ライフサイエンスコーパス: PtdIns 3-kinase

1 PtdIns 3-kinase is activated to the same extent with and

2 PtdIns 3-kinase signals cannot mimic p21ras and induce t

3 A PtdIns 3-kinase activity could also be co-immunoprecipit

4 n demonstrates that an interaction between a PtdIns 3-kinase and PI-TP occurs in vivo, which further

5 lmonary artery fibroblast DNA synthesis in a PtdIns 3-kinase-dependent manner via a G-protein-coupled

6 d was activated by PDGF-BB and thrombin in a PtdIns 3-kinase-dependent manner; this may underlie mito

7 f the other PtdIns 4-kinase gene (STT4) or a PtdIns 3-kinase gene (VPS34) did not rescue sec14-3 cell

8 or Go alpha subunits were unable to activate PtdIns 3-kinase.

9 mma12, and beta1gamma13 dimers all activated PtdIns 3-kinase about 26-fold with 4-25 nm EC50 values.

10 om LY294002, and antibodies directed against PtdIns 3-kinase did not inhibit Ca(2+)-induced alpha-gra

11 t functional connection between the Apg1 and PtdIns 3-kinase complexes.

12 l phosphorylation by PtdIns-4-P 5-kinase and PtdIns 3-kinase.

13 preferential coupling of isoforms to Raf and PtdIns-3-kinase pathways, we find that endogenous Ras is

14 ound that upon overexpression of A1PiZ, both PtdIns 3-kinase complexes were required for delivery of

15 n/IGF receptor or its intramuscular effector PtdIns-3-kinase (PI3K) causes unexpected activation of M

16 Cpk is the first PtdIns 3-kinase identified with this particular substrat

17 sponse completely, indicating a key role for PtdIns 3-kinase.

18 Our findings suggest a role for PtdIns 3-kinases and presumably for the product, PtdIns

19 Mouse p170 is also distinct from PtdIns 3-kinase or the p110 PI 3-kinases in exhibiting a

20 trast to the PI-specific yeast VPS34 homolog PtdIns 3-kinase and the p110 PI 3-kinases, which phospho

21 A unique characteristic of class II PtdIns 3-kinases is the presence of both a phox homolog

22 al function of the C2 domain of the class II PtdIns 3-kinases remains to be determined.

23 structural model of a C2 domain of class II PtdIns 3-kinases.

24 nduced a 2.3 plus minus 0.1-fold increase in PtdIns 3-kinase activity in p85 immunoprecipitates, whic

25 inhibition of phosphatidylinositol 3-kinase (PtdIns 3-kinase) activity rescues the Ca(2+) release def

26 ponent of two phosphatidylinositol 3-kinase (PtdIns 3-kinase) complexes: complex I is required for au

27 4002, a selective phosphoinositide 3-kinase (PtdIns 3-kinase) inhibitor.

28 ma isoform of phosphatidylinositol 3-kinase (PtdIns 3-kinase) was examined using pure, recombinant G

29 is activated in a phosphoinositide 3-kinase (PtdIns 3-kinase)-dependent manner upon stimulation of th

30 s oncogene is Phosphatidylinositol 3-kinase (PtdIns 3-kinase).

31 Mammalian PtdIns 3-kinases are divided into three classes based on

32 he present study, we examined the ability of PtdIns 3-kinase to initiate the Rac-1 signaling pathways

33 or thrombin resulted in rapid activation of PtdIns 3-kinase and accumulation of phosphoinositide-3,4

34 mma subunit in determining the activation of PtdIns 3-kinase was examined using gamma subunits with a

35 2)O(2) production requires the activation of PtdIns 3-kinase.

36 )) are up-regulated by the local activity of PtdIns 3-kinase.

37 nt G proteins and the p101/p110gamma form of PtdIns 3-kinase reconstituted into synthetic lipid vesic

38 issues containing the p101/p110gamma form of PtdIns 3-kinase, was ineffective.

39 hich could be reversed by activated forms of PtdIns 3-kinase and PKB/Akt.

40 l antigen receptor function independently of PtdIns 3-kinase activity.

41 PtdIns(3,4,5)P3] production as inhibition of PtdIns 3-kinase by wortmannin or deletion of the PH doma

42 roximately 100 microM), another inhibitor of PtdIns 3-kinase, and neither compound affected type II P

43 lipid transfer proteins in the regulation of PtdIns 3-kinase activity.

44 Ruk was shown to be a negative regulator of PtdIns 3-kinase activity through binding to its P85 regu

45 The role of PtdIns 3-kinase in Ras signaling in T cells has not been

46 The essential role of PtdIns 3-kinase is likely to provide PI(3,4,5)P(3) that

47 naling molecules such as Syk, p85 subunit of PtdIns 3-kinase, and p62dok, suggesting that these molec

48 e, providing proof of concept for the use of PtdIns 3-kinase inhibitors in myotubular myopathy and su

49 re most similar to that of p110, a family of PtdIns 3-kinases that mediates the responses of cells to

50 syl inhibited the activity of beta1gamma2 on PtdIns 3-kinase.

51 CR or Ras activation of AP-1 is dependent on PtdIns 3-kinase.

52 ulated the lipid kinase activity of the p150.PtdIns 3-kinase complex 3-fold.

53 Phosphatidylinositide (PtdIns) 3-kinase catalyzes the addition of a phosphate g

54 regulator, the class 3 phosphatidylinositol (PtdIns) 3-kinase vacuolar protein sorting 34 (Vps34), in

55 red complex includes a phosphatidylinositol (PtdIns) 3-kinase and associated proteins that are involv

56 R and F-actin required phosphatidylinositol (PtdIns) 3-kinase and was inhibited by SHIP, because the

57 es have shown that the phosphatidylinositol (PtdIns) 3-kinase encoded by the yeast VPS34 gene is requ

58 The phosphatidylinositol (PtdIns) 3-kinase Vps34 is a lipid kinase that regulates

59 Multiple phosphatidylinositol (PtdIns) 3-kinases (PI3Ks) can produce PtdIns3P to contro

60 on of a novel class of phosphatidylinositol (PtdIns) 3-kinases whose members contain C-terminal C2 do

61 gnaling proteins, including phosphoinositol (PtdIns) 3-kinase (EC 2.7.1.137), Cbl, GRB2, p130Cas and

62 o triggering of the T cell antigen receptor; PtdIns 3-kinase activity is both required and sufficient

63 Gbeta5gamma2 was not able to stimulate PtdIns 3-kinase despite producing a 10-fold activation o

64 ability of the betagamma dimer to stimulate PtdIns 3-kinase.

65 ayed variation in their ability to stimulate PtdIns 3-kinase.

66 ibited the ability of the dimer to stimulate PtdIns 3-kinase.

67 Gbeta(1-4) complexed with gamma2-stimulated PtdIns 3-kinase activity about 26-fold with EC50 values

68 The present data thus highlight that PtdIns 3-kinase and Akt/PKB are not universal Ras effect

69 Accumulated evidence shows that PtdIns 3-kinase can provide a critical signal for cell p

70 ced alpha-granule secretion, suggesting that PtdIns 3-kinase is not involved in alpha-granule secreti

71 ubiquitin ligase complex, components of the PtdIns 3-kinase complex, and the ESCRT machinery.

72 associated with reduced accumulation of the PtdIns 3-kinase product phosphatidylinositol 3,4,5-trisp

73 n PtdIns(3)P, Pep12p, Vps21p, Vps45p, or the PtdIns 3-kinase, Vps34p.

74 These data demonstrate that the PtdIns 3-kinase/protein kinase B pathway represents a ke

75 n PtdIns 4-kinases by its sensitivity to the PtdIns 3-kinase inhibitor wortmannin (WT).

76 ribution and activation of enzymes distal to PtdIns 3-kinase, including those that promote Rac activa

77 ular myopathy and suggesting that unbalanced PtdIns 3-kinase activity plays a critical role in the pa

78 g the production of PtdIns(3)P by the Vps34p PtdIns 3-kinase and the subsequent Fab1p- dependent phos

79 1p, which converts the product of the Vps34p PtdIns 3-kinase PtdIns(3)P into PtdIns(3,5)P2, also is r

80 Recombinant p150 associated with PtdIns 3-kinase in vitro in a stable manner, resulting i

81 150 similar to that previously observed with PtdIns 3-kinase.

82 ception of beta5, interact equally well with PtdIns 3-kinase.