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1  develop allosteric potentiators of this key prostaglandin receptor.
2 cy by inactivating the gene encoding the EP2 prostaglandin receptor.
3  activate nociceptive neurons independent of prostaglandin receptors.
4 uced by PGF2alpha is mediated by FP or other prostaglandin receptors.
5  and antisense primers for each of the three prostaglandin receptors.
6 onsistent with the proposed phylogeny of the prostaglandin receptors.
7 ed as having anticancer activity that target prostaglandin receptors.
8 ased COX-2 in H9c2 cells, which also express prostaglandin receptors.
9 mine whether prostaglandin E2 (PGE2), E-type prostaglandin receptor 2 (EP2), and NADPH oxidase 2 (NOX
10 demonstrating the first intersection between prostaglandin receptor activation and NFAT signaling.
11                                          EP2 prostaglandin receptor activation with butaprost blocks
12  we added recombinant GDF-9, prostaglandins, prostaglandin receptor agonists, or cyclooxygenase inhib
13 or off-target activation observed with other prostaglandin receptor agonists.
14 he enhancement is not prevented by AH6809, a prostaglandin receptor antagonist, but is blocked by cap
15 ts is probably dependent on which downstream prostaglandin receptors are activated.
16                                      Because prostaglandin receptors are known to undergo ligand-indu
17 ronotropic mechanisms such as muscarinic and prostaglandin receptor binding, stretch, extracelluar Ca
18            Blockade of G-protein-coupled EP4 prostaglandin receptor by AH 23848 prevented LPS-induced
19 e fashion by a pathway involving EP2 and EP4 prostaglandin receptors, cyclooxygenase-2-dependent reac
20 gs demonstrate that COX-2 and its downstream prostaglandin receptor EP(1) signaling pathway accelerat
21 ceptors have been described, termed E-series prostaglandin receptors (EP(1)-EP(4)), that can be furth
22                                 Blocking the prostaglandin receptor, EP(1), prevented LPS/d-GalN-indu
23                 Our results suggest that the prostaglandin receptor EP2 is critically involved in neu
24  subjects, there is a surprising lack of the prostaglandin receptor EP2 on Th17 cells; therefore, we
25 PGE2, most likely by signaling through the E prostaglandin receptor EP2, reduces radiation-induced ap
26  human purified naive T cells, PGE2 acts via prostaglandin receptor EP2- and EP4-mediated signaling a
27 well as concomitant downstream expression of prostaglandin receptors EP2 and EP3a1.
28 GE2) on the brain and appears to require EP3 prostaglandin receptors (EP3Rs), but the specific neuron
29                    The administration of the prostaglandin receptor EP4 antagonist AE3-208 (10 mg/kg
30 , these results demonstrate a novel role for prostaglandin receptor EP4 in the mediation of barrier-e
31 isome proliferator-activated receptor delta, prostaglandin receptor EP4, and c-myc), each containing
32 pha (FP), thromboxane A2 (TP)] suggests that prostaglandin receptors evolved functionally from an anc
33 on reflects involvement of G protein-coupled prostaglandin receptors expressed by mucosal epithelial
34 amily have been evaluated at the eight human prostaglandin receptors for potential use in the treatme
35 mmation and injury, although the responsible prostaglandin receptors have not been fully identified.
36                                  Lastly, EP4 prostaglandin receptor inhibitor GW627368 pretreatment i
37 A activator 6-benzoyl-cAMP, and agonists for prostaglandin receptors IP, EP2, and EP4 in infected but
38 ibe a mechanism in which Epac2 activation by prostaglandin receptors leads to phosphorylation of pyru
39 e the role of the extracellular sequences in prostaglandin receptor-ligand interaction, chimeras were
40                                              Prostaglandin receptors may be activated by their cognat
41 bitors of cyclooxygenase-2 or antagonists of prostaglandin receptors may have therapeutic potential f
42 o restore both of the high- and low-affinity prostaglandin receptor numbers to within normal ranges i
43                     Targeting of the nuclear prostaglandin receptor peroxisome proliferator-activated
44 (COX-2) inhibitors for inflammatory disease, prostaglandin receptors provide alternative targets for
45 scular effects of antagonists for individual prostaglandin receptors remain uncharacterized.
46          Pharmacologic inhibition of EP2/EP4 prostaglandin receptor signaling or WNT ligand secretion
47                      Endogenous G(s)-coupled prostaglandin receptors stimulated PRG binding to membra
48 uggest that isoPGE2 effects were mediated by prostaglandin receptor subtypes EP2/DP on preosteoclasts
49 ty ratio for the hFP receptor over the other prostaglandin receptors tested.
50  support the concept of targeting protective prostaglandin receptors therapeutically after stroke.
51 , acts in an autocrine/paracrine fashion via prostaglandin receptors to activate G alpha s and increa
52 ding evidence that these cells express EP(4) prostaglandin receptors, which are known to activate G(s
53 hey act mainly via plasma membrane localized prostaglandin receptors, which belong to the G-protein c