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1 a modulator of cell growth (mainly acting at A3 receptors).
2 ture MDDCs as native expressers of the human A3 receptor.
3 AB-MECA binding confirmed the site to be the A3 receptor.
4 e is not coupled to the xanthine-insensitive A3 receptor.
5 e cardioprotective role of a novel adenosine A3 receptor.
6 ting the presence of phospholipase C-coupled A3 receptors.
7 e, genistein, also bound only very weakly at A3 receptors.
8 receptors, respectively, and 3.0 nM at human A3 receptors.
9 m intracellular stores via the activation of A3 receptors.
10 thesized and found to be selective for human A3 receptors.
11 ed to arginine, the homologous amino acid in A3 receptors.
12 dioligands to recombinant canine A1, A2A, or A3 receptors.
13 t A1 and A2A receptors and 3 microM at human A3 receptors.
14 wed 14-fold greater affinity at human vs rat A3 receptors.
15 r affinity but 15-fold selectivity for human A3 receptors.
16 tors, respectively, and 3.25 microM at human A3 receptors.
17 increased selectivity of flavonols for human A3 receptors.
18 (Ki = 14 nM), while it lacks affinity at rat A3 receptors.
19 , had Ki values of 0.3 - 0.4 microM at human A3 receptors.
20 5-ethyl diester was > 600-fold selective for A3 receptors.
21 l cyclase in CHO cells expressing cloned rat A3 receptors.
22 its complete selectivity toward A1, A2A, and A3 receptors.
23 the anti-ischemic effect of adenosine A1 and A3 receptors.
24 chieve the anti-ischemic effect of adenosine A3 receptors.
25 Neither cells expressed A1 or A3 receptors.
26 selective enhancement of agonist binding at A3 receptors.
27 effect that is mediated by adenosine A1 and A3 receptors.
28 and which had a Ki value of 248 nM at human A3 receptors.
29 yl analogue was clearly less potent at human A3 receptors.
30 to enhance potency and selectivity at human A3 receptors.
31 gues were nearly equipotent at rat and human A3 receptors.
32 1 and A2A receptors and at recombinant human A3 receptors.
33 measurable affinity at adenosine A1, A2A, or A3 receptors.
34 ne) has high affinity for recombinant A1 and A3 receptors.
37 previous work, using a fluorescent adenosine-A3 receptor (A3AR) agonist and fluorescence correlation
44 oropropyl ester (26) was favorable for human A3 receptor affinity, resulting in Ki values of 4.2 and
45 nophils with the highly potent and selective A3 receptor agonist CI-IB-MECA clearly induced Ca2+ rele
47 2-chloro-N6-cyclopentyladenosine (CCPA) and A3 receptor agonist N6-(3-iodobenzyl)-adenosine-5'-N-met
49 ophil membranes were characterized using the A3 receptor agonist radioligand 125I-labeled AB-MECA, wh
50 terized the actions of a selective adenosine A3 receptor agonist, 2-chloro-N6-(3-lodobenzyl)-adenosin
51 lopentyladenosine and not with the selective A3-receptor agonist 4-aminobenzyl-5'-N methylcarboxamido
52 t of the concentration-response curve of the A3 receptor agonists in the presence of antagonist and,
53 ist 2-Chloro-N6-cyclopentyladenosine and the A3 receptor agonists N6-Benzyl-NECA and 1-deoxy-1-[6-[[(
54 ryonic kidney 293 cells expressing the human A3 receptor and a chimeric Galphaq-i3 protein, which was
56 ocytes with enhanced expression of the human A3 receptor and showed significantly higher ATP content,
57 tive, 28, displayed a Ki value of 31.4 nM at A3 receptors and 1300-fold selectivity vs A1 receptors.
61 poxia, ischemia, or seizures), activation of A3 receptors and subsequent heterologous desensitization
62 displayed a Ki value of 4.8 microM at human A3 receptors and was inactive at rat A1/A2a receptors.
63 13, displayed a Ki value of 0.59 nM at human A3 receptors and was moderately selective for that subty
64 antagonists of competitive binding at human A3 receptors, and K(i) values ranging from 120 nM to 101
65 , 3, which had a Ki value of 7.7 nM at human A3 receptors, and was 40- and 14-fold selective vs rat A
66 ethyluronamide (Cl-IB-MECA), and a selective A3 receptor antagonist, 3-ethyl-5-benzyl-2-methyl-4-phen
68 e signaling pathways activated by the A1 and A3 receptors are distinct and involve selective coupling
73 upregulation; (2) the A2a, but not the A1 or A3, receptors are the major expressed and functionally c
74 peripheral blood eosinophils express the ADO A3 receptor as indicated by detection of the transcript
75 imidazo[2.1-i]pur in-5-one (PSB-11) from the A3 receptors, as well as [3H]N6-[(R)-phenylisopropyl]ade
76 ed the effects of an agonist in a functional A3 receptor assay, i.e. inhibition of adenylyl cyclase i
77 ), may be substituted with L (present in the A3 receptor) but not with D (in biogenic amine receptors
80 ding pyridine derivative reduced affinity at A3 receptors by 88-fold and slightly increased affinity
83 cells with cDNA encoding the human adenosine A3 receptor causes a sustained A3 agonist-mediated cardi
84 y transfected with the human adenosine A1 or A3 receptor cDNA individually or they were cotransfected
85 ene transfer and overexpression of the human A3 receptor cDNA, renders the myocytes resistant to the
86 at least two populations of agonist-occupied A3-receptor complexes, showing different motilities with
87 with xanthines allows selective detection of A3 receptors despite the lack of selectivity of the liga
88 degree of selectivity for cloned human brain A3 receptors, determined in competitive binding assays v
89 e protection mediated by prior activation of A3 receptors exhibits a significantly longer duration th
90 t of timing of hypertonic saline exposure on A3 receptor expression and degranulation was studied in
91 myl methionyl-leucyl-phenylalanine inhibited A3 receptor expression and degranulation, whereas hypert
94 ence that semaphorins, activating the Plexin-A3 receptor, function as retraction inducers to trigger-
95 ine-2,4-dione derivatives as human adenosine A3 receptor (hA3R) antagonists to determine their kineti
97 ding of flavonoids to adenosine A1, A2A, and A3 receptors has been conducted using comparative molecu
101 pt that an increased expression of the human A3 receptor in the cardiac myocyte can be an important c
102 indicated by detection of the transcript for A3 receptors in polymerase chain reaction-amplified cDNA
103 d high specific activity, the low density of A3 receptors in rat brain appears insufficient to allow
108 ovides the first evidence that the adenosine A3 receptor is present on ventricular myocytes and can m
109 way, suggesting that selective activation of A3 receptors is an effective means of protecting the isc
116 e affinity of flavones at both rat and human A3 receptors may explain some of the previously observed
117 y of neonatal mononuclear cells to adenosine A3 receptor-mediated accumulation of cAMP, a second mess
118 ominant negative RhoA (RhoAT19N) blocked the A3 receptor-mediated phospholipase D activation and card
120 The study indicates that cardiac adenosine A3 receptor mediates a sustained cardioprotective functi
121 s as TNF-alpha inhibitors suggested that the A3 receptor might be involved (N6-(3-iodobenzyl)-9-[5-(m
122 -356 nM), and heteromeric GluA1/A2 and GluA2/A3 receptors nonselectively, with IC(50) values in the m
124 These results attest to the existence of ADO A3 receptors on eosinophils and suggest that ADO stimula
126 n the dissociation kinetics of 125I-ABA from A3 receptors or [125I]-[2-(4-amino-3-iodo-phenyl)ethylam
128 ease and autocrine feedback through P2Y2 and A3 receptors provide signal amplification, controlling g
129 by > 95%, indicating that xanthine-resistant A3 receptors represent a quantitatively minor subtype.
130 Ki values of 41.3 and 1.90 microM at A1 and A3 receptors, respectively, and was inactive at A2A rece
131 hich was less potent than 27 at A1, A2A, and A3 receptors, retained moderate potency at A2B receptors
132 ibution of neural adenosine A1, A2a, A2b, or A3 receptors (Rs) in the human intestine was investigate
137 ine (BW-A1433), an antagonist of A1, A2, and A3 receptors, significantly reduced the vasoconstrictor
139 led in myocytes cotransfected with the human A3 receptor than in those cells expressing the human A1
141 ne ring, esters were much more selective for A3 receptors than closely related thioester, amide, and
143 was determined at cloned human and rat brain A3 receptors using [125I]-AB-MECA [N6-(4-amino-3-iodoben
144 Affinity was determined at cloned human A3 receptors using [125I]AB-MECA (N6-(4-amino-3-iodobenz
145 inity was determined at cloned human and rat A3 receptors using [125I]AB-MECA [N6-(4-amino-3-iodobenz
146 inity was determined at cloned human and rat A3 receptors using [125I]AB-MECA [N6-(4-amino-3-iodobenz
148 o bind with 14-17-fold selectivity for human A3 receptors vs rat A1 and A2A receptors, with a Ki valu
150 umulation in intact cells that express human A3 receptors was employed as a functional index of A3 re
151 ioligand binding by BTH4 (7) at cloned human A3 receptors was negligible but one slightly A3 selectiv
153 erivative, 26, with a Ki value of 58.3 nM at A3 receptors, was > 1700-fold selective vs either A1 rec
154 tive, 24, with a Ki value of 0.670 microM at A3 receptors, was 24-fold selective vs A1 receptors (Ki
155 oned media was maximal if both HMC-1 A2B and A3 receptors were activated, whereas activation of A2B r
156 f the adenosine A1 receptor with CCPA or the A3 receptor with C1-IB-MECA can replace preconditioning
158 quinazolin-5-amine (CGS15943) binds to human A3 receptors with high affinity (Ki = 14 nM), while it l
160 lectron-withdrawing groups were specific for A3 receptors with nanomolar Ki values and selectivity as
163 tive and highly potent at both human and rat A3 receptors, with Ki values of 18.9 and 113 nM, respect
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