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1 (IGF-IR inhibitor), LY294002, or Wortmannin (phosphoinositide-3-kinase inhibitor).
2 nal phenotype, and this could be reversed by phosphoinositide 3-kinase inhibitors.
3 bitor K252a, as well as protein kinase A and phosphoinositide 3-kinase inhibitors.
4 e response was only slightly affected by the phosphoinositide 3-kinase inhibitor 2-(4-morpholinyl)-8-
5 nhibit autophagy, pDCs were treated with the phosphoinositide-3 kinase inhibitor 3-methyladenine (3-M
6                                              Phosphoinositide 3-kinase inhibitors abrogated Akt phosp
7 athways that activate macropinocytosis, with phosphoinositide 3-kinase inhibitor activation stimulati
8                                              Phosphoinositide 3-kinase inhibitors and an actin polyme
9                                  Indeed, pan-phosphoinositide 3-kinase inhibitors are being evaluated
10                                The class III phosphoinositide 3-kinase inhibitors attenuated DAPK dep
11                                Wortmannin, a phosphoinositide 3-kinase inhibitor, attenuated basal ph
12                                              Phosphoinositide-3-kinase inhibitor-known to be involved
13 ptor (EGFR) inhibitor AG1478, but not by the phosphoinositide-3 kinase inhibitor LY292004 or the mito
14 or AG1478 caused a small inhibition, but the phosphoinositide 3 kinase inhibitor LY294002 potentiated
15                       Preincubation with the phosphoinositide 3'-kinase inhibitor LY294002 significan
16 ssion by insulin was blocked by the specific phosphoinositide 3-kinase inhibitor LY294002 and mammali
17 However, pretreatment of C4-2 cells with the phosphoinositide 3-kinase inhibitor LY294002 restored pa
18 RAS mutation, and this was suppressed by the phosphoinositide 3-kinase inhibitor LY294002.
19 , which was unaffected by treatment with the phosphoinositide 3-kinase inhibitor LY294002.
20 lls and serum-starved cells treated with the phosphoinositide 3-kinase inhibitors, LY294002 and wortm
21                    Treatment with either the phosphoinositide-3-kinase inhibitor, LY294002 and pan-mT
22 uggesting that rapamycin in combination with phosphoinositide 3-kinase inhibitors may be therapeutic
23 tion in the presence of either Rho-kinase or phosphoinositide 3-kinase inhibitors or an intracellular
24                                 Importantly, phosphoinositide 3-kinase inhibitor/protein kinase B (PI
25 benzopyran-4-one hydrochloride (LY294002) (a phosphoinositide 3-kinase inhibitor) reduced the VPA act
26     Pretreatment of muscles with wortmannin (phosphoinositide 3-kinase inhibitor), TMB-8 (antagonist
27                   In contrast, Wortmannin, a phosphoinositide 3-kinase inhibitor upstream of protein
28 uggest that chronic (hours) drug exposure to phosphoinositide 3-kinase inhibitors used in cancer can
29 diol (1 mg/kg), or 17beta-estradiol plus the phosphoinositide 3-kinase inhibitor wortmannin (1 mg/kg)
30 tment with tyrosine kinase inhibitors or the phosphoinositide 3-kinase inhibitor wortmannin demonstra
31                                          The phosphoinositide 3-kinase inhibitor wortmannin significa
32 eNOS is inhibited by pertussis toxin, by the phosphoinositide 3-kinase inhibitor wortmannin, and by t
33 nnel blockers iberiotoxin and paxilline, the phosphoinositide 3-kinase inhibitor wortmannin, the prot
34 G, and preincubation of neutrophils with the phosphoinositide 3-kinase inhibitor wortmannin, which ab
35 by dominant-negative Ras and Rac1 and by the phosphoinositide 3-kinase inhibitor Wortmannin.
36 oprotein (GP) IIb-IIIa, are sensitive to the phosphoinositide 3-kinase inhibitor wortmannin.
37 , many studies relying instead on use of the phosphoinositide 3-kinase inhibitors wortmannin and LY29
38  NF-kappa B activation is not reduced by the phosphoinositide-3 kinase inhibitors wortmannin and LY29
39 n vitro was abolished in the presence of the phosphoinositide 3-kinase inhibitor, wortmannin, thus re
40 ction was prevented by pretreatment with the phosphoinositide 3-kinase inhibitors, wortmannin (50 nmo
41 Treatment of hepatocytes or WIF-B cells with phosphoinositide 3-kinase inhibitors, wortmannin or LY29

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