterial and eukaryotic sources, confirms t
215 hod to discriminate three "Tropea Red Onion" PGI ecotypes (TrT, TrMC and TrA) from each other and the
216 , 2,3-dinor 6-keto PGF(1alpha) (PGI-M), only PGI-M was depressed by the COX-2 inhibitor.
217 hacin or by genetic inactivation of COX-1 or PGI(2) synthase with small interfering (si)RNA.
218  threonine, in place of a glutamine in other PGI enzymes, which could permit rotation of the C-2-C-3
219  AMs to a much greater degree than the other PGI(2) analogs and more closely resembled the effects of
220                        Mice that overexpress PGI(2) synthase selectively in bronchial epithelium are
221 post-injury treatment with the ZJ-43 prodrug PGI-02776 reduces both acute neuronal pathology and long
222 y important stable analogues of prostacyclin PGI(2), namely benzindene prostacyclins, has been achiev
223                                Prostacyclin (PGI(2)) is the major prostaglandin generated downstream
224                                Prostacyclin (PGI(2)) is widely used to treat pulmonary arterial hyper
225 n to the production of PGE(2), prostacyclin (PGI(2)), and thromboxane A(2) in human coronary artery e
226 ular Cyclooxygenase-2 (COX-2), prostacyclin (PGI(2)), restrains atherogenesis, inhibition and deletio
227 s, (c) hypoxia and (d) altered prostacyclin (PGI(2)) and enhanced isoprostane formation.
228 ostanglandin E(2) (PGE(2)) and prostacyclin (PGI(2)) production.
229 othelial nitric oxide (NO) and prostacyclin (PGI(2)) production.
230 n augmented expression of both prostacyclin (PGI(2)) and thromboxane (Tx) synthases in endothelial ce
231 cyclooxygenase (COX)-2 depress prostacyclin (PGI(2)) without a concomitant inhibition of platelet COX
232  suppression of PGHS-2-derived prostacyclin (PGI(2)) and PGE(2).
233 clooxygenase 2 (COX-2)-derived prostacyclin (PGI(2)) is sufficient to explain most elements of the ca
234 normally caused by endothelial prostacyclin (PGI(2)).
235 roduced just prior to labor is prostacyclin (PGI(2)), a smooth muscle relaxant.
236 d the subsequent production of prostacyclin (PGI(2)) is an important mechanism responsible for the re
237 latory proteins, production of prostacyclin (PGI(2)), and cAMP were determined.
238 s, likely due to inhibition of prostacyclin (PGI(2)).
239 ched angiotensin II-stimulated prostacyclin (PGI(2))-dependent relaxation into a persistent vasoconst
240 lial cell COX-2 coupled to the prostacyclin (PGI(2)) synthase (PGIS) activates the nuclear receptor p
241             The GRIPHON trial (Prostacyclin [PGI(2)] Receptor Agonist In Pulmonary Arterial Hypertens
242 l 150 mg (78.2%) and 300 mg (84.7%) reported PGI-C improvement relative to placebo (39.7%; both p < 0
243 roduction and is replenished by the reversed PGI reaction.
244 ess observed for the Deltamec/Deltamec/(RNAi)PGI double mutant when compared with the single mutants,
245 ta agonist GW501516 but not by the selective PGI(2) receptor agonist cicaprost.
246  graveolens L.) "sedano bianco di Sperlonga" PGI ecotype was investigated to obtain the metabolic pro
247 ation, short-tag pooled genomic indexing (ST-PGI), was also introduced to further improve the economy
248                         In the present study PGI-02776, a newly designed di-ester prodrug of the urea
249                               The subjective PGI-I scale was largely unchanged during both study peri
250 tecting against RSV-induced illness and that PGI(2) is a potential therapeutic target in the treatmen
251                             We conclude that PGI(2) exerts anti-inflammatory action by inhibiting STA
252 al of bacterial enzymes, we demonstrate that PGI-LysAP has broad exopeptidase activity which may enha
253 of PGI(2.) In this study, we determined that PGI(2) analogs modulate dendritic cell (DC) cytokine pro
254 hough there are many studies indicating that PGI/AMF has been implicated in progression of metastasis
255                    We therefore propose that PGI(2)-mediated upregulation of contractile proteins and
256                               We report that PGI(2) analogs (iloprost, cicaprost, treprostinil) diffe
257                           We now report that PGI-02776 (10mg/kg) is neuroprotective when administered
258                          We also report that PGI/AMF degradation is mainly regulated by the ubiquitin
259                 In vitro studies showed that PGI(2) did not affect IL-4 and IL-5 production or the le
260               Molecular analysis showed that PGI/AMF suppressed epithelial marker expressions and enh
261        Together, these findings suggest that PGI(2) plays a key immunoregulatory role by promoting th
262                  These findings suggest that PGI(2) signaling through the IP may exert anti-inflammat
263 Collectively, these experiments suggest that PGI(2), which is generated by endothelial cells during l
264 her, the results presented here suggest that PGI/AMF is involved in oxidative stress-induced cellular
265                      The data suggested that PGI veal has higher variability for most fatty acids tha
266 hese results suggest for the first time that PGI/AMF is a key gene to both EMT in the initiating step
267       Here we show, for the first time, that PGI/AMF overexpression led to an increase in the DNA-bin
268                                          The PGI(2) analogs decreased BMDC production of proinflammat
269                                          The PGI/AMF siRNA caused cells to change shape dramatically
270  finding that the COX product PGE(2) and the PGI(2) analogs cicaprost decreased Alternaria extract-in
271 hern Italy (Siracusa), have been awarded the PGI (Protected Geographical Indication) recognition as '
272 al 18 months of treatment as assessed by the PGI-I scale, with mean scores of 4.1 points [0.2] in the
273 ctive change was detected as assessed by the PGI-I scale: mean scores at month 18 were 4.6 points (SE
274 these effects were strongly inhibited by the PGI/AMF, VEGF, or VEGF receptor inhibitors.
275 rved in the thymus of naive mice lacking the PGI(2) receptor IP, as well as in the lungs during aller
276 ces, confirms this enzyme as a member of the PGI superfamily.
277 h muscle cells, similar to the effect of the PGI(2) analog iloprost.
278 deleted mice have shown that ablation of the PGI(2) receptor (the IP) predisposes to an exaggerated r
279               Intramedullary infusion of the PGI(2) receptor agonist increased urine volume and sodiu
280                     Although deletion of the PGI(2) receptor fosters atherogenesis, the importance of
281 f "much better" or "very much better" on the PGI-C.
282 ng that hypoxia-inducible VEGF regulates the PGI/AMF expression.
283 , with energies significantly lower than the PGI/PGII conformations characteristic of polyglycine str
284 nderlying such regulation, we found that the PGI(2) receptor, IP, is preferentially expressed by effe
285                        Signaling through the PGI(2) receptor (IP) has been shown to inhibit inflammat
286 he concentration and time of exposure to the PGI(2) analog iloprost and was blocked by both RO3244794
287                                        Those PGI/AMF siRNA-transfected cells showed epithelial phenot
288 n as the catalytic base in the eukaryal-type PGIs.
289 chanisms of these two structurally unrelated PGIs may be similar and based on an enediol intermediate
290 , we sought to define the effects of various PGI(2) analogs on resident alveolar macrophage (AM) and
291                              The vasodilator PGI(2) analog, cicaprost, increased Rap1 activity and de
292 enge remains to identify a mechanism whereby PGI(2) and PGE(2) expression can be suppressed while avo
293 s; however, the molecular mechanism by which PGI/AMF regulates EMT is not known.
294                Furthermore, tumor cells with PGI/AMF deficiency lost their abilities to form tumor ma
295 ification system to authenticate honeys with PGI.
296 se-14 (PARP-14) to be a binding partner with PGI/AMF.
297 an improvement in cognitive performance with PGI-02776 treatment.
298 ransfer of DO11.10 Th2 cells pretreated with PGI(2) resulted in considerably attenuated pulmonary inf
299 genous PGI/AMF, were stably transfected with PGI/AMF small interfering RNA (siRNA).
300 as markedly reduced following treatment with PGI(2), whereas IP-deficient Th2 cells were unaffected a

 
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