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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.
35 er to the 3-position lowered the affinity at A3 receptors 3-fold.
36 ctivity and stability of the human adenosine A3 receptor (A3) were investigated.
37 previous work, using a fluorescent adenosine-A3 receptor (A3AR) agonist and fluorescence correlation
38                                    Adenosine A3 receptor (A3AR) having an identical N-terminal region
39 tion and degranulation of mast cells via the A3 receptor (A3AR).
40                      Thus, adenosine A2B and A3 receptors act in a functional cooperative fashion to
41 eptors was employed as a functional index of A3 receptor activation.
42                                          The A3 receptor (ADORA3) was expressed only in mouse islets
43 etalloproteinase (MMP)2, MMP7, and adenosine A3 receptor (ADORA3).
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
46  BK-induced responses were unaffected by the A3 receptor agonist IB-MECA (1 microM).
47  2-chloro-N6-cyclopentyladenosine (CCPA) and A3 receptor agonist N6-(3-iodobenzyl)-adenosine-5'-N-met
48                             In addition, the A3 receptor agonist N6-(3-iodobenzyl)adenosine-5'-N-meth
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
55 it is natural to consider a link between the A3 receptor and eosinophils.
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.
58             Cardiac atrial cells lack native A3 receptors and exhibit a shorter duration of cardiopro
59 nd the compound is thus nonselective between A3 receptors and L-type Ca2+ channels.
60 44, displayed a Ki value of 7.94 nM at human A3 receptors and selectivity of 5200-fold.
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
67 ceptor antagonist CGS15943, but not by A1 or A3 receptor antagonists.
68 e signaling pathways activated by the A1 and A3 receptors are distinct and involve selective coupling
69                       Thus, adenosine A1 and A3 receptors are linked to different G-proteins.
70                       Since rodent adenosine A3 receptors are not blocked by theophylline, selective
71 he rat and human adenosine A1, A2A, A2B, and A3 receptors are presented.
72                                       Rodent A3 receptors are relatively insensitive to xanthines; in
73  early a3-subunit-containing GABA(A) (GABA(A)a3) receptors are a key developmental organizer.
74 upregulation; (2) the A2a, but not the A1 or A3, receptors are the major expressed and functionally c
75 peripheral blood eosinophils express the ADO A3 receptor as indicated by detection of the transcript
76 imidazo[2.1-i]pur in-5-one (PSB-11) from the A3 receptors, as well as [3H]N6-[(R)-phenylisopropyl]ade
77 ed the effects of an agonist in a functional A3 receptor assay, i.e. inhibition of adenylyl cyclase i
78 ), may be substituted with L (present in the A3 receptor) but not with D (in biogenic amine receptors
79 ic and electrostatic regions with the A1 and A3 receptors, but not the A2A.
80 nyl or 3-furyl group reduced the affinity at A3 receptors by 4- and 9-fold, respectively.
81 ding pyridine derivative reduced affinity at A3 receptors by 88-fold and slightly increased affinity
82                            A novel adenosine A3 receptor can mediate this protective function.
83            Also, increased expression of the A3 receptor caused an enhanced cardioprotective effect b
84 cells with cDNA encoding the human adenosine A3 receptor causes a sustained A3 agonist-mediated cardi
85 y transfected with the human adenosine A1 or A3 receptor cDNA individually or they were cotransfected
86 ene transfer and overexpression of the human A3 receptor cDNA, renders the myocytes resistant to the
87 at least two populations of agonist-occupied A3-receptor complexes, showing different motilities with
88 with xanthines allows selective detection of A3 receptors despite the lack of selectivity of the liga
89 degree of selectivity for cloned human brain A3 receptors, determined in competitive binding assays v
90 e protection mediated by prior activation of A3 receptors exhibits a significantly longer duration th
91 t of timing of hypertonic saline exposure on A3 receptor expression and degranulation was studied in
92 myl methionyl-leucyl-phenylalanine inhibited A3 receptor expression and degranulation, whereas hypert
93 l-leucyl-phenylalanine-stimulation augmented A3 receptor expression and degranulation.
94                 Polymorphonuclear neutrophil A3 receptors expression determines whether hypertonic sa
95 ence that semaphorins, activating the Plexin-A3 receptor, function as retraction inducers to trigger-
96 ine-2,4-dione derivatives as human adenosine A3 receptor (hA3R) antagonists to determine their kineti
97             In the CA1 region, activation of A3 receptors had no direct effects on synaptically evoke
98 ding of flavonoids to adenosine A1, A2A, and A3 receptors has been conducted using comparative molecu
99 enosine receptor subtypes, A1, A2A, A2B, and A3 receptors, have been cloned and characterized.
100                              At A1, A2A, and A3 receptors however the optimum occurs with four methyl
101 criminating hydrophobic region occurs in the A3 receptor in proximity to the N5-substituent.
102 pt that an increased expression of the human A3 receptor in the cardiac myocyte can be an important c
103 indicated by detection of the transcript for A3 receptors in polymerase chain reaction-amplified cDNA
104 d high specific activity, the low density of A3 receptors in rat brain appears insufficient to allow
105 ful for localization and characterization of A3 receptors in rat brain.
106                Therefore, involvement of ADO A3 receptors in the bronchoconstrictor and/or inflammato
107                                          The A3 receptor is coupled via RhoA to activate phospholipas
108                                The adenosine A3 receptor is expressed in brain, but the consequences
109 ovides the first evidence that the adenosine A3 receptor is present on ventricular myocytes and can m
110 way, suggesting that selective activation of A3 receptors is an effective means of protecting the isc
111              Thus, activation of both A1 and A3 receptors is required to mediate the cardioprotective
112 selective (approximately 200-fold) for human A3 receptors (Ki = 0.56 microM).
113 ertonic saline resuscitation was assessed in A3 receptor knockout and wild-type mice.
114                                 Mortality in A3 receptor knockout mice remained only 50% regardless o
115 ed hypertonic saline-treatment was absent in A3 receptor knockout mice.
116                 Here we investigated whether A3 receptors may diminish the efficacy of hypertonic sal
117 e affinity of flavones at both rat and human A3 receptors may explain some of the previously observed
118 y of neonatal mononuclear cells to adenosine A3 receptor-mediated accumulation of cAMP, a second mess
119 ominant negative RhoA (RhoAT19N) blocked the A3 receptor-mediated phospholipase D activation and card
120     I870R preferentially inhibited the human A3 receptor-mediated protection from ischemia.
121   The study indicates that cardiac adenosine A3 receptor mediates a sustained cardioprotective functi
122 s as TNF-alpha inhibitors suggested that the A3 receptor might be involved (N6-(3-iodobenzyl)-9-[5-(m
123 -356 nM), and heteromeric GluA1/A2 and GluA2/A3 receptors nonselectively, with IC(50) values in the m
124                                              A3 receptors on eosinophil membranes were characterized
125 These results attest to the existence of ADO A3 receptors on eosinophils and suggest that ADO stimula
126                                The effect of A3 receptors on the efficacy of hypertonic saline resusc
127 n the dissociation kinetics of 125I-ABA from A3 receptors or [125I]-[2-(4-amino-3-iodo-phenyl)ethylam
128                Activation of adenosine A1 or A3 receptors protects heart cells from ischemia-induced
129 ease and autocrine feedback through P2Y2 and A3 receptors provide signal amplification, controlling g
130 by > 95%, indicating that xanthine-resistant A3 receptors represent a quantitatively minor subtype.
131  Ki values of 41.3 and 1.90 microM at A1 and A3 receptors, respectively, and was inactive at A2A rece
132 hich was less potent than 27 at A1, A2A, and A3 receptors, retained moderate potency at A2B receptors
133 ibution of neural adenosine A1, A2a, A2b, or A3 receptors (Rs) in the human intestine was investigate
134 of the 6-phenyl substituent was tolerated in A3 receptor selective agents.
135                                The adenosine A3 receptor-selective antagonist 3-ethyl 5-benzyl-2-meth
136       Inclusion of a 6-phenyl group enhanced A3 receptor selectivity: Compound 28 (MRS1097; 3,5-dieth
137                                          The A3 receptor signals via RhoA and phospholipase D (PLD) t
138 ine (BW-A1433), an antagonist of A1, A2, and A3 receptors, significantly reduced the vasoconstrictor
139 eceptors with particular selectivity for the A3 receptor subtype.
140 led in myocytes cotransfected with the human A3 receptor than in those cells expressing the human A1
141  3-keto derivative was 5-fold more potent at A3 receptors than a related open-ring analogue.
142 ne ring, esters were much more selective for A3 receptors than closely related thioester, amide, and
143                                              A3 receptor transcript was substantially diminished, and
144 was determined at cloned human and rat brain A3 receptors using [125I]-AB-MECA [N6-(4-amino-3-iodoben
145      Affinity was determined at cloned human 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
147 inity was determined at cloned human and rat A3 receptors using [125I]AB-MECA [N6-(4-amino-3-iodobenz
148 one visnagin was 30-fold selective for human A3 receptors vs either rat A1 or A2A receptors.
149 o bind with 14-17-fold selectivity for human A3 receptors vs rat A1 and A2A receptors, with a Ki valu
150         A rhodopsin-based model of the human A3 receptor was built, and the pyridine reference ligand
151 umulation in intact cells that express human A3 receptors was employed as a functional index of A3 re
152 ioligand binding by BTH4 (7) at cloned human A3 receptors was negligible but one slightly A3 selectiv
153 , whereas messenger RNA expression of A1 and A3 receptors was reduced (both, p = .03).
154 erivative, 26, with a Ki value of 58.3 nM at A3 receptors, was > 1700-fold selective vs either A1 rec
155 tive, 24, with a Ki value of 0.670 microM at A3 receptors, was 24-fold selective vs A1 receptors (Ki
156 oned media was maximal if both HMC-1 A2B and A3 receptors were activated, whereas activation of A2B r
157 f the adenosine A1 receptor with CCPA or the A3 receptor with C1-IB-MECA can replace preconditioning
158                       However, activation of A3 receptors with Cl-IB-MECA antagonized the adenosine A
159 quinazolin-5-amine (CGS15943) binds to human A3 receptors with high affinity (Ki = 14 nM), while it l
160 ) binds nonselectively to human A1, A2A, and A3 receptors with high affinity.
161 lectron-withdrawing groups were specific for A3 receptors with nanomolar Ki values and selectivity as
162 derivative was the most potent derivative at A3 receptors, with a Ki value of 0.36 nM.
163 carboxylate , 38, was highly potent at human A3 receptors, with a Ki value of 20 nM.
164 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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