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1 NECA (10 microM) induced a 1.9 +/- 0.06-fold increase in
2 NECA activated ERK and CREB in HRECs.
3 NECA also increased insulin-like growth factor-I and bas
4 NECA and CGS21680 increased cAMP production within 10 mi
5 NECA and forskolin had no effect on AP-1 activation, c-j
6 NECA binding to GRP94 was efficiently blocked by geldana
7 NECA enhanced JunB binding to the murine VEGF promoter,
8 NECA enhanced tube formation on the matrix, whereas both
9 NECA failed to prevent cytokine-induced beta-cell death
10 NECA increases canine mastocytoma cell cAMP, Ca2+, and i
11 NECA induced proliferation in a concentration-dependent
12 NECA inhibited cytosolic protein phosphatase activity by
13 NECA inhibited diabetes in A2A receptor KO mice and the
14 NECA or N(6)-(2-iodo)benzyl-5'-N-methylcarboxamidodoaden
15 NECA stimulated chemotaxis in a concentration-dependent
16 NECA stimulation activates p38 mitogen-activated protein
17 NECA stimulation is blocked by the A3 AR antagonist 3-et
18 NECA, in parallel with the activation of ERK, also stimu
19 NECA-induced secretion of IL-8 and VEGF was verified by
20 NECA-stimulated degranulation is not prevented by pertus
21 NECA-treated BMDC also expressed reduced levels of MHC c
22 vating cells in the presence of IL-1, IL-1 + NECA, or IL-1 + forskolin and culturing cells in the pre
24 affect LPS-induced TNF-alpha and CXCL10; (4) NECA and CGS21680 similarly inhibited LPS-induced TNF-al
25 er (XAC), 5'-(N-ethyl carboxamido)adenosine (NECA), and adenosine, respectively] and reduced by coexp
26 hages with 5'-N-ethyl-carboxamido-adenosine (NECA), a nonselective adenosine A(2) receptor agonist, o
27 1 agonist), 5'-N-ethylcarboxamide adenosine (NECA) (10 muM; agonist for all adenosine receptor subtyp
28 agonist) and 5-N-ethylcarboxamide adenosine (NECA) (AdoRA2A/ADoRA2B agonist) inhibited LAK cell cytot
29 r CGS21680, 5'-N-ethylcarboxamido adenosine (NECA), UK432097 [6-(2,2-diphenylethylamino)-9-[(2R,3R,4S
30 or agonist 5'-(N-ethylcarboxamido)adenosine (NECA) and blocked by the adenosine receptor antagonist,
31 neither 5'-( N-ethylcarboxamido)-adenosine (NECA; activating the A2b adenosine receptor) nor prostag
32 ne analogue 5'-N-ethylcarboxamido-adenosine (NECA) in the absence or presence of AdoR antagonists.
33 cell surface SERT protein are elevated after NECA or sildenafil stimulation of AR/SERT-cotransfected
36 pts, only the nonselective adenosine agonist NECA (5'-N-ethylcarboxamidoadenosine), but not the selec
37 ffects of the nonselective adenosine agonist NECA, the relatively selective adenosine A2 agonist CV-1
38 ng regions for the 9H-purine ring in agonist NECA 3 and the 1H-[1,2,4]triazolo[1,5-c]quinazoline ring
39 n cooperativity with the orthosteric agonist NECA were different in PD81723 and VCP171; positive coop
43 he selective A(2)-adenosine receptor agonist NECA but not the A(1)-adenosine agonist CCPA replicated
44 The non-selective adenosine receptor agonist NECA effectively inhibited IAC by 79.3 +/- 2.9 % (n = 24
48 namics substantially differ between agonist (NECA) and inverse agonist (ZM241385) bound receptors, wi
50 popolysaccharide (LPS) and the A2AR agonists NECA and CGS21680 synergistically augment VEGF transcrip
51 boxamidoadenosine (NECA) >> N(6)-aminobenzyl-NECA approximately 2-chloroadenosine > 2-[4-(2-carboxyet
52 on of HMC-1 with the stable adenosine analog NECA (5'-N-ethylcarboxamidoadenosine) activated p21(ras)
53 n vitro, whereas the stable adenosine analog NECA [5'-(N-ethylcarboxamido)adenosine] downregulated ex
54 13 secretion induced by the adenosine analog NECA, but did not mimic the enhanced Ag-induced degranul
58 nduced TIMP-1 release, as both adenosine and NECA were less efficacious in augmenting TIMP-1 release
59 e anti-inflammatory effects of adenosine and NECA, which was lost in macrophages isolated from A2aR-d
63 ; positive cooperativity between PD81723 and NECA was reduced on alanine substitution of a number of
64 osine and the A3 receptor agonists N6-Benzyl-NECA and 1-deoxy-1-[6-[[(3-iodophenyl)methyl]amino]-9H-p
66 se (MAPK), whereas p38 MAPK inhibitors block NECA stimulation of SERT activity, as does the protein p
69 (50) < 10 ng/ml), but not of IFN-gamma, both NECA and CGS21680 synergistically up-regulate VEGF expre
70 Studies of mRNA half-life showed that both NECA and forskolin decreased the half-life of collagenas
72 tokine-induced beta-cell death in vitro, but NECA strongly suppressed expression of the proinflammato
75 GF 109203X failed to block ERK activation by NECA or UTP, however, another PKC inhibitor, Ro 31-8220,
78 (RTI-55) whole-cell binding is increased by NECA or sildenafil, and both surface binding and cell su
80 he down-regulation of Gi proteins induced by NECA treatment and was not associated with sustained or
82 mitogenic effect of adenosine is mimicked by NECA, CCPA, and R-PIA, but not by CGS21680and 2-Cl-IB-ME
84 )adenosine) > CHA (N6-cyclohexyladenosine) = NECA (5'-N-ethylcarboxamidoadenosine) > 2-CADO (2-chloro
85 , adenosine A2 receptor (A2R) agonists DPMA, NECA, and CGS21680 increased VEGF mRNA in a dose-depende
87 agonists was 5'-N-ethylcarboxamidoadenosine (NECA) > N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide
88 > N6 benzyl 5'-N-ethylcarboxamidoadenosine (NECA) > NECA > CGS21680 > N6-cyclohexyladenosine), and t
89 tency order: 5'-N-ethylcarboxamidoadenosine (NECA) >> N(6)-aminobenzyl-NECA approximately 2-chloroade
90 osine analog 5'-N-ethylcarboxamidoadenosine (NECA) (10 microM) increased mRNA expression of IL-1beta,
91 HEK-293 cells, N-ethylcarboxamidoadenosine (NECA) activates endogenous A2BARs that signal through Gs
92 tive agonist 5'-N-ethylcarboxamidoadenosine (NECA) but not by the A3-selective agonist N6-(3-iodobenz
93 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) decreased collagenase production by IL-1-stimulate
94 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) increased both arginase activity (EC(50)=261.8 nM)
95 sine agonist 5'-N-ethylcarboxamidoadenosine (NECA) increased expression of interleukin-8 (IL-8), basi
96 (AR) agonist 5'-N-ethylcarboxamidoadenosine (NECA) induces an increase in 5-HT uptake Vmax in rat bas
98 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) prevented diabetes development in both MLDS-challe
99 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) protected CD73(-/-) mice against T. gondii-induced
100 In this report, N-ethylcarboxamidoadenosine (NECA) was used to investigate the nucleotide binding pro
101 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) while cell activity was monitored with whole-cell
102 nstrate that 5'-N-ethylcarboxamidoadenosine (NECA), a nonspecific ADO analogue, and 2-p-(2-carbonyl-e
103 adenosine or 5'-N-ethylcarboxamidoadenosine (NECA), a stable adenosine analog, to modify the response
104 AR agonist, 5'-N-ethylcarboxamidoadenosine (NECA), at an early stage after immunization had an inhib
105 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA), in a concentration-dependent manner, increased bo
107 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA; IC50 = 30 nM; p < 0.0001, analysis of variance).
108 E-NECA], [3H]5'-N-ethylcarboxamidoadenosine [NECA], and R(-)N6-(2-phenylisopropyl)adenosine [R-PIA])
109 ptor agonist 5'-N-ethylcarboxamidoadensoine (NECA) increased fasting blood glucose and slowed glucose
110 ive agonist, N(6)-ethylcarboximidoadenosine (NECA, 0.03-0.1 micromol/kg, ip.), lowered 1-4 Hz amplitu
113 nzyl 5'-N-ethylcarboxamidoadenosine (NECA) > NECA > CGS21680 > N6-cyclohexyladenosine), and this was
118 2-hexynyl-5'-N-ethylcarboxamidoadenosine [HE-NECA], [3H]5'-N-ethylcarboxamidoadenosine [NECA], and R(
120 everal selective A(2B) antagonists inhibited NECA-stimulated calcium mobilization in HEK-A(2B) cells.
121 ntagonists, enprofylline and IPDX, inhibited NECA-stimulated proliferation, ERK activation, cell migr
123 es from the VEGF promoter did not affect LPS/NECA-induced VEGF promoter activity, suggesting that NF-
124 F expression is strongly up-regulated by LPS/NECA in macrophages from A(3)-/- but not A(2A)-/- mice,
125 Taken together, these data indicate that LPS/NECA-induced VEGF expression involves transcriptional re
126 acrophages in an NF-kappaB-dependent manner; NECA strongly increased these levels in an A2AR-dependen
127 s verified using RT-PCR and ELISA; 10 microM NECA increased IL-13 concentrations in HMC-1 conditioned
129 ersed the capacity of dibutyryl cAMP but not NECA to increase pp1 activity (p < 0.01, n = 5) in keepi
132 ses, whereas injection of the same amount of NECA at a late stage inhibited the Th1 response but had
134 ly dissociated, that the enhancing effect of NECA on Th17 responses was modulated by gammadelta T cel
138 R antagonist MRS1754 prevented the effect of NECA, we conclude that the stimulatory effect of adenosi
140 ermeant analog of cGMP, mimic the effects of NECA on 5-HT uptake, whereas the protein kinase G (PKG)
146 e with K(I) determinations for inhibition of NECA-stimulated cAMP accumulation in HEK-A(2B) cells.
153 ith extremely high concentrations of CADO or NECA, mild inhibition of LAK cytotoxicity was observed t
156 ) agonist 2-p-(2-carboxyethyl)phenethylamino-NECA nor the selective A(3) agonist N(6)-(3-iodobenzyl)-
158 agonist 2-p-(2-carboxyethyl)phenylethylamino-NECA (CGS 21680) had no effect on expression of these an
161 hanism of action was pre-translational since NECA decreased collagenase, but not stromelysin or tissu
162 The findings of this study demonstrate that NECA and forskolin decrease collagenase gene expression
164 -/-) and A(2B)AR(-/-)mice, it was shown that NECA modulates TNF-alpha, IL-12, IL-10, and CD86 respons
167 channel blocker rTertiapin-Q diminished the NECA-evoked inhibitory current by 56 +/- 12%, whereas th
172 Moreover, a decrease in cAMP levels upon NECA stimulation of naive macrophages was counterbalance
173 AR agonists in inducing IL-10 production was NECA > IB-MECA > CCPA >/= CGS21680, and the A(2B)AR anta
175 an B lymphocytes cocultured for 12 days with NECA-stimulated HMC-1 produced 870 +/- 33 pg IgE per 10(
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