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1 tential mediator of angiogenesis through the A2B receptor.
2 eptor other than A1, A2A or A3, possibly the A2B receptor.
3 cutely isolated astrocytes is coupled to the A2B receptor.
4 t the effect is likely to be mediated by the A2b receptor.
5 which was prevented by blockade of adenosine A2B receptors.
6 receptors and HMEC-1 preferentially express A2B receptors.
7 xanthine 3 was >13-fold more potent at human A2B receptors.
8 a pA2 value of 8.0 but was not selective for A2B receptors.
9 d A3 receptors, retained moderate potency at A2B receptors.
10 c fibroblast proliferation via activation of A2B receptors.
11 A2A receptors and suggested a major role for A2B receptors.
14 y of p73 to upregulate the expression of the A2B receptor, a recently characterized p53 target that e
19 ular permeability occurred through adenosine A2B receptor activation and was accompanied by a paralle
22 roarray analysis revealed that the adenosine A2B receptor (AdoRA2B) is selectively up-regulated by hy
28 ing pathway: both treatments act through the A2b receptor and specifically activate the Epac1/RapGef3
29 ol-induced hepatic steatosis via both A1 and A2B receptors and suggest that targeting adenosine recep
30 human mast cell line HMC-1 expresses A2A and A2B receptors, and that both receptors activate adenylat
32 ne mimicked the effect of MTX, and adenosine A2b receptor antagonist (3,7-dimethyl-1-propargylxanthin
34 effect of NECA was reversed by the selective A2B receptor antagonist N-(4-cyanophenyl)-2-[4-(2,3,6,7-
35 ar accumulation, which were inhibited by the A2B receptor antagonist PSB603 [(8-[4-[4-((4-chlorophenz
36 2A receptor antagonist), but not by MRS1754 (A2B receptor antagonist), and it was mimicked by the A2A
39 tial therapeutic implications given that A2A/A2B receptor antagonists have already entered clinical t
42 enylate cyclase via Gs-protein but that only A2B receptors are also coupled to phospholipase C via Gq
43 al cancer (DCC), neogenin, and the adenosine A2b receptor] are expressed by the fetal mucosal epithel
45 the 3-position favored affinity at the human A2B receptor, as indicated by 1-allyl-3-methyl-8-phenylx
47 a luciferase reporter in HMEC-1 showed that A2B receptors, but not A1, A2A, or A3, activated IL-8 an
48 athophysiological conditions, the purinergic A2b receptor can regulate cell motility, but the underly
49 er ovary cells stably transfected with human A2B receptor cDNA, inhibition of agonist-induced cyclic
52 ntracellular signaling, we demonstrated that A2B receptor-dependent accumulation of JunB protein and
53 PK pathways are essential steps in adenosine A2B receptor-dependent stimulation of IL-8 production in
54 s, our data suggest an important role of the A2B receptor-dependent upregulation of JunB in VEGF prod
58 To better understand the regulation of the A2b receptor in intestinal epithelia, we studied the eff
59 report increased expression of the adenosine A2b receptor in meniscus cells after stimulation at the
64 otective effects of HPC are negated when the A2B receptor is nonfunctional, the hypoxia-->adenosine--
65 enal perfusion by endothelial cell adenosine A2B receptors is antagonized by adenosine reuptake into
67 f Sca-1(+)CD31(-) cells generated from WT or A2B receptor knockout (A2BKO) mice or the same volume of
69 ther apical or basolateral adenosine induces A2b receptor-mediated increase in IL-6 secretion, which
70 indings demonstrate that inosine acts via an A2B receptor-mediated pathway that impinges on specific
73 ribozyme that would specifically cleave the A2B receptor mRNA and examine its effect on retinal angi
74 the plasmid expressing the ribozyme reduced A2B receptor mRNA levels by 45+/-4.8% (P=5.1x10(-5)).
75 lls were transfected with these plasmids and A2B receptor mRNA levels were determined by quantitative
76 Ribozymes specific for the mouse and human A2B receptor mRNAs were designed and cloned in expressio
80 is nonfunctional, the hypoxia-->adenosine-->A2B receptor pathway plays a critical role in the preven
86 ituted in the 1-, 3-, 7-, and 8-positions as A2B receptor-selective antagonists have been identified.
87 in expression or membrane recruitment of the A2b receptor, shown to be essential for its function.
88 actors, we hypothesized that ablation of the A2B receptor signaling in these cells would reduce their
90 sine agonist, the desensitization of A2a and A2b receptor-stimulated adenylyl cyclase in dominant neg
91 lls, the rates of desensitization of A2a and A2b receptor-stimulated adenylyl cyclase were markedly s
93 oalkylacyl derivatives demonstrated that for A2B receptors the optimal chain length occurs with three
95 ses (PDEs) confines cAMP generated by apical A2B receptors to a microdomain that includes the CFTR ch
96 product of ATP hydrolysis by ENTPD, acts via A2B receptors to counterbalance the pro-fibrotic respons
99 current study, we tested the hypothesis that A2B receptors upregulate JunB, which can contribute to s
100 king ecto-5'-nucleotidase or adenosine A1 or A2B receptors were protected from developing fatty liver
101 osine A2A receptor; 12-fold versus adenosine A2B receptor) with improved oral efficacy in the rat diu
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