ライフサイエンスコーパス: NECA

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

23 inding of the radioligands [3H]CGS21680, [3H]NECA, and [3H]XAC.

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 s identified 5'N-ethylcarboxamido adenosine (NECA) as a Grp94-selective ligand.

30 r CGS21680, 5'-N-ethylcarboxamido adenosine (NECA), UK432097 [6-(2,2-diphenylethylamino)-9-[(2R,3R,4S

31 or agonist 5'-(N-ethylcarboxamido)adenosine (NECA) and blocked by the adenosine receptor antagonist,

32 neither 5'-( N-ethylcarboxamido)-adenosine (NECA; activating the A2b adenosine receptor) nor prostag

33 ne analogue 5'-N-ethylcarboxamido-adenosine (NECA) in the absence or presence of AdoR antagonists.

34 cell surface SERT protein are elevated after NECA or sildenafil stimulation of AR/SERT-cotransfected

35 bited VEGF protein production by HRECs after NECA stimulation.

36 The adenosine agonist NECA (100 micromol/L) increased interleukin-8 (IL-8), va

37 pts, only the nonselective adenosine agonist NECA (5'-N-ethylcarboxamidoadenosine), but not the selec

38 ffects of the nonselective adenosine agonist NECA, the relatively selective adenosine A2 agonist CV-1

39 ng regions for the 9H-purine ring in agonist NECA 3 and the 1H-[1,2,4]triazolo[1,5-c]quinazoline ring

40 n cooperativity with the orthosteric agonist NECA were different in PD81723 and VCP171; positive coop

41 the nonselective adenosine receptor agonist NECA (5'-N-ethylcarboxamidoadenosine).

42 reated with the general Ado receptor agonist NECA and abolished by Ado receptor antagonists.

43 s mimicked by the adenosine receptor agonist NECA and the A2B receptor agonist BAY60-6583.

44 he selective A(2)-adenosine receptor agonist NECA but not the A(1)-adenosine agonist CCPA replicated

45 The non-selective adenosine receptor agonist NECA effectively inhibited IAC by 79.3 +/- 2.9 % (n = 24

46 The adenosine receptor agonist NECA inhibited interferon-gamma and stimulated interleuk

47 agonist adenosine and the synthetic agonist NECA.

48 antagonist MRS 1220, but not by the agonist NECA (up to 300 nM), consistent with labeling of R.

49 namics substantially differ between agonist (NECA) and inverse agonist (ZM241385) bound receptors, wi

50 cacy to the reference high efficacy agonist, NECA, in an assay of ERK1/2 phosphorylation assay.

51 popolysaccharide (LPS) and the A2AR agonists NECA and CGS21680 synergistically augment VEGF transcrip

52 n microscopy of A(2B)R bound to its agonists NECA and BAY60-6583, each coupled to an engineered G(s)

53 boxamidoadenosine (NECA) >> N(6)-aminobenzyl-NECA approximately 2-chloroadenosine > 2-[4-(2-carboxyet

54 ng-assisted enzymatic cascade amplification (NECA) comprises an on-loop amplification reaction using

55 on of HMC-1 with the stable adenosine analog NECA (5'-N-ethylcarboxamidoadenosine) activated p21(ras)

56 n vitro, whereas the stable adenosine analog NECA [5'-(N-ethylcarboxamido)adenosine] downregulated ex

57 13 secretion induced by the adenosine analog NECA, but did not mimic the enhanced Ag-induced degranul

58 Adenosine and NECA also stimulated gap junctional intercellular commun

59 Adenosine and NECA markedly induced HO-1 and blocked LPS-induced TNF-a

60 rence abrogated the effects of adenosine and NECA on TNF-alpha.

61 nduced TIMP-1 release, as both adenosine and NECA were less efficacious in augmenting TIMP-1 release

62 A(2B)R recognizes its ligands adenosine and NECA with relatively low affinity, but the detailed mech

63 e anti-inflammatory effects of adenosine and NECA, which was lost in macrophages isolated from A2aR-d

64 he inhibitory effects of adenosine, CADO and NECA.

65 Hypoxia and NECA increased VEGF protein secretion 4.7 times, whereas

66 Adenosine (EC50: 0.5 microM) and NECA (universal adenosine receptor agonist; EC50 0.1 mic

67 ; positive cooperativity between PD81723 and NECA was reduced on alanine substitution of a number of

68 osine and the A3 receptor agonists N6-Benzyl-NECA and 1-deoxy-1-[6-[[(3-iodophenyl)methyl]amino]-9H-p

69 Whereas Hsp90 did not bind NECA, GRP94 bound NECA in a saturable manner with a K(d)

70 se (MAPK), whereas p38 MAPK inhibitors block NECA stimulation of SERT activity, as does the protein p

71 ethy]-5-isoquinoline-sulfonamide (H8) blocks NECA, hydroxylamine, and 8-bromo-cGMP effects.

72 Whereas p38 MAPK inhibition blocks NECA stimulation of 5-HT activity, it fails to blunt sti

73 (50) < 10 ng/ml), but not of IFN-gamma, both NECA and CGS21680 synergistically up-regulate VEGF expre

74 Studies of mRNA half-life showed that both NECA and forskolin decreased the half-life of collagenas

75 Whereas Hsp90 did not bind NECA, GRP94 bound NECA in a saturable manner with a K(d) of 200 nm.

76 tokine-induced beta-cell death in vitro, but NECA strongly suppressed expression of the proinflammato

77 regulated kinase 1/2 (ERK), are activated by NECA and UTP.

78 ERK activation by NECA or UTP is unaffected by a tyrosine kinase inhibitor

79 GF 109203X failed to block ERK activation by NECA or UTP, however, another PKC inhibitor, Ro 31-8220,

80 0 ligand on HMC-1 surface was not altered by NECA.

81 antagonists diminished activation of ERK by NECA exposure.

82 (RTI-55) whole-cell binding is increased by NECA or sildenafil, and both surface binding and cell su

83 Cyclic AMP levels were increased by NECA, and a direct adenylate cyclase activator (forskoli

84 he down-regulation of Gi proteins induced by NECA treatment and was not associated with sustained or

85 This effect is fully mimicked by NECA (nonselective agonist), largely mimicked by CCPA (A

86 mitogenic effect of adenosine is mimicked by NECA, CCPA, and R-PIA, but not by CGS21680and 2-Cl-IB-ME

87 ncrease in intracellular calcium produced by NECA.

88 clopentyl 5'-N-ethylcarboxamidoadenosine (CP-NECA) were synthesized, and their potency and selectivit

89 )adenosine) > CHA (N6-cyclohexyladenosine) = NECA (5'-N-ethylcarboxamidoadenosine) > 2-CADO (2-chloro

90 s, with N(6)-2-(3-bromobenzyloxy)cyclopentyl-NECA and N(6)-2-(3-methoxyphenoxy)cyclopentyl-NECA showi

91 ECA and N(6)-2-(3-methoxyphenoxy)cyclopentyl-NECA showing ~1500-fold improved A(1)R selectivity compa

92 , adenosine A2 receptor (A2R) agonists DPMA, NECA, and CGS21680 increased VEGF mRNA in a dose-depende

93 of existing surface SERTs fails to eliminate NECA stimulation of SERT.

94 agonists was 5'-N-ethylcarboxamidoadenosine (NECA) > N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide

95 > N6 benzyl 5'-N-ethylcarboxamidoadenosine (NECA) > NECA > CGS21680 > N6-cyclohexyladenosine), and t

96 tency order: 5'-N-ethylcarboxamidoadenosine (NECA) >> N(6)-aminobenzyl-NECA approximately 2-chloroade

97 osine analog 5'-N-ethylcarboxamidoadenosine (NECA) (10 microM) increased mRNA expression of IL-1beta,

98 HEK-293 cells, N-ethylcarboxamidoadenosine (NECA) activates endogenous A2BARs that signal through Gs

99 tive agonist 5'-N-ethylcarboxamidoadenosine (NECA) but not by the A3-selective agonist N6-(3-iodobenz

100 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) decreased collagenase production by IL-1-stimulate

101 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) increased both arginase activity (EC(50)=261.8 nM)

102 sine agonist 5'-N-ethylcarboxamidoadenosine (NECA) increased expression of interleukin-8 (IL-8), basi

103 (AR) agonist 5'-N-ethylcarboxamidoadenosine (NECA) induces an increase in 5-HT uptake Vmax in rat bas

104 sine agonist 5'-N-ethylcarboxamidoadenosine (NECA) or the adenylate cyclase activator forskolin.

105 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) prevented diabetes development in both MLDS-challe

106 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) protected CD73(-/-) mice against T. gondii-induced

107 In this report, N-ethylcarboxamidoadenosine (NECA) was used to investigate the nucleotide binding pro

108 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) while cell activity was monitored with whole-cell

109 nstrate that 5'-N-ethylcarboxamidoadenosine (NECA), a nonspecific ADO analogue, and 2-p-(2-carbonyl-e

110 adenosine or 5'-N-ethylcarboxamidoadenosine (NECA), a stable adenosine analog, to modify the response

111 AR agonist, 5'-N-ethylcarboxamidoadenosine (NECA), at an early stage after immunization had an inhib

112 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA), in a concentration-dependent manner, increased bo

113 gonist [(3)H]5'-N-ethylcarboxamidoadenosine (NECA).

114 ptor agonist 5'-N-ethylcarboxamidoadenosine (NECA; IC50 = 30 nM; p < 0.0001, analysis of variance).

115 E-NECA], [3H]5'-N-ethylcarboxamidoadenosine [NECA], and R(-)N6-(2-phenylisopropyl)adenosine [R-PIA])

116 ptor agonist 5'-N-ethylcarboxamidoadensoine (NECA) increased fasting blood glucose and slowed glucose

117 ive agonist, N(6)-ethylcarboximidoadenosine (NECA, 0.03-0.1 micromol/kg, ip.), lowered 1-4 Hz amplitu

118 Finally, NECA-dependent VEGF secretion and reporter activity were

119 Conditioned media from NECA-activated HMC-1 stimulated human umbilical vein end

120 nzyl 5'-N-ethylcarboxamidoadenosine (NECA) > NECA > CGS21680 > N6-cyclohexyladenosine), and this was

121 SCH58261 > HE-NECA = CSC = CGS 21680 = XAC > NECA = R-PIA.

122 In [(3)H]NECA displacement assays, GRP94 displayed binding intera

123 ation of another radiolabeled agonist, [(3)H]NECA, from the receptor.

124 On the other hand, NECA and CGS-21680 dose-dependently potentiated the prod

125 2-hexynyl-5'-N-ethylcarboxamidoadenosine [HE-NECA], [3H]5'-N-ethylcarboxamidoadenosine [NECA], and R(

126 opropyl)adenosine [R-PIA]) was SCH58261 > HE-NECA = CSC = CGS 21680 = XAC > NECA = R-PIA.

127 everal selective A(2B) antagonists inhibited NECA-stimulated calcium mobilization in HEK-A(2B) cells.

128 ntagonists, enprofylline and IPDX, inhibited NECA-stimulated proliferation, ERK activation, cell migr

129 LPS/NECA treatment also increased HIF-1alpha protein and DNA

130 es from the VEGF promoter did not affect LPS/NECA-induced VEGF promoter activity, suggesting that NF-

131 F expression is strongly up-regulated by LPS/NECA in macrophages from A(3)-/- but not A(2A)-/- mice,

132 Taken together, these data indicate that LPS/NECA-induced VEGF expression involves transcriptional re

133 acrophages in an NF-kappaB-dependent manner; NECA strongly increased these levels in an A2AR-dependen

134 s verified using RT-PCR and ELISA; 10 microM NECA increased IL-13 concentrations in HMC-1 conditioned

135 lag and hydrodynamic size increase of MNPs, NECA-based target quantification provided a wide dynamic

136 d collagenase promoter activity, and neither NECA nor forskolin blocked this action.

137 ersed the capacity of dibutyryl cAMP but not NECA to increase pp1 activity (p < 0.01, n = 5) in keepi

138 the zeta-isoform, and prevents UTP- but not NECA-induced ERK activation.

139 The stimulatory action of NECA, a non-selective analogue, was blocked neither by t

140 ses, whereas injection of the same amount of NECA at a late stage inhibited the Th1 response but had

141 that cAMP mediates the inhibitory effect of NECA on collagenase production.

142 ly dissociated, that the enhancing effect of NECA on Th17 responses was modulated by gammadelta T cel

143 es, indicating that the beneficial effect of NECA was due to immunomodulation.

144 This proliferative effect of NECA was inhibited by the addition of anti-human VEGF an

145 The effect of NECA was reversed by the selective A2B receptor antagoni

146 R antagonist MRS1754 prevented the effect of NECA, we conclude that the stimulatory effect of adenosi

147 e of A(2B) receptors prevented the effect of NECA.

148 ermeant analog of cGMP, mimic the effects of NECA on 5-HT uptake, whereas the protein kinase G (PKG)

149 We also showed that the effects of NECA on Th1 and Th17 responses were completely dissociat

150 The effects of NECA were not significantly attenuated by either the A(2

151 mino-NECA caused any of the above effects of NECA.

152 congener completely inhibited the effects of NECA.

153 Focal ejections of NECA evoked outward currents in all cells tested and red

154 e with K(I) determinations for inhibition of NECA-stimulated cAMP accumulation in HEK-A(2B) cells.

155 site (-1093 to -1086) resulted in a loss of NECA-dependent VEGF reporter activity.

156 t derivatives that lengthen the 5' moiety of NECA improve selectivity for Grp94 over Hsp90alpha.

157 chniques indicated that GRP94 bound 1 mol of NECA/mol of GRP94 dimer.

158 To accommodate the 0.5 mol of NECA:mol of GRP94 binding stoichiometry observed for the

159 d alone in the absence or in the presence of NECA, produced no IgE.

160 Inhibition of IAC by adenosine or NECA was eliminated by substituting GDP-beta-S for GTP i

161 We examined whether LPS and/or NECA induce HIF-1alpha expression.

162 ith extremely high concentrations of CADO or NECA, mild inhibition of LAK cytotoxicity was observed t

163 sence of the A(2A) ligands SCH58261, CSC, or NECA, or in the absence of A(2A) receptors.

164 agonist 2-p-(2-carboxyethyl) phenethylamino-NECA caused any of the above effects of NECA.

165 ) agonist 2-p-(2-carboxyethyl)phenethylamino-NECA nor the selective A(3) agonist N(6)-(3-iodobenzyl)-

166 osine > 2-[4-(2-carboxyethyl)phenethylamino]-NECA (CGS21680) > N(6)-aminobenzyladenosine.

167 agonist 2-p-(2-carboxyethyl)phenylethylamino-NECA (CGS 21680) had no effect on expression of these an

168 OP with the following rank order of potency: NECA > CV-1808 > > R-PIA = CGS-21680.

169 Transfection of HRECs reduced NECA-stimulated migration of cells by 47.3+/-1.2% (P=7x1

170 )-1-deoxy-N-ethyl-beta-d-ribofuranuronamide (NECA) and the selective 1-deoxy-1-[6-[[(3-iodophenyl)met

171 hanism of action was pre-translational since NECA decreased collagenase, but not stromelysin or tissu

172 The findings of this study demonstrate that NECA and forskolin decrease collagenase gene expression

173 We found that NECA inhibited TNF-alpha and IL-12 in a concentration-de

174 -/-) and A(2B)AR(-/-)mice, it was shown that NECA modulates TNF-alpha, IL-12, IL-10, and CD86 respons

175 The NECA-evoked current was abolished by the A(1) antagonist

176 the SK channel blocker apamin decreased the NECA-induced current by 42 +/- 7%.

177 channel blocker rTertiapin-Q diminished the NECA-evoked inhibitory current by 56 +/- 12%, whereas th

178 In general, the NECA-based compounds displayed greater A(1)R selectivity

179 The SK component of the NECA-evoked current coincided with an increase in intrac

180 d that the response of gammadelta T cells to NECA was determined by their activation status.

181 -fold improved A(1)R selectivity compared to NECA.

182 interleukin (IL)-6 production in response to NECA due to activation of protein kinases A and C.

183 orskolin, but weakly affects the response to NECA or UTP.

184 Moreover, a decrease in cAMP levels upon NECA stimulation of naive macrophages was counterbalance

185 Here we use NECA and its derivatives to probe the properties of site

186 AR agonists in inducing IL-10 production was NECA > IB-MECA > CCPA >/= CGS21680, and the A(2B)AR anta

187 The whole NECA reaction is homogeneous and isothermal.

188 W156ECL2 decreased VCP171 cooperativity with NECA.

189 an B lymphocytes cocultured for 12 days with NECA-stimulated HMC-1 produced 870 +/- 33 pg IgE per 10(

190 LPS with NECA strongly up-regulates VEGF expression by macrophage

191 Treatment of PMNs with NECA increased the pp1 activity of crude membrane prepar

192 Further stimulation with NECA did not increase HIF-1alpha promoter activity, indi

193 Analysis of the pEC(50) values of XAC, NECA, and adenosine for the ABA-X-BY630-occupied A(3)-re