ライフサイエンスコーパス: phosphatidylinositol-3-OH kinase

1 phosphatase antagonizing the activity of the phosphatidylinositol 3-OH kinase.

2 ithin 1 hour of treatment and is mediated by phosphatidylinositol 3-OH kinase.

3 sistent with the model that PTEN antagonizes phosphatidylinositol 3-OH kinase.

4 t affecting signalling events that depend on phosphatidylinositol-3-OH kinase.

5 roteins including phospholipase C-gamma1 and phosphatidylinositol-3-OH kinase.

6 le to recruit the adaptor molecule Crk-L and phosphatidylinositol-3-OH kinase.

7 sphosphate, antagonizing the activity of the phosphatidylinositol 3'-OH kinase.

8 on Rac can be stimulated by a Ras-dependent phosphatidylinositol-3-OH kinase, a mechanism could exis

9 s septin-independent pathway was mediated by phosphatidylinositol-3-OH kinase activation through a co

10 ase acting through a pathway that involves a phosphatidylinositol-3-OH kinase activity.

11 clude an insulin-like receptor (daf-2) and a phosphatidylinositol 3-OH kinase (age-1) regulating a fo

12 ity of an insulin-like receptor (daf-2) or a phosphatidylinositol-3-OH kinase (age-1) favour entry in

13 cells, LMP2A has been shown to activate the phosphatidylinositol 3'-OH kinase/Akt and beta-catenin s

14 Phosphatidylinositol 3-OH kinase/AKT is a potent pro-sur

15 T activation; when cells were incubated with phosphatidylinositol-3-OH kinase/AKT inhibitor or infect

16 Activation of the phosphatidylinositol-3-OH kinase/Akt pathway results in

17 rations that promote oncogenesis through the phosphatidylinositol-3-OH kinase/AKT pathway.

18 ifferentiation-inducing cytokine, results in phosphatidylinositol-3-OH kinase/Akt1 kinase-dependent p

19 lcium/calmodulin-dependent protein kinase 2, phosphatidylinositol 3-OH-kinase and by rapamycin.

20 s, we showed that neuregulin signals through phosphatidylinositol-3'-OH kinase and Akt to enhance sur

21 asoprotection was prevented by inhibitors of phosphatidylinositol-3-OH kinase and extracellular signa

22 ion of Akt activity induced by PKD3 required phosphatidylinositol-3-OH kinase and p38.

23 xtending (Age) mutations, such as the age-1 (phosphatidylinositol 3-OH kinase) and daf-2 (insulin/IGF

24 s of insulin were abolished by inhibitors of phosphatidylinositol 3-OH kinase, and by rapamycin, a sp

25 ologue of the catalytic subunit of mammalian phosphatidylinositol 3-OH kinase) arrest development at

26 s as an adaptor) and VEGFR2 (which activates phosphatidylinositol-3-OH kinase) comprise a mechanosens

27 : activation by Gbetagamma heterodimers in a phosphatidylinositol-3-OH kinase-dependent fashion, and

28 ter treatment with LY294002, an inhibitor of phosphatidylinositol 3-OH kinase, fully consistent with

29 Notably, genetic disruption of phosphatidylinositol-3-OH kinase-gamma (PI(3)Kgamma) dec

30 r a novel beta gamma-sensitive complex, p101.phosphatidylinositol-3-OH kinase-gamma, in the transduct

31 n 76%, oxidative stress response in 21%, and phosphatidylinositol-3-OH kinase in 36% of the tested tu

32 ting with the regulatory p85alpha subunit of phosphatidylinositol-3-OH kinase in mast cells and disru

33 The phosphatidylinositol 3-OH-kinase inhibitor LY294002 has

34 is, ip 1-E1A-Axl cells were treated with the phosphatidylinositol-3'-OH kinase inhibitor wortmannin o

35 This effect was blocked by the phosphatidylinositol-3-OH kinase inhibitor LY294002 and

36 tein kinase kinase inhibitor PD98059 and the phosphatidylinositol-3-OH kinase inhibitor LY294002 both

37 ediated by mitogen-activated protein kinase, phosphatidylinositol-3-OH kinase, interferons, and G pro

38 TPA), insulin, or forskolin to activate PKC, phosphatidylinositol-3-OH kinase, or protein kinase A (P

39 , thrombospondin-4, KR18, latrophilin-3, and phosphatidylinositol-3-OH kinase P101 subunit) showed la

40 rs, inhibited by inhibitors of dynamin, Rac, phosphatidylinositol-3-OH kinase, PAK1 and actin polymer

41 the receptor tyrosine kinase, PDGFRalpha and phosphatidylinositol 3-OH kinase pathway.

42 34%, squamous differentiation genes in 44%, phosphatidylinositol-3-OH kinase pathway genes in 47%, a

43 TCF3 activated the pro-survival phosphatidylinositol-3-OH kinase pathway in BL, in part

44 Inhibitors of phosphatidylinositol 3'(OH)-kinase (PI-3K) activity dimi

45 A and BDNF were reduced by inhibitors of the phosphatidylinositol 3'-OH kinase (PI 3-kinase) signal t

46 xpression of dominant-negative and wild-type phosphatidylinositol 3-OH kinase (PI 3-kinase) subunits,

47 Here, we demonstrate that FTI-277 inhibits phosphatidylinositol 3-OH kinase (PI 3-kinase)/AKT2-medi

48 ) alpha-thrombin activates the MAPK(ERK) and phosphatidylinositol 3-OH-kinase (PI 3-kinase)/Akt pathw

49 ha(v) integrins, also requires p130(CAS) and phosphatidylinositol-3-OH kinase (PI 3-kinase).

50 ose uptake through stabilization of EGFR and phosphatidylinositol-3-OH kinase (PI(3)K) activation, an

51 TNF activates phosphatidylinositol-3-OH kinase (PI(3)K) and its downst

52 stream cell-survival effectors-most notably, phosphatidylinositol-3-OH kinase (PI(3)K) and mitogen-ac

53 of KLF2 expression in a pathway dependent on phosphatidylinositol-3-OH kinase (PI(3)K) and the kinase

54 the IL-7R but not the pre-BCR was coupled to phosphatidylinositol-3-OH kinase (PI(3)K) and the kinase

55 Phosphatidylinositol-3-OH kinase (PI(3)K) and the nutrie

56 ll-like receptor (TLR)-induced activation of phosphatidylinositol-3-OH kinase (PI(3)K) by promoting t

57 age-1 encodes a homologue of mammalian phosphatidylinositol-3-OH kinase (PI(3)K) catalytic subu

58 , receiving stimulatory signals from Ras and phosphatidylinositol-3-OH kinase (PI(3)K) downstream fro

59 e nucleotide exchange factor (GEF) for PIKE (phosphatidylinositol-3-OH kinase (PI(3)K) enhancer).

60 lass IA isoforms (p110alpha and p110beta) of phosphatidylinositol-3-OH kinase (PI(3)K) generate lipid

61 ells, we found that the p110delta isoform of phosphatidylinositol-3-OH kinase (PI(3)K) induced intern

62 Activation of phosphatidylinositol-3-OH kinase (PI(3)K) is required fo

63 The p110delta subunit of phosphatidylinositol-3-OH kinase (PI(3)K) is selectively

64 f PtdIns(3,4,5)P(3) or inhibition of class I phosphatidylinositol-3-OH kinase (PI(3)K) mimicked this

65 This effect required the activation of the phosphatidylinositol-3-OH kinase (PI(3)K) pathway, speci

66 eral cell lines is due to stimulation of the phosphatidylinositol-3-OH kinase (PI(3)K) pathway, which

67 tensin homolog (PTEN) and activation of the phosphatidylinositol-3-OH kinase (PI(3)K) pathway.

68 ght genes, including in three members of the phosphatidylinositol-3-OH kinase (PI(3)K) pathway.

69 EN) functions as a negative regulator of the phosphatidylinositol-3-OH kinase (PI(3)K)-Akt pathway, w

70 mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-OH kinase (PI(3)K)-AKT signalling

71 Here we found that Nck also controlled the phosphatidylinositol-3-OH kinase (PI(3)K)-kinase Akt pat

72 InR1, acting via the phosphatidylinositol-3-OH kinase (PI(3)K)-protein kinase

73 in of 4,128 amino acids and belonging to the phosphatidylinositol-3-OH kinase (PI(3)K)-related protei

74 manner to the p85alpha regulatory subunit of phosphatidylinositol-3-OH kinase (PI(3)K).

75 p70 S6 kinase, or Rho, but instead requires phosphatidylinositol-3-OH kinase (PI(3)K).

76 hat are both independent of and dependent on phosphatidylinositol-3-OH kinase (PI(3)K).

77 timember family and the critically important phosphatidylinositol-3-OH kinase (PI(3)K)/Akt pathway is

78 Treg cells is differences in the activity of phosphatidylinositol-3-OH kinase (PI(3)K); only Tconv ce

79 g the protein-tyrosine phosphatase Shp-2 and phosphatidylinositol-3-OH kinase (PI(3)K); they are also

80 ellular signal-regulated kinase (ERK)1/2 and phosphatidylinositol-3-OH kinase (PI-3K) pathways signif

81 pid messenger PtdIns(3,4,5)P(3), the class I phosphatidylinositol-3-OH kinases (PI(3)Ks) support many

82 The phosphatidylinositol-3-OH kinase [PI(3)K] pathway is fre

83 An insulin-like phosphatidylinositol 3-OH kinase (PI3'K) signaling pathw

84 Phosphatidylinositol-3-OH kinase (PI3 kinase) mediates c

85 ular signal-regulated kinase-1/-2 (ERK-1/2), phosphatidylinositol-3-OH kinase (PI3-K), or Src kinases

86 CAM-1) through a novel pathway that includes phosphatidylinositol 3 OH-kinase (PI3K), AKT, and nitric

87 Phosphatidylinositol 3' OH kinase (PI3K) signaling and F

88 domembrane trafficking-as a regulator of the phosphatidylinositol 3'-OH kinase (PI3K) pathway.

89 r growth, including activation of NF-kappaB, phosphatidylinositol 3'-OH kinase (PI3K) signaling, and

90 These proteins activate the phosphatidylinositol 3'-OH kinase (PI3K)/Akt pathway, wh

91 gen-activated protein kinase (MAPK), but not phosphatidylinositol 3'-OH kinase (PI3K, Pik3r1), signal

92 ction and proximal signals including Ca(2+), phosphatidylinositol 3'OH kinase (PI3K), and phospho-ext

93 Both MAP kinase and phosphatidylinositol 3-OH kinase (PI3K) activation are i

94 variety of experiments employing a specific phosphatidylinositol 3-OH kinase (PI3K) inhibitor (LY294

95 bited activity of Akt, a key effector in the phosphatidylinositol 3-OH kinase (PI3K) pathway; loss of

96 We have studied the role of phosphatidylinositol 3-OH kinase (PI3K)-Akt signaling in

97 4 (DLL4)-induced Notch signaling potentiates phosphatidylinositol 3-OH kinase (PI3K)-dependent signal

98 been intimately linked to the activation of phosphatidylinositol 3-OH kinase (PI3K).

99 find that KSHV infection also activates the phosphatidylinositol 3-OH-kinase (PI3K)/Akt cell signali

100 ys, including the VEGF/VEGF receptor and the phosphatidylinositol-3'-OH-kinase (PI3K) pathway.

101 Here, we show that a functional link between phosphatidylinositol-3-OH kinase (PI3K) and Ras is suppr

102 ancers, directly antagonizes the activity of phosphatidylinositol-3-OH kinase (PI3K) by dephosphoryla

103 monstrate elevated kinase levels of AKT2 and phosphatidylinositol-3-OH kinase (PI3K) in 32 of 80 prim

104 investigate how signaling downstream of the phosphatidylinositol-3-OH kinase (PI3K) pathway controls

105 Activation of the phosphatidylinositol-3-OH kinase (PI3K) signaling cascad

106 gh a pathway that sequentially involves Ras, phosphatidylinositol-3-OH kinase (PI3K), and protein kin

107 eptor and the p85alpha regulatory subunit of phosphatidylinositol-3-OH kinase (PI3K), leading to incr

108 The phosphatidylinositol-3-OH kinase (PI3K)-Akt pathway is a

109 rins requires activation of the lipid kinase phosphatidylinositol-3-OH kinase (PI3K).

110 actor signaling coupled to activation of the phosphatidylinositol-3-OH kinase (PI3K)/Akt pathway play

111 or suppressor PTEN, a major inhibitor of the phosphatidylinositol-3-OH kinase (PI3K)/Akt pathway, is

112 Activation of the phosphatidylinositol-3-OH kinase (PI3K)/Akt pathway, whi

113 Both trigger the phosphatidylinositol-3-OH-kinase (PI3K)-AKT-Forkhead-box

114 ation of an epidermal growth factor receptor/phosphatidylinositol-3-OH kinase/protein kinase B (AKT)/

115 Neither inhibition of phosphatidylinositol-3-OH kinase (PtdIns-3-OH kinase) wi

116 gnaling, mediated by DAF-2 through the AGE-1 phosphatidylinositol-3-OH kinase, regulates reproduction

117 eduction in the phosphorylation of Gab2, the phosphatidylinositol 3-OH kinase regulatory subunit p85,

118 ratory role, procaspase-8 interacts with the phosphatidylinositol-3-OH kinase regulatory subunit p85a

119 ammaH2AX formation can be prevented with the phosphatidylinositol 3-OH kinase-related kinase inhibito

120 ion, at an evolutionary conserved C-terminal phosphatidylinositol 3-OH-kinase-related kinase (PI3KK)

121 controls, suggesting that SSeCKS attenuates phosphatidylinositol-3-OH kinase signaling.

122 mologue (PTEN) or genomic alterations in the phosphatidylinositol-3-OH kinase-signalling pathway are

123 on the adapter Grb2-associated binder 2 and phosphatidylinositol 3-OH kinase, SphK2 showed minimal d

124 ed by platelet-derived growth factor through phosphatidylinositol-3-OH kinase, suggesting that AKT2 m

125 hough signaling via the lipid kinase PI(3)K (phosphatidylinositol-3-OH kinase), the serine-threonine

126 Activation of phosphatidylinositol-3-OH kinase was required for perios

127 r example, mitogen-activated protein kinase, phosphatidylinositol-3-OH kinase, Wnt/beta-catenin and r