ライフサイエンスコーパス: phosphoinositide 3-kinase inhibitor

1 (IGF-IR inhibitor), LY294002, or Wortmannin (phosphoinositide-3-kinase inhibitor).

2 bitor K252a, as well as protein kinase A and phosphoinositide 3-kinase inhibitors.

3 nal phenotype, and this could be reversed by 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 cluding several chemoimmunotherapy regimens, phosphoinositide 3-kinase inhibitors, and lenalidomide p

10 Indeed, pan-phosphoinositide 3-kinase inhibitors are being evaluated

11 The class III phosphoinositide 3-kinase inhibitors attenuated DAPK dep

12 Wortmannin, a phosphoinositide 3-kinase inhibitor, attenuated basal ph

13 Phosphoinositide-3-kinase inhibitor-known to be involved

14 ptor (EGFR) inhibitor AG1478, but not by the phosphoinositide-3 kinase inhibitor LY292004 or the mito

15 or AG1478 caused a small inhibition, but the phosphoinositide 3 kinase inhibitor LY294002 potentiated

16 Preincubation with the phosphoinositide 3'-kinase inhibitor LY294002 significan

17 ssion by insulin was blocked by the specific phosphoinositide 3-kinase inhibitor LY294002 and mammali

18 However, pretreatment of C4-2 cells with the phosphoinositide 3-kinase inhibitor LY294002 restored pa

19 , which was unaffected by treatment with the phosphoinositide 3-kinase inhibitor LY294002.

20 RAS mutation, and this was suppressed by the phosphoinositide 3-kinase inhibitor LY294002.

21 lls and serum-starved cells treated with the phosphoinositide 3-kinase inhibitors, LY294002 and wortm

22 Treatment with either the phosphoinositide-3-kinase inhibitor, LY294002 and pan-mT

23 uggesting that rapamycin in combination with phosphoinositide 3-kinase inhibitors may be therapeutic

24 revalence OR incidence OR epidemiology) and (phosphoinositide 3 kinase inhibitors OR PI3K inhibitors)

25 tion in the presence of either Rho-kinase or phosphoinositide 3-kinase inhibitors or an intracellular

26 a detoxified TLR4 agonist, and Wortmannin, a phosphoinositide 3-kinase inhibitor, prevented the LPS-m

27 Importantly, phosphoinositide 3-kinase inhibitor/protein kinase B (PI

28 benzopyran-4-one hydrochloride (LY294002) (a phosphoinositide 3-kinase inhibitor) reduced the VPA act

29 Phosphoinositide 3-kinase inhibitors remain available bu

30 Pretreatment of muscles with wortmannin (phosphoinositide 3-kinase inhibitor), TMB-8 (antagonist

31 In contrast, Wortmannin, a phosphoinositide 3-kinase inhibitor upstream of protein

32 uggest that chronic (hours) drug exposure to phosphoinositide 3-kinase inhibitors used in cancer can

33 can then be reactivated by the addition of a phosphoinositide 3-kinase inhibitor, which has previousl

34 domide with or without anti-CD20 (n=37), and phosphoinositide 3-kinase inhibitors with or without ant

35 diol (1 mg/kg), or 17beta-estradiol plus the phosphoinositide 3-kinase inhibitor wortmannin (1 mg/kg)

36 tment with tyrosine kinase inhibitors or the phosphoinositide 3-kinase inhibitor wortmannin demonstra

37 However, treatment with the phosphoinositide 3-kinase inhibitor wortmannin did not d

38 The phosphoinositide 3-kinase inhibitor wortmannin significa

39 eNOS is inhibited by pertussis toxin, by the phosphoinositide 3-kinase inhibitor wortmannin, and by t

40 nnel blockers iberiotoxin and paxilline, the phosphoinositide 3-kinase inhibitor wortmannin, the prot

41 G, and preincubation of neutrophils with the phosphoinositide 3-kinase inhibitor wortmannin, which ab

42 by dominant-negative Ras and Rac1 and by the phosphoinositide 3-kinase inhibitor Wortmannin.

43 oprotein (GP) IIb-IIIa, are sensitive to the phosphoinositide 3-kinase inhibitor wortmannin.

44 , many studies relying instead on use of the phosphoinositide 3-kinase inhibitors wortmannin and LY29

45 NF-kappa B activation is not reduced by the phosphoinositide-3 kinase inhibitors wortmannin and LY29

46 n vitro was abolished in the presence of the phosphoinositide 3-kinase inhibitor, wortmannin, thus re

47 ction was prevented by pretreatment with the phosphoinositide 3-kinase inhibitors, wortmannin (50 nmo

48 Treatment of hepatocytes or WIF-B cells with phosphoinositide 3-kinase inhibitors, wortmannin or LY29