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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 sponse to nitrate treatments were blocked by U73122, a pharmacological inhibitor of phospholipase C,
43 by group I mGluR agonists in the presence of U73122, a phospholipase C (PLC) blocker.
44                                              U73122, a phospholipase C inhibitor, also abolished TXA2
45                                              U73122, a phospholipase C inhibitor, was able to complet
46 oked TRPC6/C7 activity, which was blocked by U73122, a phospholipase C inhibitor.
47 )-trisphosphate-induced Ca2+ release, and by U73122, a phospholipase C inhibitor.
48 s a Ca(2+)-independent cytoplasmic PLA2, and U73122, a selective inhibitor of phospholipase C (PLC).
49 n involved a Gq-coupled receptor inasmuch as U73122, a specific PLC inhibitor, abolished the response
50  C (PLC) mediated calcium store release with U73122, abrogated formyl peptide induced calcium elevati
51       Further evidence of the specificity of U73122 action was inhibition of the increase in InsP3 ma
52                    However, PD98059, BIM and U73122 all reduced phosphorylation of ERK1/2 determined
53 Y294002, or by blocking phospholipase C with U73122 all significantly increased the incidence of adap
54                The phospholipase C inhibitor U73122 almost fully blocked MSHA (P = 0.001, n = 10), wi
55                                              U73122 also prevented the accompanying rise in intracell
56 nt with the conventional PLC-gamma inhibitor U73122 also showed similar results.
57                                 Furthermore, U73122 also suppresses the spontaneous hyperactivity exh
58 I3-K (LY294002 and Wortmannin) and PLCgamma (U73122) also block cyclin D2 expression and S phase entr
59           Preincubation with either 5 microM U73122 (an inhibitor of IP8 formation) or 10 microM cycl
60 spholipase C (PLC) during fertilization with U73122, an aminosteroid.
61                                              U73122, an inhibitor of phosphoinositidase C, inhibited
62 se in intracellular calcium was inhibited by U73122, an inhibitor of phospholipase C, and by thapsiga
63 h PI(4,5)P(2) in a manner similar to that of U73122, an inhibitor of PI(4,5)P(2) hydrolysis, suggesti
64 l proliferation was significantly reduced by U73122, an inhibitor of PI-PLC.
65 ic amphiphiles, U73343 (a less electrophilic U73122 analogue) and a range of kinase inhibitors were w
66 hronotropic effect that could be reversed by U73122 and 2-APB.
67 s inhibited by the phospholipase C inhibitor U73122 and by the inositol 1,4,5-trisphosphate receptor
68 resence of a phospholipase C (PLC) inhibitor U73122 and calcium chelator BAPTA (5,5'-dimethyl-bis(o-a
69                    Pretreatment of CCDs with U73122 and calphostin C, inhibitors of phospholipase C (
70 ors of PI- and PC-specific phospholipases C (U73122 and D609) as well as PI3-kinase inhibitor (wortma
71                            The PLC inhibitor U73122 and dialysis of PtdIns(4,5)P2 or PtdIns(4)P throu
72  treated with the phospholipase C inhibitors U73122 and ET-18-OCH(3) and were accompanied by an incre
73 tmannin, and the phospholipase C inhibitors, U73122 and ET-18-OCH3.
74  all inhibited activation of TRPC1 SOCs, and U73122 and GF109203X also reduced store-operated PKC-dep
75 e C-dependent phosphoinositide hydrolysis by U73122 and neomycin, suggesting that signaling from phos
76 erstanding of molecular interactions between U73122 and PLCs.
77 tol trisphosphate (IP3) receptor antagonists U73122 and xestospongin C, demonstrating involvement of
78 en-17-yl]amino]hexyl]-1H-pyrrole-2,5-dion e (U73122) and edelfosine.
79 FAT activity, whereas the inhibitors of PLC (U73122) and the inositol trisphosphate and ryanodine rec
80 , attenuated by a phospholipase C inhibitor (U73122), and is abolished by a MEK inhibitor (PD098059)
81 ost of these PLCs were directly activated by U73122, and a simple mechanism for the activation is pro
82 inhibitor W-7, the phospholipase-C inhibitor U73122, and anti-psychotic phenothiazines.
83                                Thapsigargin, U73122, and pertussis toxin inhibited the percentage of
84 c-Src, as demonstrated by inhibitors SU1498, U73122, and PP1, respectively.
85       By using inhibitors of PLC activation, U73122, and the inositol 1,4,5-triphosphate (IP(3)) rece
86 , anti-Galphaq antibodies, the PLC inhibitor U73122, and the PKC inhibitor GF109203X all inhibited ac
87 [wortmannin], the phospholipase C inhibitor [U73122] and the Src-SH2 antagonist [PP2].
88                  Importantly, the effects of U73122 are selective to dopamine-mediated hyperactivity,
89 gly suggest a need to re-evaluate the use of U73122 as a general inhibitor of PLC isozymes.
90 ic analysis confirmed covalent reaction with U73122 at eight cysteines, although maximum activation w
91 enyl borate) or a phospholipase C inhibitor (U73122) attenuated Ca(2+) waves, global Ca(2+) and myoge
92                                     PLCz- or U73122-augmented mitogenesis was not observed in three n
93 ospholipase C (PLC) inhibitors, neomycin and U73122 block mastoparan-induced increases of [Ca2+]i and
94                                              U73122 blocked contraction in adult antral cells but not
95       The PLC inhibitors 3-nitrocoumarin and U73122 blocked vacuole fusion in vitro, whereas their in
96 ase inhibitor herbimycin A and PLC inhibitor U73122 both blocked CD43-induced enhancement of adhesion
97 rate (2-APB) and the phospholipase C blocker U73122 but continued in the presence of caffeine.
98 A-(AM)3 and by the phospholipase C inhibitor U73122 but not by its inactive analogue U73433.
99 issociation was blocked by the PLC inhibitor U73122 but was not affected by the phosphoinositide (PI)
100 ated by pre-treatment with the PLC inhibitor U73122, but not affected by treatment with the inactive
101 ussis toxin, and the phospholipase inhibitor U73122, but not neutralizing antibodies to CXCR4.
102 ttenuated by infusions of the PLC inhibitor, U73122, but not vehicle, to the VTA.
103 inhibited by thapsigargin, herbimycin A, and U73122, but only partially reduced by low extracellular
104 en-17-yl] amino]hexyl)-1H-pyrrole-2,5-dione (U73122), by the intracellular Ca2+ chelator 1,2-bis(2-am
105 rolysis with 500 microM neomycin or 5 microM U73122 completely abolished the CCh-induced positive chr
106     Pharmacological inhibition of PLC gamma (U73122) confirmed that PLC gamma signaling suppressed pr
107 e the aminosteroid phospholipase C inhibitor U73122 could block the DPDPE effect.
108            In contrast, the PI-PLC inhibitor U73122 decreased both phagocytosis and PKC-epsilon accum
109                                    2-APB and U73122 decreased the frequency of spontaneous Ca(2+) tra
110     Inhibition of phospholipase C (PLC) with U73122 did not inhibit either ImAHP or IsAHP in OT neuro
111  of cells with the phospholipase C inhibitor U73122 does not inhibit ac electric field-induced increa
112                        The PLCbeta inhibitor U73122 down-regulates TNFalpha expression by macrophages
113 nd the further addition of Plc1p blocks this U73122 effect.
114 e-dependent manner, although above 15 microM U73122 eggs showed an elevated resting [Ca2+]i and a low
115 hospholipase C (PLC) since the PLC inhibitor U73122 eliminated the Ca(2+) oscillations.
116 activity in wild-type mice by its inhibitor, U73122, exacerbated adriamycin-induced cardiac dysfuncti
117 ntrast to its reported inhibitory potential, U73122 failed to inhibit several purified PLCs.
118 e was abolished by 2-APB but not affected by U73122 [GenBank] or 8Br-cADPR.
119 ot affected by the phospholipase C inhibitor U73122 [GenBank] or by the cADP receptor inhibitor 8-bro
120                                 Furthermore, U73122 (Gqalpha-PLC specific uncoupler) and GP2A (Gqalph
121 sitol-specific phospholipase C (PI-PLC) with U73122 had no effect on the response to elevated [Ca2+]0
122                                              U73122 had similar effects on the cation current evoked
123 d to confirm this by using the PLC inhibitor U73122; however, this was found to act as a novel inhibi
124 -specific phospholipase C (PI-PLC) inhibitor U73122 (IC50=4 microM).
125                            Pretreatment with U73122 (IC50=7 microM) results in an 87% inhibition of N
126          The phospholipase C (PLC) inhibitor U73122 increased spontaneous activity which implies a ro
127                                Surprisingly, U73122 increased the activity of hPLCbeta3 in a concentr
128 + responses by the phospholipase C inhibitor U73122 indicated that H218 and Edg3 mobilized Ca2+ throu
129       c-Src phosphorylation was inhibited by U73122, indicating it was downstream of phospholipase (P
130 or the peritoneal lymphocyte gamma inhibitor U73122, indicating that both TrkB and PI3K activities ar
131 ker nifedipine and phospholipase C inhibitor U73122 inhibited NO formation and thus implicated partic
132          The phospholipase C (PLC) inhibitor U73122 inhibited the amplitude of the noradrenaline-acti
133                                 In addition, U73122 inhibited the GTPgammaS-induced Ca2+ release and
134                                              U73122 inhibited the sperm-induced Ca2+ release in a dos
135 98059, but not the phospholipase C inhibitor U73122, inhibited the outward current evoked by 10 micro
136 ium, thapsigargin [inhibitor of Ca-ATPases], U73122 [inhibitor of phospholipase C], and pertussis tox
137                                 We show that U73122 inhibits the locomotor-stimulating effects of apo
138 e pre-treated with phospholipase C inhibitor U73122 no 5-HT-induced sK(Ca) channel openings were seen
139                        Hence, the effects of U73122 on human PLCbeta3 (hPLCbeta3) were evaluated in a
140  However, when these cells were treated with U73122 or Calphostin C, the mitogenic responses are not
141 ion of JNK and NF-kappaB was not affected by U73122 or Dap12/FcRgamma deletion.
142 phorylation, an increase that was reduced by U73122 or PI-PLCgamma2 siRNA.
143            The presence of the PLC inhibitor U73122 or the calcium chelator 1,2-bis(2-aminophenoxy)et
144                       Inhibition of PLC with U73122 or transfection of a PLCgamma1 antisense cDNA con
145  a phospholipase C (PLC) inhibitor (40.0 mum U73122) or a protein kinase C (PKC) inhibitor (10.0 mum
146 armacological agents used to antagonize PLC (U73122) or the inositol phosphate receptor (Xestospongin
147 sitization was inhibited by pertussis toxin, U73122, or chelerythrine chloride, inhibitors of Gi-prot
148 the IR, we used a specific inhibitor of PLC, U73122, or microinjection of SH2 domain glutathione S-tr
149 romazine or by the phospholipase C inhibitor U73122, perturbants of the lipid phase of the membrane.
150                                              U73122 pretreatment has no effect on NGF stimulated Akt
151                The phospholipase C inhibitor U73122 prevented FBP-induced increases in [Ca2+]i and el
152    Treatment of cells with the Plc inhibitor U73122 prevented increases in inositol phosphate levels
153 swell).) The phospholipase C (PLC) inhibitor U73122 reduced the amplitude of I(Cl(swell)) whereas the
154     Blocking cellular PLC with an inhibitor (U73122) reduced inositol phosphate turnover in all of th
155                   Activation of hPLCbeta3 by U73122 required covalent modification of cysteines as ev
156 rylation, while cotreatment with PD98059 and U73122 results in 97% inhibition.
157                                              U73122 selectively inhibits mitogen-activated protein ki
158 ctivity and significant 3-nitrocoumarin- and U73122-sensitive fusion, suggesting that there is anothe
159       In contrast, PLCgamma1 inhibition with U73122 significantly decreased persistence on immobilize
160     Treatment with phospholipase C inhibitor U73122 significantly reversed P2X3 current inhibition in
161                                         Like U73122, Spry2 over-expression inhibited wild type Gag re
162 obilization by the phospholipase C inhibitor U73122 strongly suggested that Edg2 and Edg4 mobilize Ca
163 ivation of TrpL was blocked more than 70% by U73122, suggesting that the effect of these agents was d
164  by including the phospholipase C antagonist U73122, the inositol 1,4,5-trisphosphate receptor antago
165 cked by the phospholipase C (PLC) inhibitor, U73122, the phosphatidylinositol (PI) PLC inhibitor 1-O-
166 PD98059, the phospholipase C (PLC) inhibitor U73122, the protein kinase C (PKC) inhibitor GF102390X,
167 llular Ca(2+), the phospholipase C inhibitor U73122, the protein kinase inhibitor staurosporine, or s
168  is strikingly enhanced by the PLC inhibitor U73122 through enhanced binding of Vam7p SNARE domain to
169 gamma signaling suppressed prostin-1 in that U73122 treatment caused induction of prostin-1 in PLC ga
170 e of D1- and D2-mediated signaling following U73122 treatment modifies the locomotor output of animal
171 phosphorylation by the general PLC inhibitor U73122 was associated with a delayed and reduced phospho
172          The inhibition of Ca2+ transient by U73122 was not due to a failure of fertilization, since
173              A selective blocker of PLCbeta, U73122, was used to assess the physiological relevance o
174 ation is suggested by using a PLC inhibitor, U73122, which blocks both adhesion- and M-CSF-mediated c

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