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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.
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
29 is inhibition is blocked by a PLC inhibitor (U73122, 1-(6-{[(17beta)-3-Methoxyestra-1,3,5(10)-trien-1
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
34 wever, they were unaffected by 10 micrometer U73122, 20 micrometer nifedipine, or removal of Ca(2+) f
37 g PLC formation in the VTA, via infusions of U73122 (400nM/side), should reduce progestin (5alpha-pre
39 microM), selective ETA receptor antagonist, U73122 (5 microM), or SKF 96365 (3 x 10(-5) M), an inhib
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,
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
53 Y294002, or by blocking phospholipase C with U73122 all significantly increased the incidence of adap
58 I3-K (LY294002 and Wortmannin) and PLCgamma (U73122) also block cyclin D2 expression and S phase entr
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
65 ic amphiphiles, U73343 (a less electrophilic U73122 analogue) and a range of kinase inhibitors were w
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
70 ors of PI- and PC-specific phospholipases C (U73122 and D609) as well as PI3-kinase inhibitor (wortma
72 treated with the phospholipase C inhibitors U73122 and ET-18-OCH(3) and were accompanied by an incre
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
77 tol trisphosphate (IP3) receptor antagonists U73122 and xestospongin C, demonstrating involvement of
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
86 , anti-Galphaq antibodies, the PLC inhibitor U73122, and the PKC inhibitor GF109203X all inhibited ac
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
93 ospholipase C (PLC) inhibitors, neomycin and U73122 block mastoparan-induced increases of [Ca2+]i and
96 ase inhibitor herbimycin A and PLC inhibitor U73122 both blocked CD43-induced enhancement of adhesion
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
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
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
114 e-dependent manner, although above 15 microM U73122 eggs showed an elevated resting [Ca2+]i and a low
116 activity in wild-type mice by its inhibitor, U73122, exacerbated adriamycin-induced cardiac dysfuncti
119 ot affected by the phospholipase C inhibitor U73122 [GenBank] or by the cADP receptor inhibitor 8-bro
121 sitol-specific phospholipase C (PI-PLC) with U73122 had no effect on the response to elevated [Ca2+]0
123 d to confirm this by using the PLC inhibitor U73122; however, this was found to act as a novel inhibi
128 + responses by the phospholipase C inhibitor U73122 indicated that H218 and Edg3 mobilized Ca2+ throu
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
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
138 e pre-treated with phospholipase C inhibitor U73122 no 5-HT-induced sK(Ca) channel openings were seen
140 However, when these cells were treated with U73122 or Calphostin C, the mitogenic responses are not
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.
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
158 ctivity and significant 3-nitrocoumarin- and U73122-sensitive fusion, suggesting that there is anothe
160 Treatment with phospholipase C inhibitor U73122 significantly reversed P2X3 current inhibition in
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
174 ation is suggested by using a PLC inhibitor, U73122, which blocks both adhesion- and M-CSF-mediated c
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