ライフサイエンスコーパス: U73122

1 production by the phospholipase C inhibitor U73122.

2 y ryanodine or the phospholipase C inhibitor U73122.

3 red both ICl(Ca) and ICat in the presence of U73122.

4 ely prevented by pretreatment with 10 microM U73122.

5 nt with a specific phospholipase C inhibitor U73122.

6 ment or by the phospholipase Cbeta inhibitor U73122.

7 ocytes and 3T3-L1 adipocytes pretreated with U73122.

8 nsulin in 3T3-L1 adipocytes is unaffected by U73122.

9 as inhibited by a phospholipase C inhibitor, U73122.

10 s inhibited by the phospholipase C inhibitor U73122.

11 abolished by the phospholipase C inhibitor, U73122.

12 e peptide-induced changes were unaffected by U73122.

13 by the PI-phospholipase C (PI-PLC) inhibitor U73122.

14 Galpha(q) or treated with the PLC inhibitor U73122.

15 rane to the cytosol, which were inhibited by U73122.

16 Q123 and the phospholipase C (PLC) inhibitor U73122.

17 rtan and the phospholipase C (PLC) inhibitor U73122.

18 ished by the phospholipase C (PLC) inhibitor U73122.

19 nd the phospholipase C (PLC)-gamma inhibitor U73122.

20 ors and is blocked by the PLCgamma inhibitor U73122.

21 n at the phagosome, and their sensitivity to U73122.

22 ctivation and was prevented by the inhibitor U73122.

23 retreated with the phospholipase C inhibitor U73122.

24 d by a selective phospho-lipase C inhibitor, U73122.

25 Inhibition of PLC gamma activation by U73122 (1 microM) augmented the EGF-induced [3H]thymidin

26 ng PLC activity with the pharmacologic agent U73122 (1 microM) diminished both this mobilization of g

27 letely abolished by pretreatment with either U73122 (1 microM, 4 min), a phospholipase C inhibitor, o

28 U73122 (1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-

29 is inhibition is blocked by a PLC inhibitor (U73122, 1-(6-{[(17beta)-3-Methoxyestra-1,3,5(10)-trien-1

30 Interestingly, U73122 (10 mum) also activated hPLCgamma1 (>10-fold) and

31 contrast, inhibition of phospholipase C with U73122 (10(-7) to 10(-5) mol/L) attenuated the oscillati

32 d-surface contact found that EGTA (5 mM) and U73122 (16 nM), an inhibitor of phospholipase C, inhibit

33 The phospholipase C inhibitor U73122 (2 microM) blocked histamine activation of ICl(Ca

34 wever, they were unaffected by 10 micrometer U73122, 20 micrometer nifedipine, or removal of Ca(2+) f

35 The phospholipase C inhibitor U73122 (3 microM) reduced the CS-induced increases in [C

36 The phospholipase C inhibitor U73122 (4 micro M) blocked the constriction responses to

37 g PLC formation in the VTA, via infusions of U73122 (400nM/side), should reduce progestin (5alpha-pre

38 The phospholipase C inhibitor U73122 (5 microM) had no significant effects on amino ac

39 microM), selective ETA receptor antagonist, U73122 (5 microM), or SKF 96365 (3 x 10(-5) M), an inhib

40 In contrast, the addition of U73122 (a phospholipase C inhibitor), calphostin C (a pr

41 atment with thapsigargin (5 microM) nor with U73122 (a phospholipase C inhibitor; 10 microM) blocked

42 , inhibited M3G-induced Ca(2+) influx, while U73122 (a PLC inhibitor) and 2-aminoethoxydiphenyl borat

43 sponse to nitrate treatments were blocked by U73122, a pharmacological inhibitor of phospholipase C,

44 by group I mGluR agonists in the presence of U73122, a phospholipase C (PLC) blocker.

45 U73122, a phospholipase C inhibitor, also abolished TXA2

46 U73122, a phospholipase C inhibitor, was able to complet

47 oked TRPC6/C7 activity, which was blocked by U73122, a phospholipase C inhibitor.

48 )-trisphosphate-induced Ca2+ release, and by U73122, a phospholipase C inhibitor.

49 s a Ca(2+)-independent cytoplasmic PLA2, and U73122, a selective inhibitor of phospholipase C (PLC).

50 n involved a Gq-coupled receptor inasmuch as U73122, a specific PLC inhibitor, abolished the response

51 C (PLC) mediated calcium store release with U73122, abrogated formyl peptide induced calcium elevati

52 Further evidence of the specificity of U73122 action was inhibition of the increase in InsP3 ma

53 However, PD98059, BIM and U73122 all reduced phosphorylation of ERK1/2 determined

54 Y294002, or by blocking phospholipase C with U73122 all significantly increased the incidence of adap

55 The phospholipase C inhibitor U73122 almost fully blocked MSHA (P = 0.001, n = 10), wi

56 U73122 also prevented the accompanying rise in intracell

57 nt with the conventional PLC-gamma inhibitor U73122 also showed similar results.

58 Furthermore, U73122 also suppresses the spontaneous hyperactivity exh

59 I3-K (LY294002 and Wortmannin) and PLCgamma (U73122) also block cyclin D2 expression and S phase entr

60 Preincubation with either 5 microM U73122 (an inhibitor of IP8 formation) or 10 microM cycl

61 spholipase C (PLC) during fertilization with U73122, an aminosteroid.

62 U73122, an inhibitor of phosphoinositidase C, inhibited

63 se in intracellular calcium was inhibited by U73122, an inhibitor of phospholipase C, and by thapsiga

64 h PI(4,5)P(2) in a manner similar to that of U73122, an inhibitor of PI(4,5)P(2) hydrolysis, suggesti

65 l proliferation was significantly reduced by U73122, an inhibitor of PI-PLC.

66 ic amphiphiles, U73343 (a less electrophilic U73122 analogue) and a range of kinase inhibitors were w

67 hronotropic effect that could be reversed by U73122 and 2-APB.

68 s inhibited by the phospholipase C inhibitor U73122 and by the inositol 1,4,5-trisphosphate receptor

69 resence of a phospholipase C (PLC) inhibitor U73122 and calcium chelator BAPTA (5,5'-dimethyl-bis(o-a

70 Pretreatment of CCDs with U73122 and calphostin C, inhibitors of phospholipase C (

71 ors of PI- and PC-specific phospholipases C (U73122 and D609) as well as PI3-kinase inhibitor (wortma

72 The PLC inhibitor U73122 and dialysis of PtdIns(4,5)P2 or PtdIns(4)P throu

73 treated with the phospholipase C inhibitors U73122 and ET-18-OCH(3) and were accompanied by an incre

74 tmannin, and the phospholipase C inhibitors, U73122 and ET-18-OCH3.

75 all inhibited activation of TRPC1 SOCs, and U73122 and GF109203X also reduced store-operated PKC-dep

76 e C-dependent phosphoinositide hydrolysis by U73122 and neomycin, suggesting that signaling from phos

77 erstanding of molecular interactions between U73122 and PLCs.

78 tol trisphosphate (IP3) receptor antagonists U73122 and xestospongin C, demonstrating involvement of

79 en-17-yl]amino]hexyl]-1H-pyrrole-2,5-dion e (U73122) and edelfosine.

80 FAT activity, whereas the inhibitors of PLC (U73122) and the inositol trisphosphate and ryanodine rec

81 , attenuated by a phospholipase C inhibitor (U73122), and is abolished by a MEK inhibitor (PD098059)

82 ost of these PLCs were directly activated by U73122, and a simple mechanism for the activation is pro

83 inhibitor W-7, the phospholipase-C inhibitor U73122, and anti-psychotic phenothiazines.

84 Thapsigargin, U73122, and pertussis toxin inhibited the percentage of

85 c-Src, as demonstrated by inhibitors SU1498, U73122, and PP1, respectively.

86 By using inhibitors of PLC activation, U73122, and the inositol 1,4,5-triphosphate (IP(3)) rece

87 , anti-Galphaq antibodies, the PLC inhibitor U73122, and the PKC inhibitor GF109203X all inhibited ac

88 [wortmannin], the phospholipase C inhibitor [U73122] and the Src-SH2 antagonist [PP2].

89 Importantly, the effects of U73122 are selective to dopamine-mediated hyperactivity,

90 gly suggest a need to re-evaluate the use of U73122 as a general inhibitor of PLC isozymes.

91 ic analysis confirmed covalent reaction with U73122 at eight cysteines, although maximum activation w

92 enyl borate) or a phospholipase C inhibitor (U73122) attenuated Ca(2+) waves, global Ca(2+) and myoge

93 PLCz- or U73122-augmented mitogenesis was not observed in three n

94 ospholipase C (PLC) inhibitors, neomycin and U73122 block mastoparan-induced increases of [Ca2+]i and

95 U73122 blocked contraction in adult antral cells but not

96 The PLC inhibitors 3-nitrocoumarin and U73122 blocked vacuole fusion in vitro, whereas their in

97 ase inhibitor herbimycin A and PLC inhibitor U73122 both blocked CD43-induced enhancement of adhesion

98 rate (2-APB) and the phospholipase C blocker U73122 but continued in the presence of caffeine.

99 A-(AM)3 and by the phospholipase C inhibitor U73122 but not by its inactive analogue U73433.

100 issociation was blocked by the PLC inhibitor U73122 but was not affected by the phosphoinositide (PI)

101 ated by pre-treatment with the PLC inhibitor U73122, but not affected by treatment with the inactive

102 ussis toxin, and the phospholipase inhibitor U73122, but not neutralizing antibodies to CXCR4.

103 ttenuated by infusions of the PLC inhibitor, U73122, but not vehicle, to the VTA.

104 inhibited by thapsigargin, herbimycin A, and U73122, but only partially reduced by low extracellular

105 en-17-yl] amino]hexyl)-1H-pyrrole-2,5-dione (U73122), by the intracellular Ca2+ chelator 1,2-bis(2-am

106 rolysis with 500 microM neomycin or 5 microM U73122 completely abolished the CCh-induced positive chr

107 Pharmacological inhibition of PLC gamma (U73122) confirmed that PLC gamma signaling suppressed pr

108 e the aminosteroid phospholipase C inhibitor U73122 could block the DPDPE effect.

109 In contrast, the PI-PLC inhibitor U73122 decreased both phagocytosis and PKC-epsilon accum

110 2-APB and U73122 decreased the frequency of spontaneous Ca(2+) tra

111 Inhibition of phospholipase C (PLC) with U73122 did not inhibit either ImAHP or IsAHP in OT neuro

112 of cells with the phospholipase C inhibitor U73122 does not inhibit ac electric field-induced increa

113 The PLCbeta inhibitor U73122 down-regulates TNFalpha expression by macrophages

114 nd the further addition of Plc1p blocks this U73122 effect.

115 e-dependent manner, although above 15 microM U73122 eggs showed an elevated resting [Ca2+]i and a low

116 hospholipase C (PLC) since the PLC inhibitor U73122 eliminated the Ca(2+) oscillations.

117 activity in wild-type mice by its inhibitor, U73122, exacerbated adriamycin-induced cardiac dysfuncti

118 ntrast to its reported inhibitory potential, U73122 failed to inhibit several purified PLCs.

119 e was abolished by 2-APB but not affected by U73122 [GenBank] or 8Br-cADPR.

120 ot affected by the phospholipase C inhibitor U73122 [GenBank] or by the cADP receptor inhibitor 8-bro

121 Furthermore, U73122 (Gqalpha-PLC specific uncoupler) and GP2A (Gqalph

122 sitol-specific phospholipase C (PI-PLC) with U73122 had no effect on the response to elevated [Ca2+]0

123 U73122 had similar effects on the cation current evoked

124 d to confirm this by using the PLC inhibitor U73122; however, this was found to act as a novel inhibi

125 -specific phospholipase C (PI-PLC) inhibitor U73122 (IC50=4 microM).

126 Pretreatment with U73122 (IC50=7 microM) results in an 87% inhibition of N

127 The phospholipase C (PLC) inhibitor U73122 increased spontaneous activity which implies a ro

128 Surprisingly, U73122 increased the activity of hPLCbeta3 in a concentr

129 + responses by the phospholipase C inhibitor U73122 indicated that H218 and Edg3 mobilized Ca2+ throu

130 c-Src phosphorylation was inhibited by U73122, indicating it was downstream of phospholipase (P

131 or the peritoneal lymphocyte gamma inhibitor U73122, indicating that both TrkB and PI3K activities ar

132 ker nifedipine and phospholipase C inhibitor U73122 inhibited NO formation and thus implicated partic

133 The phospholipase C (PLC) inhibitor U73122 inhibited the amplitude of the noradrenaline-acti

134 In addition, U73122 inhibited the GTPgammaS-induced Ca2+ release and

135 U73122 inhibited the sperm-induced Ca2+ release in a dos

136 98059, but not the phospholipase C inhibitor U73122, inhibited the outward current evoked by 10 micro

137 ium, thapsigargin [inhibitor of Ca-ATPases], U73122 [inhibitor of phospholipase C], and pertussis tox

138 We show that U73122 inhibits the locomotor-stimulating effects of apo

139 e pre-treated with phospholipase C inhibitor U73122 no 5-HT-induced sK(Ca) channel openings were seen

140 pratropium nor the phospholipase C inhibitor U73122, nor the protein kinase C inhibitor chelerythrine

141 Hence, the effects of U73122 on human PLCbeta3 (hPLCbeta3) were evaluated in a

142 However, when these cells were treated with U73122 or Calphostin C, the mitogenic responses are not

143 ion of JNK and NF-kappaB was not affected by U73122 or Dap12/FcRgamma deletion.

144 phorylation, an increase that was reduced by U73122 or PI-PLCgamma2 siRNA.

145 The presence of the PLC inhibitor U73122 or the calcium chelator 1,2-bis(2-aminophenoxy)et

146 Inhibition of PLC with U73122 or transfection of a PLCgamma1 antisense cDNA con

147 a phospholipase C (PLC) inhibitor (40.0 mum U73122) or a protein kinase C (PKC) inhibitor (10.0 mum

148 armacological agents used to antagonize PLC (U73122) or the inositol phosphate receptor (Xestospongin

149 sitization was inhibited by pertussis toxin, U73122, or chelerythrine chloride, inhibitors of Gi-prot

150 the IR, we used a specific inhibitor of PLC, U73122, or microinjection of SH2 domain glutathione S-tr

151 romazine or by the phospholipase C inhibitor U73122, perturbants of the lipid phase of the membrane.

152 U73122 pretreatment has no effect on NGF stimulated Akt

153 The phospholipase C inhibitor U73122 prevented FBP-induced increases in [Ca2+]i and el

154 Treatment of cells with the Plc inhibitor U73122 prevented increases in inositol phosphate levels

155 swell).) The phospholipase C (PLC) inhibitor U73122 reduced the amplitude of I(Cl(swell)) whereas the

156 Blocking cellular PLC with an inhibitor (U73122) reduced inositol phosphate turnover in all of th

157 Activation of hPLCbeta3 by U73122 required covalent modification of cysteines as ev

158 rylation, while cotreatment with PD98059 and U73122 results in 97% inhibition.

159 U73122 selectively inhibits mitogen-activated protein ki

160 ctivity and significant 3-nitrocoumarin- and U73122-sensitive fusion, suggesting that there is anothe

161 In contrast, PLCgamma1 inhibition with U73122 significantly decreased persistence on immobilize

162 Treatment with phospholipase C inhibitor U73122 significantly reversed P2X3 current inhibition in

163 Like U73122, Spry2 over-expression inhibited wild type Gag re

164 obilization by the phospholipase C inhibitor U73122 strongly suggested that Edg2 and Edg4 mobilize Ca

165 ivation of TrpL was blocked more than 70% by U73122, suggesting that the effect of these agents was d

166 by including the phospholipase C antagonist U73122, the inositol 1,4,5-trisphosphate receptor antago

167 cked by the phospholipase C (PLC) inhibitor, U73122, the phosphatidylinositol (PI) PLC inhibitor 1-O-

168 PD98059, the phospholipase C (PLC) inhibitor U73122, the protein kinase C (PKC) inhibitor GF102390X,

169 llular Ca(2+), the phospholipase C inhibitor U73122, the protein kinase inhibitor staurosporine, or s

170 is strikingly enhanced by the PLC inhibitor U73122 through enhanced binding of Vam7p SNARE domain to

171 gamma signaling suppressed prostin-1 in that U73122 treatment caused induction of prostin-1 in PLC ga

172 e of D1- and D2-mediated signaling following U73122 treatment modifies the locomotor output of animal

173 phosphorylation by the general PLC inhibitor U73122 was associated with a delayed and reduced phospho

174 The inhibition of Ca2+ transient by U73122 was not due to a failure of fertilization, since

175 A selective blocker of PLCbeta, U73122, was used to assess the physiological relevance o

176 ation is suggested by using a PLC inhibitor, U73122, which blocks both adhesion- and M-CSF-mediated c