ライフサイエンスコーパス: phosphatidyl inositol

1 n of a phosphate group to the 3'-position of phosphatidyl inositol.

2 human GPIT is EtN-P-2Manalpha1-4GlcN-(acyl)-phosphatidyl-inositol.

3 ERK (extracellular signal-regulated kinase), phosphatidyl inositol 3 (PI3)-kinase/Akt, and RalGEF/Ral

4 oss-linking of the FcepsilonRI activates the phosphatidyl inositol 3 kinase (PI3K) and mitogen-activa

5 epidermal growth factor receptor (ERBB1) or phosphatidyl inositol 3 kinase (PI3K) enhanced BBR3610 t

6 We found that inhibition of Ras, p38, phosphatidyl inositol 3 kinase (PI3K) or Akt signaling r

7 afenib cooperated with clinically relevant , phosphatidyl inositol 3 kinase (PI3K)-thymoma viral prot

8 ll as integrin-induced activation of Rho and phosphatidyl inositol 3 kinase, were compromised in Pyk2

9 This metabolic switch depends on the phosphatidyl inositol 3'-kinase/Akt pathway, is antagoni

10 teric site in complex with the head group of phosphatidyl inositol 3,4,5-trisphosphate and N-terminal

11 , RT-PCR using primers flanking the putative phosphatidyl inositol 3-kinase (PI3-K) binding site of E

12 3-methyl-adenine (3-MA), an inhibitor of phosphatidyl inositol 3-kinase (PI3-kinase) prevented in

13 on activation of the IGF-I receptor and the phosphatidyl inositol 3-kinase (PI3-kinase)-Akt pathway

14 ing, CD28 costimulation, and signals through phosphatidyl inositol 3-kinase (PI3K) and related metabo

15 wer cholesterol, possibly via recruitment of phosphatidyl inositol 3-kinase (PI3K) and the serine/thr

16 tivity to myeloid cell leukemia-1 (MCL1) and phosphatidyl inositol 3-kinase (PI3K) inhibitors.

17 Phosphatidyl inositol 3-kinase (PI3K) is activated by IL

18 mitogen-activated protein kinase (MAPK) and phosphatidyl inositol 3-kinase (PI3K) signaling on the s

19 s glucose uptake through the insulin, IGF-1, phosphatidyl inositol 3-kinase (PI3K), and MAPK pathways

20 cation of a pharmacological inhibitor of the phosphatidyl inositol 3-kinase (PI3K).

21 le of nuclear factor kappa B (NF-kappaB) and phosphatidyl inositol 3-kinase (PI3K)/Akt signaling in t

22 was designed to investigate the role of the phosphatidyl inositol 3-kinase (PI3K)/AKT/p70(S6K) signa

23 ecombination, we assessed the effects of the phosphatidyl inositol 3-kinase inhibitor wortmannin on t

24 the pharmacological inhibitors wortmannin, a phosphatidyl inositol 3-kinase inhibitor, and leupeptin

25 the proteasome inhibitor, MG-132, or by the phosphatidyl inositol 3-kinase inhibitor, wortmannin.

26 In contrast, the activity of phosphatidyl inositol 3-kinase is not required for OGD p

27 ism of dual targeting of casein kinase 1 and phosphatidyl inositol 3-kinase isoforms as key effectors

28 nases (MAPKs) or protein kinase B/Akt of the phosphatidyl inositol 3-kinase pathway.

29 fects of anisomycin largely involved p38 and phosphatidyl inositol 3-kinase signaling mechanisms.

30 or OGD preconditioning because inhibition of phosphatidyl inositol 3-kinase with a chemical inhibitor

31 f NF-kappaB and found that they included the phosphatidyl inositol 3-kinase, protein kinase C, mitoge

32 ail of EGFR and attenuate phosphorylation of phosphatidyl inositol 3-kinase, which is recruited by EG

33 The phosphatidyl inositol 3-kinase-like kinases (PIKKs), ata

34 The stability of the genome relies on phosphatidyl inositol 3-kinase-related kinases (PIKKs) t

35 ne mutations that block its interaction with phosphatidyl inositol 3-kinase.

36 /11, protein kinase C, tyrosine kinases, and phosphatidyl inositol 3-kinase.

37 rotection was mediated, in part, through the phosphatidyl inositol 3-kinase/Akt and GSK-3beta pathway

38 laces the FRAP/mTOR kinase downstream of the phosphatidyl inositol 3-kinase/Akt-signaling pathway, wh

39 te, and a FYVE domain that selectively binds phosphatidyl inositol 3-phosphate.

40 ough nuclear factor kappa B (NF kappa B) and phosphatidyl-inositol 3 kinase (PI 3-kinase) since addit

41 rivatives or disruption of PDGFRalpha-driven phosphatidyl-inositol 3' kinase (PI3K) activity resulted

42 Nalpha treatment resulted in an mTOR- and/or phosphatidyl-inositol 3'(PI 3') kinase-dependent phospho

43 te myocytes is promoted by activation of the phosphatidyl-inositol 3'-kinase (PI3 kinase) pathway and

44 mma-32P]ATP results in the formation of [32P]phosphatidyl-inositol 3,4, 5-trisphosphate [PtdIns(3,4,5

45 It was also found that though inhibition of phosphatidyl-inositol 3-kinase (PI-3K) by LY294002 in al

46 tions in genes that encode components of the phosphatidyl-inositol 3-kinase (PI3-kinase) signaling pa

47 Extension formation requires phosphatidyl-inositol 3-kinase activity, whereas Rho kin

48 e plasma membrane via the Golgi complex in a phosphatidyl-inositol 3-kinase-dependent and actin-indep

49 g is dependent upon downstream activation of phosphatidyl-inositol 3-kinase/Akt, inactivation of the

50 In human lymphoblasts, NRG1-mediated phosphatidyl-inositol,3,4,5 triphosphate [PI(3,4,5)P3] s

51 als mediated by SRC family kinases SYK, CBL, phosphatidyl inositol-3 (PI-3) kinase, and Rac are direc

52 r tyrosine kinases, is a potent activator of phosphatidyl inositol-3 kinase (PI3K) and mammalian targ

53 ulated by growth factors and is sensitive to phosphatidyl inositol-3 kinase (PI3K) inhibitors.

54 The phosphatidyl inositol-3 kinase (PI3K) signaling pathway

55 ddition, other signaling pathways, including phosphatidyl inositol-3 kinase (PI3K), have the potentia

56 luding insulin receptor substrate-1 (IRS-1), phosphatidyl inositol-3 kinase (PI3K), Mammalian target

57 y inhibitors of ceramide-mediated apoptosis, phosphatidyl inositol-3 kinase activity, or tyrosine kin

58 cellular signal-regulated kinase kinase 1 or phosphatidyl inositol-3 kinase inhibition.

59 Incubation with a phosphatidyl inositol-3 kinase inhibitor or expression o

60 Our results show that inhibiting phosphatidyl inositol-3 kinase or blocking the interacti

61 hand, blockade of Ca2+, phospholipase C, or phosphatidyl inositol-3 kinase signaling pathways did no

62 Radiation-induced activation of the phosphatidyl inositol-3 kinase/Akt signal transduction p

63 he synthesis and biochemical validation of a phosphatidyl inositol-3 phosphate (PI3P) immunogen.

64 in monomers, and wortmannin, an inhibitor of phosphatidyl inositol-3-kinase (PI3-kinase), each disrup

65 growth factor 1 (IGF-1) signalling (IIS) via phosphatidyl inositol-3-kinase (PI3K), phosphoinositide-

66 ylates Chk1-Ser(280), the effect of Erbb2 on phosphatidyl inositol-3-kinase (PI3K)/Akt signaling duri

67 Inhibition of phosphatidyl inositol-3-kinase or mammalian target of ra

68 he BcLOV4 photoreceptor to stimulate Ras and phosphatidyl inositol-3-kinase signaling in mammalian ce

69 clic AMP; (ii) mediated by protein kinase C, phosphatidyl inositol-3-kinase, myosin light chain kinas

70 BKM-120 is a CNS-penetrant pan-class I phosphatidyl-inositol-3 kinase (PI3K) inhibitor in clini

71 The phosphatidyl-inositol-3 kinases (PI3K) pathway regulates

72 Activation of phosphatidyl-inositol-3'-OH-kinase (PI3K) and the result

73 inase (PI3K) and the resulting production of phosphatidyl-inositol-3,4,5-trisphosphate (PIP3) are ubi

74 nsequences of biochemical inhibition of KIT, phosphatidyl-inositol-3-kinase (PI3-K), PLCgamma, MAPK/E

75 ain-of-function alterations in MET, HER2, or Phosphatidyl-Inositol-3-Kinase (PI3K), catalytically ina

76 primary classes of effectors, namely, Rafs, phosphatidyl-inositol-3-kinases (PI3Ks) and Ral guanine

77 AP activity is stimulated by lipid messenger phosphatidyl inositol 4,5 bisphoshate (PI4,5P2) and is r

78 ossibly in combination with the reduction in phosphatidyl inositol 4,5 bisphosphate (PIP2).

79 f 0.59 muM and that this activation required phosphatidyl inositol 4,5-bisphosphate (PIP(2)).

80 gamma accumulation at cell-cell contacts and phosphatidyl inositol 4,5-bisphosphate production, which

81 we show cholesterol and the signaling lipid phosphatidyl-inositol 4,5 bisphosphate (PIP(2)) regulate

82 e inner leaflet of the plasma membrane (PM), phosphatidyl-inositol 4,5-bisphosphate [PI(4,5)P(2)] com

83 es interaction with plasma-membrane-specific phosphatidyl inositol (4,5) bisphosphate (PI(4,5)P2), th

84 Sac1 is a phosphatidyl inositol-4 phosphate (PI4P) lipid phosphata

85 ARF, an ATP-dependent step that requires the phosphatidyl-inositol-4 kinase Pik1, and third ATP-depen

86 nd sequesters acidic phospholipids including phosphatidyl-inositol-4,5-bisphosphate (PIP2) [7].

87 RF6 during neurite extension by coexpressing phosphatidyl-inositol-4-phosphate 5-Kinase alpha [PI(4)P

88 of Sec2p also binds to the Golgi-associated phosphatidyl-inositol-4-phosphate, which works in concer

89 bisphosphate (PtdInsP2) levels by activating phosphatidyl-inositol-4-phosphate-5-OH kinase (PtdIns-5-

90 ith its binding partners Ypt32p, Sec15p, and phosphatidyl-inositol-4-phosphate.

91 re that the N-WASP EVH1 domain does not bind phosphatidyl inositol-(4,5)-bisphosphate, as previously

92 nities for MT1-MMP and TACE, to the glycosyl-phosphatidyl inositol anchor of prions to create a membr

93 s to the cell surface by means of a glycosyl-phosphatidyl-inositol anchor.

94 rminal domain with homology to GPI (glycosyl-phosphatidyl-inositol) anchor-containing proteins are se

95 CD16B is a glycosyl-phosphatidyl inositol-anchored molecule, whereas CD32A i

96 hosphatidic acid and phosphorylated forms of phosphatidyl inositol at least in part through the bindi

97 d implicates tubby domains as phosphorylated-phosphatidyl- inositol binding factors.

98 Changes in phosphatidyl inositol bisphosphate (PIP2) concentration

99 that mice who are deficient in the glycosyl-phosphatidyl inositol (GPI) -linked protein GFRalpha1 (G

100 essing site close to the C-terminal glycosyl phosphatidyl inositol (GPI) membrane anchor site, which

101 and the sequence predicted it was a glycosyl phosphatidyl inositol (GPI)-anchored protein that had a

102 action was further examined using a glycosyl phosphatidyl inositol (GPI)-linked form of CD45Null (lac

103 ision abnormally delayed (dally), a glycosyl-phosphatidyl inositol (GPI)-linked glypican, as a hepara

104 en used to manipulate and concentrate glycan-phosphatidyl inositol (GPI)-tethered proteins in planar

105 lipoprotein lipase (LpL) with a glycosylated phosphatidyl-inositol (GPI) anchor in cardiomyocytes hav

106 R) has been identified as an axonal glycosyl-phosphatidyl-inositol (GPI)-anchored protein, whereas th

107 Glutamate stimulates phosphatidyl inositol hydrolysis and mobilizes intracell

108 ctasia mutated ( ATM ) gene, a member of the phosphatidyl inositol kinase-like (PIKL) family of prote

109 Consecutive phosphatidyl inositol kinase-like kinase (PIKK)-dependen

110 expressing neurons also express the glycosyl-phosphatidyl inositol-linked (GPI-linked) GDNF binding c

111 tastasis-associated protein CD24, a glycosyl phosphatidyl inositol-linked surface protein, as a downs

112 Phosphatidyl-inositol mannosides (PIM) are glycolipids u

113 ocalised production of PI(4,5)P(2) by type 1 phosphatidyl inositol phosphate kinase type 1gamma (PIPK

114 tion, which is triggered on membranes by the phosphatidyl inositol phosphate PIP(3), or in solution b

115 d composition, including bilayers containing phosphatidyl inositol phosphates.

116 transduction pathway requires Akt binding to phosphatidyl-inositol phosphates (PIP) on the cell membr

117 pheral membrane proteins which interact with phosphatidyl-inositol phosphates (PIPs) in cell membrane

118 eads to an increase in phospholipids such as phosphatidyl inositols, phosphatidyl serines, phosphatid

119 yclic GMP, protein kinase G, Ca(2+), and the phosphatidyl inositol phospholipase C affects Ca(2+) ent

120 Inhibition of the phosphatidyl inositol (PI) 3-kinase intermediate in IGF-

121 studied biochemical response: stimulation of phosphatidyl inositol (PI) hydrolysis].

122 In vitro phosphatidyl inositol (PI) kinase assay demonstrated tha

123 LRH-1-which reveal that these receptors bind phosphatidyl inositol second messengers and that ligand

124 osphorylation of several proteins, including phosphatidyl inositol-specific phospholipase C-gammal.

125 ants and that prevention of this accelerated phosphatidyl-inositol turnover in turn negates suppressi

126 atidyl ethanolamine, phosphatidyl serine and phosphatidyl inositol) under cold stress.

127 Conversion of phosphatidic acid to phosphatidyl inositol was the most active pathway in lam

128 lipid classes, i.e. phosphatidyl-choline and phosphatidyl-inositol, were differentially affected by t