ライフサイエンスコーパス: PI-3K

1 PI-3K activates Akt by phosphorylation of threonine 308

2 PI-3K activity in capsule-epithelium and fiber cell laye

3 PI-3K activity was found in both lens epithelial cells a

4 PI-3K inhibitors wortmannin and LY294002 blocked the IGF

5 PI-3K initiates a cell signaling pathway that inhibits a

6 PI-3K signaling is known to regulate protein translation

7 PI-3K, in turn, regulated 2 distinct pathways.

8 uction, while the recruitment of PI-3Kinase (PI-3K) is necessary but not sufficient for this effect.

9 A PI-3K inhibitor blocked Akt phosphorylation in JSRV Env-

10 ding FLIP, and protect from Apo2L/TRAIL in a PI-3K/Akt-dependent manner.

11 Furthermore, we found that Akt is a PI-3K downstream mediator for 5-MCDE-induced AP-1 transa

12 Akt induce NF-kappaB activation, Ly294002 (a PI-3K inhibitor), dominant-negative PI-3K, and kinase-de

13 Thus, activation of a PI-3K/Akt signaling pathway is required for cytokine-dep

14 inase reduces cell-matrix adhesion through a PI-3K-dependent, but ROCK-independent, mechanism.

15 the AP-1 induction is specifically through a PI-3K/Akt-dependent and p70(S6K)-independent pathway.

16 ation and Cap43 protein expression through a PI-3K/Akt-dependent and p70(S6k)-independent pathway.

17 ion, protects cells from apoptosis through a PI-3K/Akt/Bad pathway but not through an ERK1/2 pathway.

18 ocytes from mice deficient in the class I(A) PI-3K p85alpha regulatory subunit.

19 t hyperactivation of the p21(ras)-class I(A) PI-3K pathway is the mechanism for this phenotype.

20 intercrosses between Nf1 +/- and class I (A)-PI-3K-deficient mice, we demonstrate that hyperactivatio

21 Accordingly, PI-3K is involved in TPO-mediated inhibition of apoptosi

22 leaving the mechanism by which they activate PI-3K unclear.

23 /ERK activation but only minimally activated PI-3K and Akt.

24 n inactivation (and by extension, activation PI-3K signaling) on myelinating oligodendrocytes and the

25 Whereas constitutively active PI-3K and Akt induce NF-kappaB activation, Ly294002 (a P

26 hibited CEC transmigration without affecting PI-3K activity.

27 s were stimulated with insulin or IGF-1, and PI-3K activity was determined after immunoprecipitation

28 egulated serine/threonine kinase (ERK-2) and PI-3K by expression of dominant-negative proteins or che

29 increased survival signaling via GM-CSF and PI-3K and reduced ROS and apoptosis.

30 ments to determine the control of GM-CSF and PI-3K by calmodulin in Amo showed that GM-CSF expression

31 IGF-1 activated the MAPK/ERK and PI-3K pathways.

32 A, Casein kinase-II, and the Raf-MEK-ERK and PI-3K-Akt pathways, are not required for HSF1-mediated n

33 to TrkB, and heightened downstream ERK2 and PI-3K activities in prefrontal cortex and in lymphocytes

34 lin in Amo showed that GM-CSF expression and PI-3K activation could not be induced when calmodulin wa

35 reported an interaction between the HIF and PI-3K/Akt pathways in HER2-overexpressing cancer cells.

36 rly pathway dependent on tyrosine kinase and PI-3K and a late pathway dependent on protein kinase C.

37 The contribution of the MAPK and PI-3K pathways and, where possible, individual elements

38 rough manipulation of the PI-3K/Akt/mTOR and PI-3K/GSK-3beta/APC pathways.

39 by inhibiting their association with p38 and PI-3K.

40 lar leakage; NF-kappaB, HIF-1alpha, p38, and PI-3K activity; and VEGF, TNF-alpha, and IL-1beta levels

41 MEK inhibitor PD98059 and PI-3K inhibitors wortmannin and LY294002 inhibited a car

42 f the compounds were potent mixed DNA-PK and PI-3K inhibitors.

43 ndent with maximal benefit seen when PKB and PI-3K were inhibited before ischaemia or during both isc

44 igration by activation of PI-3K/PKCmicro and PI-3K/RhoA pathways independent of Akt.

45 plicated in control of GM-CSF production and PI-3K activation in other immune cell types.

46 via this receptor, whereas NF-kappaB/Rel and PI-3K are crucial for CD40-induced proliferation.

47 This process is mediated by SOS and PI-3K and requires coordinate upstream signals through S

48 tion, suggesting the contribution of another PI-3K family members in MEK1/2 and p42/44ERK activation.

49 nduced AP-1 transactivation, whereas another PI-3K downstream kinase, p70(S6K), was not involved in A

50 e of the mechanisms by which ZNF217 augments PI-3K/Akt signaling.

51 interest because it provided a link between PI-3K, an enzyme known to play a critical role in cellul

52 c2 as a novel mediator of cross-talk between PI-3K and the p21(ras)-ERK pathway which functions to al

53 ced NOi release requires stimulation of both PI-3K/Akt and IP3-dependent Ca2+ signalling.

54 hus, we demonstrated p85alpha-associated but PI-3K-independent cell death in response to UVR and iden

55 Bcl-2 family, an effect that was blocked by PI-3K inhibitors but not by ERK1/2 inhibition.

56 utralization of virus entry and infection by PI-3K and other cellular tyrosine kinase inhibitors sugg

57 of the Bcl-2 family), which was inhibited by PI-3K inhibitors, but not by the p70 S6K inhibitor rapam

58 s phosphorylation appears to be regulated by PI-3K activity.

59 actors FOXO1 or KLF2, which are repressed by PI-3K signaling.

60 ts indicate that Th17 cytokines are tuned by PI-3K signaling in CCR6(+) T(M) cells, which may contrib

61 analysis demonstrates that the Ras-dependent PI-3K pathway is also critical for controlling Myc prote

62 Two different PI-3K inhibitors, wortmannin and LY294002, showed Akt-in

63 ggest that cytokine receptors lacking direct PI-3K binding sites activate Akt via a Shc/Grb2/Gab2/PI-

64 Id1 expression correlates with dysregulated PI-3K signaling in multiple established GBM cell lines.

65 e beta(2)-AR-stimulated changes in MAPK/ERK, PI-3K, and Akt/protein kinase B.

66 Therefore, we examined PI-3K-deficient embryos generated by a targeted deletion

67 Finally, PI-3K inhibition increases PPM1G activity when assessed

68 ect, suggesting an alternative mechanism for PI-3K-dependent regulation of Id1 translation.

69 hat removal of a minimal domain required for PI-3K signaling abrogated the ability of EPO to override

70 her, these findings suggest a novel role for PI-3K/Akt pathways in the modulation of growth arrest re

71 nding sites activate Akt via a Shc/Grb2/Gab2/PI-3K pathway, thereby regulating cell survival and/or p

72 proteins, we show that Ras and Rac GTPases, PI-3K, and PKC participate in cell migration mediated by

73 ults suggest that activation of Akt1 by HER2/PI-3K plays an important role in conferring a broad-spec

74 , we delineated a pathway that involves HER2/PI-3K/Akt in mediating multidrug resistance in human bre

75 Collectively, these data identify PI-3K as an important regulator of HSC function and pote

76 HSC/P) function, and recent studies identify PI-3K as a therapeutic target in treating different leuk

77 dstone, United Kingdom) was used to identify PI-3K reaction products.

78 evious reports have suggested that increased PI-3K/Akt or decreased PTEN activity may activate the HI

79 HHV-8 gB Delta TM-induced PI-3K was essential for the induction of RhoA and Cdc42

80 ceptor (IL-6R) signaling (eg, IKK/NF-kappaB, PI-3K/Akt, and Raf/MAPK) and downstream effectors (eg, p

81 d EGF-induced phosphatidylinositol-3 kinase (PI-3K) and Akt activation.

82 ctivating the phosphatidylinositol-3 kinase (PI-3K) and mitogen-associated protein kinase (MAPK) sign

83 inase C (PKC) and phosphoinositide-3 kinase (PI-3K) appeared to be required for SDF-1alpha-mediated p

84 e presence of phosphatidylinositol-3 kinase (PI-3K) inhibitors (wortmannin and LY294002), HGF did not

85 Class I(A) phosphatidylinositol-3 kinase (PI-3K) is a lipid kinase, which is activated in blood ce

86 horylates the phosphatidylinositol-3 kinase (PI-3K) product PI3,4,5P3.

87 how increased phosphatidylinositol-3 kinase (PI-3K) signaling, we sought to determine whether this pa

88 inhibition of phosphotidylinositol-3 kinase (PI-3K) with LY294002 reverted the radioresistant phenoty

89 antibody, or with inhibitors of PI-3 kinase (PI-3K), c-Jun kinase (JNK), or Akt, suppressed retinal A

90 ibitor of the phosphatidylinositol-3 kinase (PI-3K), LY294002.

91 The role of Src kinases, PI-3 kinase (PI-3K), Rac1, and CD47 was determined by incubating cell

92 press HER3 caused a phosphoinoside-3 kinase (PI-3K)-dependent activation of Akt, and was associated w

93 (Erk1/2) and phosphatidylinositol-3 kinase (PI-3K).

94 d activity of phosphatidylinositol-3 kinase (PI-3K).

95 ced activation of phosphoinositide-3 kinase (PI-3K).

96 essed through the phosphoinositide-3 kinase (PI-3K)/Akt and p53 pathways.

97 can activate phosphatidylinositol-3 kinase (PI-3K)/Akt pathways and plays an important role in media

98 including Stat5, phosphoinositide-3 kinase (PI-3K)/Akt, and p42/44 mitogen-activated protein kinase

99 on and of the phosphatidylinositol-3 kinase (PI-3K)/Akt-1 pathway prevented the action of EGF on TGF-

100 activation of phosphatidylinositol-3 kinase (PI-3K)/Akt/mammalian target of rapamycin (mTOR) and glyc

101 activation of phosphatidylinositol 3'kinase (PI-3K) and its subsequent up-regulation of specific NF-k

102 n as well as phosphatidylinositol-3'-kinase (PI-3K) activity and Akt/protein kinase B phosphorylation

103 ists to activate the phosphatidyl 3'-kinase (PI-3K) prosurvival pathway.

104 ctivation of phosphatidylinositol-3'-kinase (PI-3K).

105 e mediated by phosphatidylinositol 3-kinase (PI-3K) activation.

106 ependent upon phosphatidylinositol 3-kinase (PI-3K) activity as evidenced by inhibition of glucose up

107 ade involving phosphatidylinositol 3-kinase (PI-3K) and Akt.

108 ation of both phosphatidylinositol 3-kinase (PI-3K) and NF-kappaB/Rel transcription factors is crucia

109 activation of phosphatidylinositol 3-kinase (PI-3K) and p38 kinases.

110 ross-talk between phosphoinositide 3-kinase (PI-3K) and the classical p21(ras)-Raf-Mek-ERK pathway to

111 nhibition of phosphatidyl-inositol 3-kinase (PI-3K) by LY294002 in alpha(IIb)beta(3)(+) cells induced

112 ry subunit of phosphatidylinositol 3-kinase (PI-3K) exerted a proapoptotic role in response to UVR th

113 Phosphatidylinositol 3-kinase (PI-3K) has been linked to promitogenic responses in sple

114 A or with the phosphatidylinositol 3-kinase (PI-3K) inhibitors wortmannin and LY294002 blocked the ea

115 unit (p85) of the phosphoinositide 3-kinase (PI-3K) is homologous with the Cdc42GAP and contains the

116 inhibition of phosphatidylinositol 3-kinase (PI-3K) or adenovirus expression of PTEN or dominant nega

117 Inhibition of phosphoinositide 3-kinase (PI-3K) or Akt signaling selectively prevents Th17 cytoki

118 eceptors (VEGFRs), phosphoinositol 3-kinase (PI-3K) or Rac1 was measured in CECs cocultured in contac

119 target of the phosphatidylinositol 3-kinase (PI-3K) pathway.

120 embers of the phosphatidylinositol 3-kinase (PI-3K) related kinase (PIKK) family unexpectedly reveale

121 igate whether phosphatidylinositol 3-kinase (PI-3K) signaling is involved in lens epithelial cell pro

122 nt activation of phosphoinositidyl 3-kinase (PI-3K) signaling.

123 y blockade of phosphatidylinositol 3-kinase (PI-3K) with wortmannin and LY 294002.

124 that the specific phosphoinositide 3-kinase (PI-3K), Akt and mammalian target of rapamycin (mTOR) inh

125 activation of phosphotidylinositol 3-kinase (PI-3K), Akt and p70 S6 kinase (p70S6k).

126 activation of phosphatidylinositol 3-kinase (PI-3K), Akt, and p70 S6 kinase (p70(S6k)).

127 FAK), Src, c-Cbl, phosphoinositide 3-kinase (PI-3K), and Rho-GTPases.

128 kinase (MAPK) and phosphoinositol 3-kinase (PI-3K), leading to both proliferative and antiapoptotic

129 y blockade of phosphatidylinositol-3-kinase (PI-3K), mammalian target of rapamycin (mTOR), and p38 MA

130 The phosphoinosotide 3-kinase (PI-3K)-Akt/protein kinase B (PKB) pathway has been shown

131 ctivated in a phosphatidylinositol 3-kinase (PI-3K)-dependent manner.

132 d through the phosphatidylinositol 3-kinase (PI-3K)-dependent pathway because inhibitors of PI-3K as

133 phorylation via a phosphoinositide 3-kinase (PI-3K)-dependent process.

134 inhibitor of phosphatidylinositol 3-kinase (PI-3K)-related PKs, including the catalytic subunit of D

135 activation of phosphatidylinositol 3-kinase (PI-3K).

136 horylation of phosphatidylinositol 3-kinase (PI-3K).

137 gnized by the phosphatidylinositol 3-kinase (PI-3K).

138 dly activated phosphatidylinositol 3-kinase (PI-3K)/Akt and p90(RSK1) to an extent similar to insulin

139 The phosphotidylinositol 3-kinase (PI-3K)/Akt pathway is critical for B(a)PDE-induced AP-1

140 The phosphatidylinositol-3-kinase (PI-3K)/Akt pathway, but not the Ras-mediated mitogen-act

141 F-1 activated the phosphoinositide 3-kinase (PI-3K)/Akt pathway.

142 receptor-coupled phosphoinositide 3-kinase (PI-3K)/Akt pathway.

143 player in the phosphatidylinositol 3-kinase (PI-3K)/Akt signal transduction pathway.

144 regulation of phosphatidylinositol 3-kinase (PI-3K)/Akt signaling pathway, taken together with the ev

145 ependent on a phosphatidylinositol 3-kinase (PI-3K)/Akt/GSKIIIbeta pathway(s) as indicated by the sup

146 inase (MAPK)/ phosphatidylinositol 3-kinase (PI-3K)/protein kinase-B (AKT)1-dependent manner.

147 RK)1/2 and phosphatidylinositol-3-OH kinase (PI-3K) pathways significantly, albeit partially, decreas

148 itors of phosphatidylinositol 3'(OH)-kinase (PI-3K) activity diminished EEA1 recruitment to newly for

149 10 (PTEN; eg, phosphatidylinositol-3-kinase [PI-3K]) have been reported to enhance axon regeneration

150 inhibitor of phosphatidylinositol-3-kinase, PI-3K) partially inhibited, and GF 109203X (GF, a specif

151 Phosphoinositide 3-kinases (PI-3Ks) are key enzymes for cell development, activation

152 MEK1/2-p42/44ERK and NF-kappaB pathways link PI-3K activity to Ag receptor-mediated cyclin D2 inducti

153 ion of the signaling intermediates that link PI-3K activity to the cell cycle remains incomplete.

154 In an attempt to link PI-3K/Akt to caspase inhibition, we evaluated the influe

155 ibitors PP2 and EPA (Src kinases), LY294002 (PI-3K), or NSC23766 (Rac1).

156 Whereas IGF-1-mediated PI-3K/Akt signaling plays a pivotal role in cell surviva

157 Inhibition of growth factor-mediated PI-3K signaling resulted in the downregulation of Cdc42

158 hanced the IGF-1-, but not the PDGF-mediated PI-3K activation, suggesting a possible integration of F

159 We propose that Akt mediates PI-3K-dependent p47(phox) phosphorylation, which contrib

160 Activated Rac, but not MEK1, PI-3K, or Akt, rescues biosynthesis of cyclin D1 and pro

161 ator of mammalian target of rapamycin (mTOR) PI-3K.

162 induced by starvation or inhibition of mTOR/PI-3K was not affected by either DRAM1 or p62 downregula

163 sion of Deltap85 (a dominant-negative mutant PI-3K) impaired B[a]PDE- and 5-MCDE-induced VEGF inducti

164 ion, overexpression of the dominant negative PI-3K mutant delta p85 reduced the induction of VEGF by

165 Moreover, dominant-negative PI-3K blocks IFN-promoted degradation of kappaBox alpha.

166 Ly294002, a dominant-negative PI-3K construct, and kinase-dead Akt block IFN-promoted

167 94002 (a PI-3K inhibitor), dominant-negative PI-3K, and kinase-dead Akt block IFN-dependent NF-kappaB

168 the cytoplasmic tyrosine kinase Src, but not PI-3K.

169 ignaling pathway that involves activation of PI-3K and Akt.

170 The activation of PI-3K and its association with specific tyrosine-phospho

171 ease in insulin/IGF-1-mediated activation of PI-3K and its downstream target Akt, with progression of

172 Insulin and IGF-1 stimulated activation of PI-3K in proliferating and differentiating cultures.

173 ap85, impaired B[a]PDE-induced activation of PI-3K, Akt and AP-1 transactivation.

174 ME fraction markedly inhibited activation of PI-3K, Akt, and p70 S6 kinase (p70(S6k)).

175 reveal that integrin-mediated activation of PI-3K-Akt is amplified by integrin-stimulated VEGF expre

176 enhanced stability of c-Myb by activation of PI-3K-dependent pathway(s) might contribute to the highe

177 Thus, selective activation of PI-3K/AKT in astrocytes expressing EGFRvIII appears to b

178 otes myeloma cell migration by activation of PI-3K/PKCmicro and PI-3K/RhoA pathways independent of Ak

179 e for CD40-mediated survival, as blocking of PI-3K activity did not lead to apoptosis of anti-CD40-tr

180 Further characterization of PI-3K-dependent Id1 regulation reveals that chemical or

181 e signals from IGF-1 bifurcate downstream of PI-3K.

182 tudy we examined the downstream effectors of PI-3K/Akt signaling and their role in cell death after o

183 igration by Rac1 activation independently of PI-3K signaling and may have importance in the developme

184 Inhibition of PI-3K activity by these inhibitors unexpectedly increase

185 Interestingly, while inhibition of PI-3K and AKT lowers 4E-BP1 phosphorylation and expressi

186 Chemical inhibition of PI-3K and mitogen-activated protein kinase kinase 1 inhi

187 In contrast, inhibition of PI-3K blocked the phosphorylation of Akt and GSK-3beta (

188 Inhibition of PI-3K impaired 5-MCDE-induced AP-1 transactivation, sugg

189 Our studies indicate that inhibition of PI-3K leads to apoptosis in primary cortical astrocytes.

190 Selective inhibition of PI-3K or Akt activity with their respective dominant-neg

191 regulate the MAPK cascade, as inhibition of PI-3K prevented activation of Mek1/2 and other downstrea

192 veals that chemical or genetic inhibition of PI-3K signaling reduces Id1 protein but not mRNA express

193 ted by chemical and biological inhibition of PI-3K suggestive of cross talk between signaling pathway

194 Inhibition of PI-3K, Akt, and p70(S6k) by overexpression of a dominant

195 Inhibition of PI-3K, PKCs, or Rho-associated kinase by pharmacologic i

196 ction correlates with that for inhibition of PI-3K-related protein kinase activity in these cells.

197 uced arrest was abolished by an inhibitor of PI-3K (LY294002) or by overexpression of dominant-negati

198 -3K)-dependent pathway because inhibitors of PI-3K as well as a dominant negative mutant of p85 (PI-3

199 EK inhibitor U0126, but not by inhibitors of PI-3K or Src kinases.

200 tro experiments using chemical inhibitors of PI-3K suggest that this kinase is potentially important

201 , we determined the potential involvement of PI-3K and its downstream kinases on the inhibition of AP

202 cells, suggesting a possible involvement of PI-3K in JSRV and ENTV Env-induced cell transformation.

203 significant differences in the modulation of PI-3K signaling by different growth factors during proli

204 rexpression of a dominant-negative mutant of PI-3K (Deltap85) impaired nickel-induced HIF-1 transacti

205 verexpression of dominant-negative mutant of PI-3K, Deltap85, impaired B[a]PDE-induced activation of

206 A balance between the nonactivation of PI-3K and the activation of Erk2 may be necessary during

207 Products of PI-3K activate several kinases, including the serine/thr

208 leptin promoter, whereas down-regulation of PI-3K influenced only HIF-1alpha binding.

209 In contrast to the absolute requirement of PI-3K and NF-kappaB/Rel for proliferation, these signali

210 However, the role of PI-3K in regulating fetal liver or adult hematopoiesis i

211 After stimulation, the p85 subunit of PI-3K was associated with 100- and 180-kDa tyrosine phos

212 direct binding sites for the p85 subunit of PI-3K, others, such as the interleukin-3 (IL-3) receptor

213 odies against p85, the regulatory subunit of PI-3K.

214 p85alpha and p85beta regulatory subunits of PI-3K (p85alpha-/-p85beta+/-).

215 also demonstrated that GSK-3 is a target of PI-3K/Akt-1.

216 -3K inhibitors, which inhibit all classes of PI-3Ks, the p85alpha regulatory subunit is not required

217 PC3 cells are dependent on PI-3K for survival and undergo caspase-dependent death w

218 FGF-2 showed no direct effect on PI-3K activation.

219 ing in Amo and that restoration of GM-CSF or PI-3K signaling will improve host response to the organi

220 s/mitogen-activated protein kinase (MAPK) or PI-3K.

221 ownstream mediators of Ras signaling (MEK or PI-3K) abrogated endothelial cell migration, invasion, a

222 Overall, PI-3K signaling appears to enhance Id1 translation with

223 s well as a dominant negative mutant of p85 (PI-3K subunit) reversed the inhibition, whereas a consti

224 ion, as well as to activate survival-related PI-3K/AKT pathways protecting cells from apoptosis.

225 The selective PI-3K inhibitor, LY 294002, also blocked beta(2)-AR-medi

226 rylation of c-Met, and its downstream signal PI-3K/Akt, but not ERK1/2 or p70S6K.

227 The presence of significant PI-3K activity throughout the lens further suggests that

228 Pretreatment with the specific PI-3K inhibitor, wortmannin, attenuated IL-10 mediated n

229 uces integrin-dependent pre-existing FAK-Src-PI-3K-Rho GTPase kinases.

230 Therefore, STAT3, PI-3K, and Akt are components of an IFN signaling pathwa

231 pression of delta-crystallin, but stimulated PI-3K.

232 se (Rpn) 6 subunit and Rpn12, and suppressed PI-3K activity.

233 gh a different mechanism by mainly targeting PI-3K/Akt signaling pathways.

234 Pyk2, rather than PI 3K/Akt or Erk, appears to be the key downstream effec

235 thway, taken together with the evidence that PI-3K/Akt plays an important role in the activation of A

236 Considering our previous findings that PI-3K is an upstream mediator for c-Jun/AP-1 activation,

237 Furthermore, our data indicate that PI-3K is indispensable for CD40-mediated NF-kappaB/Rel a

238 Furthermore, we show that PI-3K activity is necessary for the degradation of cycli

239 Here we showed that PI-3K class IB and class IA catalytic subunits, p110gamm

240 nduced AP-1 transactivation, suggesting that PI-3K is an upstream kinase involved in AP-1 activation

241 The PI-3K inhibitors wortmannin and LY294002 blocked the ins

242 The PI-3K pathway was additionally shown to exhibit cross-ta

243 The PI-3K/Akt pathway did not affect the HIF-1alpha binding

244 RvIII's differential ability to activate the PI-3K downstream signal may explain why this mutant rece

245 the ability of this integrin to activate the PI-3K-Akt pathway and, consequently, the rapamycin-sensi

246 y mimics the effect of HGF by activating the PI-3K/Akt signal involved in wound healing.

247 F-1 receptor neutralizing antibody aIR3, the PI-3K inhibitor wortmannin, and the heat shock protein-9

248 crophages of antibodies against EEA1 and the PI-3K hVPS34 reduced acquisition of late endocytic marke

249 without the PTP inhibitor bpV(phen), and the PI-3K inhibitors wortmannin and LY294002.

250 he JAK-STAT pathway (unique to TPO), and the PI-3K-AKT axis is differentially involved in TPO- and SD

251 cellular cascade through the ERK 1/2 and the PI-3K/ Akt kinase pathways and that these events could b

252 ctivation of the PI-3K pathways, because the PI-3K inhibitor LY294002 blocks the neuroprotective effe

253 nscription and is partially regulated by the PI-3K and ERK1/2 pathways.

254 w that cyclin D2 induction is blocked by the PI-3K inhibitors wortmannin and LY294002, which coincide

255 morphological changes were inhibited by the PI-3K inhibitors.

256 ses were regulated almost exclusively by the PI-3K pathway, with only minor contributions associated

257 entify a series of downstream targets in the PI-3K pathway, including glycogen synthase kinase-3beta,

258 cose utilization in B cells deficient in the PI-3K regulatory subunit p85alpha.

259 onents by mutant c-Kit, such as those in the PI-3K/Akt pathway, is demonstrated and may also be neede

260 a chronic (2-day) IGF-I exposure induced the PI-3K/Akt pathway only in MCF-7 cells.

261 Administration of the PI-3K inhibitor LY294002 also reduced JEG-3 proliferatio

262 cells and demonstrate that regulation of the PI-3K pathway plays a key role in these processes.

263 We have therefore examined the role of the PI-3K pathway, and of GSK-3beta, in regulating astrocyte

264 tive effects are linked to activation of the PI-3K pathways, because the PI-3K inhibitor LY294002 blo

265 pid translocation and phosphorylation of the PI-3K substrate Akt and phosphorylation of Akt substrate

266 neurons were linked to the activation of the PI-3K-->pAkt pro-survival pathway and the expression of

267 s important implications for the role of the PI-3K-Akt/PKB-HDM2 pathway in tumor progression and angi

268 ulans, the uvsB gene encodes a member of the PI-3K-related kinase family of proteins.

269 nhibition, we evaluated the influence of the PI-3K/Akt axis on the expression of a member of the inhi

270 8-452) was not affected by inhibition of the PI-3K/Akt pathway and was not enhanced by a proteasome i

271 ith HIF-1 transactivation, inhibition of the PI-3K/Akt pathway by either overexpression of Deltap85 o

272 expression are mediated by inhibition of the PI-3K/Akt pathway.

273 f black raspberries may be inhibition of the PI-3K/Akt/AP-1/VEGF pathway.

274 may be mediated through manipulation of the PI-3K/Akt/mTOR and PI-3K/GSK-3beta/APC pathways.

275 1 mRNA translation through inhibition of the PI-3K/Akt/mTOR/eIF4E-BP signaling pathway and triggering

276 g caspase activation, its stimulation of the PI-3K/p70 S6K cascade promotes proliferation.

277 response to wortmannin, suggesting that the PI-3K-mTOR pathway is required for this induction.

278 findings provide the first evidence that the PI-3K/AKT signaling pathway modulates PPM1G activity res

279 growth factor-I (IGF-I) signals through the PI-3K/Akt survival pathways.

280 he MEK/MAPK inhibitor PD98059 but not to the PI-3K inhibitor LY294002.

281 cial effect of p85alpha was unrelated to the PI-3K-dependent signaling pathway.

282 eptors indicate that Shc also signals to the PI-3K/Akt pathway in response to IL-2.

283 of cytokine stimulation, also signals to the PI-3K/Akt pathway.

284 production possibly by interfering with the PI-3K/Akt/mTOR signaling pathway.

285 Within the PI-3K cascade, inhibition of p70S6 kinase led to signifi

286 the activity of the core components of the 'PI-3K/Akt pathway' is modulated by a complex network of

287 F induction by B[a]PDE and 5-MCDE is through PI-3K/AP-1-dependent and HIF-1alpha-independent pathways

288 and this AP-1 induction was specific through PI-3K/Akt/JNKs-dependent and p70S6k-independent pathways

289 ogen synthase kinase 3beta and Foxo1 are two PI-3K-regulated targets that play important roles, but t

290 itaxel resistance in breast cancer cells via PI-3K/Akt/mTOR signaling pathway-dependent upregulation

291 athy by inducing retinal VEGF expression via PI-3K/Akt, HIF-1alpha, NF-kappaB, and secondarily, JNK/A

292 beta1-Mediated CLAN formation was PI-3K dependent, whereas beta3-mediated CLAN formation w

293 val and undergo caspase-dependent death when PI-3K is inhibited.

294 However, when PI-3K was inhibited with wortmannin or dominant-negative

295 these events comprise the mechanism by which PI-3K controls cell proliferation.

296 t-1 and describe a unique mechanism in which PI-3K acts as a mediator of antiproliferation in primary

297 was inhibited by pretreatment of cells with PI-3K inhibitors, wortmannin or Ly294002.

298 In contrast to studies with PI-3K inhibitors, which inhibit all classes of PI-3Ks, t

299 red growth in ER-positive cells treated with PI-3K and ERK1/ERK2 inhibitors, whereas it had no protec

300 sion of c-Myb expression upon treatment with PI-3K inhibitors or co-expression with dominant negative