ライフサイエンスコーパス: wortmannin

1 alpha), both free and bound to an inhibitor (wortmannin).

2 nuating effect of a specific PI3K inhibitor (wortmannin).

3 f PI3 kinase (PI3K) and Akt signalling using wortmannin.

4 S160 and TBC1D1 were completely inhibited by Wortmannin.

5 n-regulation was blocked by U0126 but not by wortmannin.

6 ion and were resistant to the PI3K inhibitor wortmannin.

7 tion of the p40(phox) PI3P-binding domain or wortmannin.

8 8059, but not by the PI3K-specific inhibitor wortmannin.

9 of PI3-K, which was completely inhibited by wortmannin.

10 wever, as it can be inhibited by LY294002 or wortmannin.

11 mmaR ligation, and this was also reversed by wortmannin.

12 and the effects of IGF-1 were diminished by wortmannin.

13 ction when PIP(2) synthesis was blocked with wortmannin.

14 onally in excised patches, is not blocked by wortmannin.

15 treated systemically with the PI3K inhibitor wortmannin.

16 nstimulated muscle after force inhibition by wortmannin.

17 sphatidylinositol 3-kinase (PI3K) inhibitor, wortmannin.

18 treatment and was inhibited by rapamycin and wortmannin.

19 tein, but not in the presence of PD98095 and wortmannin.

20 ich is localized to nuclei and unaffected by wortmannin.

21 BODIPY-wortmannin, and tetramethylrhodamine-wortmannin.

22 pha or in vitro by the PI4KIIIbeta inhibitor wortmannin.

23 ivator anisomycin and Akt pathway inhibitor, wortmannin.

24 trol) or with the PI3K inhibitor LY294002 or wortmannin.

25 eatment with the PI3K inhibitors LY294002 or wortmannin.

26 plus the phosphoinositide 3-kinase inhibitor wortmannin (1 mg/kg).

27 by phosphatidylinositide 3-kinase inhibitors wortmannin (100 nmol/L) and LY294002 (25 micromol/L).

28 Perfusion of tolbutamide (200 microm) or wortmannin (100-200 nm) prevented the hyperpolarization,

29 Wortmannin (150 nmol/liter), a PI3K inhibitor, reduced e

30 uantify the effects of a PI3K/Akt inhibitor, wortmannin (1mul of 1mug/mul) or vehicle was injected in

31 IP(2)) antibodies and high concentrations of wortmannin (20 microM) which depleted tissue PIP(2) leve

32 ngs was blocked by the PI4-kinase inhibitor, wortmannin (50 microM), suggesting that PIP2 re-synthesi

33 (0.1-1 microg/side) and the PI3K antagonist wortmannin (50 ng/side), supporting necessary roles for

34 hoinositol-3-kinase (PI-3-kinase) inhibitors wortmannin (50 nM) and PI-828 and by antibodies raised a

35 eatment with losartan (an AT-1R antagonist), wortmannin (a phosphoinositide 3-kinase (PI3K) inhibitor

36 osphocholine (a protein Kinase C inhibitor), wortmannin (a PI3K inhibitor), and parthenolide (an Ikap

37 nsulin effect on I(NCX) was not inhibited by wortmannin, a nitric-oxide synthase inhibitor, or disrup

38 borated using the pharmacological inhibitors wortmannin, a phosphatidyl inositol 3-kinase inhibitor,

39 ced increase in PLD activity, are altered by wortmannin, a phosphatidylinositol 3-kinase inhibitor, s

40 activation was inhibited in the presence of wortmannin, a phosphatidylinositol 3-kinase inhibitor.

41 Wortmannin, a phosphoinositide 3-kinase inhibitor, atten

42 pid A (MPLA), a detoxified TLR4 agonist, and Wortmannin, a phosphoinositide 3-kinase inhibitor, preve

43 and recovery from inhibition is prevented by wortmannin, a PI3/4 kinase inhibitor.

44 clodextrin, which disrupts caveolae, or with wortmannin, a PI3K inhibitor, blocked the increase in AN

45 tant to inhibition of cytokine production by wortmannin, a PI3K inhibitor.

46 f VEGF-induced PI3K/Akt kinase activation by wortmannin, a PI3K/Akt specific inhibitor, results in in

47 om oxo-M and 2.5 microm oxo-M plus 50 microm wortmannin, a PIP(2) synthesis inhibitor.

48 Co-administration of ICI 182,780 or Wortmannin abolished beneficial effects of estradiol-BSA

49 Coadministration of ICI 182,780 or Wortmannin abolished the beneficial effects of estrogen

50 addition, inhibition of the PI3K pathway by wortmannin abolished the O-GlcNAc response, suggesting t

51 Interestingly, EGF or wortmannin affected the interaction between NMDAR subuni

52 itor rapamycin nor the PI 3-kinase inhibitor wortmannin affects paxillin tyrosine 118 phosphorylation

53 PI 3-kinase (PI3K) inhibitors (LY294002 or wortmannin), Akt inhibitors, or Akt1 siRNA blocked adhes

54 moxic conditions and could be inhibited with wortmannin, Akt inhibitor, and rapamycin, consistent wit

55 atrunculin B, oryzalin, brefeldin A (BFA) or wortmannin--all of which have been shown to alter PIN1 a

56 Finally, we show that Wortmannin also induced the fusion of guard cell vacuole

57 In this study, we show that wortmannin also strongly inhibits Polo-like kinase 3 (Pl

58 However, wortmannin, an inhibitor of intracellular trafficking, i

59 Wortmannin, an inhibitor of phosphatidylinositol 3-kinas

60 Wortmannin, an inhibitor of PI3K, and small interfering

61 r (IGF)-1, an Akt activator, with or without wortmannin, an inhibitor of PI3K-Akt pathway, was inject

62 ct size/area at risk was increased by 98% in wortmannin and 101% in LY294002-treated TLR4(-/-) mice,

63 Pegylation of wortmannin and 17-hydroxywortmannin gives rise to conjug

64 sphatidylinositol-3-kinase (PI3K) inhibitors wortmannin and 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyr

65 lls with pharmacological inhibitors of PI3K, wortmannin and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyra

66 Wortmannin and 3-methyladenine, inhibitors of class III

67 sphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and 3-methyladenine, suggesting that it acts

68 rdingly, whereas the low-dose PI3K inhibitor wortmannin and Akt inhibitor III profoundly inhibited Ak

69 cal neurons, whereas the PI3K/Akt inhibitors wortmannin and Akti-1/2 attenuated the protective effect

70 ect of HNG on infarct size was attenuated by wortmannin and Akti-1/2.

71 phorylation, an effect that was inhibited by wortmannin and Akti-1/2.

72 of PI3 kinase inhibitors 3-methyladenine and Wortmannin and also by depletion of Atg5 and Beclin-1.

73 ect of PDGF was blocked by pretreatment with wortmannin and attenuated in cells pretreated with cytoc

74 Pharmacological (wortmannin and bafilomycin A1) and genetic (beclin siRNA

75 Moreover, wortmannin and GS-9820, but not PIK75 or TGX221, disrupt

76 s, osteoclastic resorption was suppressed by wortmannin and inhibitors of PI3Kbeta and PI3Kdelta, but

77 Wortmannin and its analogues are potent inhibitors of PI

78 Wortmannin and its analogues are potent PI3K inhibitors

79 f phosphatidylinositol 3-kinase (PI-3K) with wortmannin and LY 294002.

80 ,5-P(3) synthesis using the PI3K inhibitors, wortmannin and LY290004, protects cells from toxin-induc

81 phatidylinositol 3-kinase (PI3-K) inhibitors wortmannin and LY294001 (P < 0.05) but is diminished by

82 were investigated (targets in parentheses): wortmannin and LY294002 (pan-p110), PIK75 (alpha), GDC09

83 phosphoinositide-3' kinase (PI3K) inhibitors wortmannin and LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H

84 Inhibition of PI3-K signaling with wortmannin and LY294002 but not its inactive analogue ra

85 PI3K inhibitors wortmannin and LY294002 caused dose-dependent cellular a

86 The PI3K inhibitors wortmannin and LY294002 decreased morphine-induced micro

87 Inhibition of PI3Kinases using wortmannin and LY294002 or blockade of PI3Kgamma activit

88 We found that the PI3K inhibitors wortmannin and LY294002 significantly reduced the estrog

89 Depleters of tissue PIP(2) wortmannin and LY294002 stimulated TRPC6 activity, as di

90 Inhibition by the natural product wortmannin and LY294002 was detected with potencies cons

91 tors of phosphatidylinositol 3-kinase (PI3K; wortmannin and LY294002) and mammalian target of rapamyc

92 at inhibitors of PI3K/AKT signaling, such as wortmannin and LY294002, are able to inhibit CML and AML

93 ly and still frequently employed inhibitors, wortmannin and LY294002, have significant limitations as

94 re similarly blocked by the PI3K inhibitors, Wortmannin and LY294002, indicating that Btk-regulated e

95 1 mutants could be induced by treatment with Wortmannin and LY294002, which are inhibitors of Phospha

96 nhibitor bpV(phen), and the PI-3K inhibitors wortmannin and LY294002.

97 he induced Nrf2 activities were inhibited by wortmannin and LY294002.

98 levels by pre-treatment of preparations with wortmannin and LY294002.

99 P(2) at rest, which was greatly decreased by wortmannin and LY294002.

100 naturally occurring PI3K inhibitors such as wortmannin and quercetin, and building a pharmacophore-b

101 p70 S6 kinase activation was blocked by wortmannin and rapamycin, consistent with PI3K, mTOR, an

102 in of T3 treatment and could be inhibited by wortmannin and rapamycin.

103 of which effects were blocked by intrathecal wortmannin and rapamycin.

104 nocytosis inhibitors EIPA, blebbistatin, and wortmannin and the caveolin-mediated endocytosis inhibit

105 The PI3K inhibitor wortmannin and the protein phosphatase type 2A (PP2A) in

106 itol-tris phosphate kinase [PI3K] inhibitor, wortmannin and the Src-SH2 antagonist, PP2.

107 sulin secretion, which was also prevented by wortmannin and U0126 treatment.

108 sphorylation was only partially decreased by wortmannin and unaffected in Akt2 KO mice, suggesting ad

109 Wortmannin and YC-1 treatment prevented the increase in

110 sphatidylinositol 3-kinase (PI3K) inhibitor (wortmannin) and an ERK inhibitor (PD98059) but not by a

111 by inhibitors of phosphoinositide 3-kinase (wortmannin) and extracellular signal-regulated kinase (P

112 t inhibitor VIII), PI 3-kinase (LY294002 and wortmannin), and mTOR (rapamycin) reduced secretion of H

113 The inhibitor of PI3-K, Wortmannin, and anti-alpha5beta1 integrin antibodies abr

114 cells were treated with LPS +/- LY294002 or wortmannin, and beta 1- and alpha 3-integrins were asses

115 d for A-P guidance, because pertussis toxin, wortmannin, and expression of a p110gamma kinase-defecti

116 er with the PI3K inhibitors 3-methyladenine, wortmannin, and LY294002 or with small interfering RNA a

117 ments and was also sensitive to piceatannol, wortmannin, and LY294002, indicating additional requirem

118 y cytochalasin D, genistein, colchicine, and wortmannin, and paralleled the behavior of the Crohn's d

119 roduction studies with and without LY294002, wortmannin, and PI3Kalpha inhibitor-2, as well as with P

120 phosphoinositides are nearly insensitive to wortmannin, and surface membrane PI4-kinase activity, de

121 annin derivatives, biotin-wortmannin, BODIPY-wortmannin, and tetramethylrhodamine-wortmannin.

122 k2 inhibitor AG490, the PI3 kinase inhibitor wortmannin, and the phospholipase C inhibitors, U73122 a

123 by the PI(3) kinase inhibitors LY294002 and wortmannin, and this inhibition was rescued by the addit

124 sion of LMP2A in carcinoma cells, leading to wortmannin- and rapamycin-sensitive inhibition of the ne

125 Wortmannin application blocked the recovery of NMDA curr

126 sophageal cancer cell lines was treated with wortmannin as an Akt-signal inhibitor; the MAPK signal i

127 ion of chemotaxis when PI3K was blocked with wortmannin as compared with neutrophils isolated from bo

128 was not affected by another PI3K inhibitor, wortmannin, as well as phosphatase and tensin homologue

129 Wortmannin at 20 microm reduced phosphatidylinositol 4,5

130 Importantly, intrathecal wortmannin at anti-hyperalgesic doses reversed the evoke

131 Inhibition of PI3K by wortmannin attenuated IL-1beta-induced Akt and p65 acety

132 treatment with the specific PI-3K inhibitor, wortmannin, attenuated IL-10 mediated neuroprotection ag

133 of macropinocytosis with either amiloride or wortmannin blocked the increase in macropinocytosis medi

134 Wortmannin blocked the phosphorylation of PKC-mu (Ser744

135 esis of three wortmannin derivatives, biotin-wortmannin, BODIPY-wortmannin, and tetramethylrhodamine-

136 rafficking and/or internalization, including wortmannin, Brefeldin A, 2-Br-hexadecanoic acid, or dyna

137 he GRV2-positive endosomes were sensitive to Wortmannin but not brefeldin A (BFA), consistent with GR

138 s inhibited by pertussis toxin as well as by wortmannin but not by AG1478, indicating that Gi/o and p

139 lated Ser-473 activity that was sensitive to wortmannin but not staurosporine.

140 7 during treadmill-running were prevented by wortmannin but not vehicle treatment, whereas exercise-r

141 d by the PI3-kinase inhibitors, LY294002 and wortmannin, but not by the transcriptional inhibitor, ac

142 by AG490, C3 transferase, PP2, LY294002, and wortmannin, but not PD98059.

143 The inhibitor of ERK, PD98095, and of PI3K, wortmannin, but not that of protein kinase A, H89, of Rh

144 idylinositol 3'-kinase-like kinase inhibitor wortmannin, but not to caffeine.

145 ed by resveratrol or the inhibitors of PI3K (wortmannin), c-Src (PP1), and Akt (SH-5) through inhibit

146 Taken together, our results suggest that wortmannin can affect multiple functions of Plk3 in cell

147 shed AtCHX17-GFP fluorescence at PM, whereas wortmannin caused formation of GFP-labeled ring-like str

148 This decrease is blocked by a high wortmannin concentration (3 mum), suggesting that type I

149 3 targeted by AX7503, a tetramethylrhodamine-wortmannin conjugate.

150 e inhibition of PI3K by PIK-93, LY294002, or wortmannin decreased carbachol-induced translocation of

151 hibiting phosphatidylinositol 4 kinases with wortmannin decreased TRPV6 currents and Ca(2+) entry int

152 s or the phosphoinositide 3-kinase inhibitor wortmannin demonstrated differential effects of VEGF ver

153 Here we describe the synthesis of three wortmannin derivatives, biotin-wortmannin, BODIPY-wortma

154 Moreover, BFA and wortmannin did not alter cell death triggered by this mu

155 with the phosphoinositide 3-kinase inhibitor wortmannin did not disrupt localization of mCherry-RavD

156 of 81+/-2 microM, whereas another inhibitor wortmannin did not show any effect.

157 The phosphatidylinositol 3-kinase inhibitor, wortmannin, did not affect IGF-I-induced JNK activation.

158 enzopyran-4-one hydrochloride (LY294002) and wortmannin, differentially modulated both Cav1 and EGF r

159 Both brefeldin A (BFA) and wortmannin disturbed the motility and structural integri

160 Although both LY2 and wortmannin effectively blocked PI3K activity, wortmannin

161 Wortmannin eliminated contraction stimulation of phospho

162 Incubation with the PI 3-kinase inhibitor wortmannin eliminates insulin potentiation of NMDA recep

163 C20-6-(N-methylamino)hexanoic conjugates of wortmannin featuring a tertiary enamine attached to the

164 After force inhibition by wortmannin, filament areas were not significantly differ

165 Coadministration of wortmannin following trauma-hemorrhage abolished the pre

166 at was blocked by pretreatment of cells with wortmannin, H89, or by small interfering RNA knockdown o

167 ortmannin effectively blocked PI3K activity, wortmannin had little effect on FPR1 expression and did

168 dition, the blockade of PI3K-like kinases by wortmannin had no impact on the protective effect of caf

169 d by phosphatidylinositol 3-kinase inhibitor wortmannin (IC50 approximately 25 nmol/L) and epidermal

170 neration of LC3 punctae was not inhibited by wortmannin, implying that FMDV-induced autophagosome for

171 Finally, the PI3K inhibitor wortmannin improved motor function and prolonged lifespa

172 y, we demonstrate that inhibition of PI3K by wortmannin in neutrophil-like differentiated HL60 cells

173 d AS160 phosphorylation was fully blunted by wortmannin in vitro and in Akt2 knockout (KO) mice in vi

174 Blocking Akt phosphorylation with wortmannin increased LOX-1 expression, suggesting a modu

175 ion following I/R than males and addition of wortmannin increased ROS generation in females to the sa

176 ositol bisphosphate (PIP(2)) depletion using wortmannin increased the fraction of glucose-excited neu

177 genistein in the presence of ICI 182,780 or wortmannin, indicating a dependence on phosphatidylinosi

178 d by Concanamycin A treatment but reduced by Wortmannin, indicating that activated FLS2 receptors are

179 , cytochalasin, latrunculin, nocodazole, and wortmannin, indicating that microtubules, microfilaments

180 sus However, in cystic fibrosis neutrophils, wortmannin inhibited killing of a rough clinical isolate

181 Immunoblots demonstrated that LY 294002 and wortmannin inhibited PI3 kinase-dependent Akt phosphoryl

182 However, wortmannin inhibition of PI3K did impair the ability of

183 4) Wortmannin inhibition of PI3K did not correlate with PI(

184 Wortmannin inhibition of the S. aureus oxidase response

185 nd without compound C (inhibitor of AMPK) or Wortmannin (inhibitor of phosphatidylinositol [PI] 3-kin

186 regulation was not inhibited by caffeine and wortmannin, inhibitors of ATM/ATR signaling.

187 Treatment with brefeldin A (BFA) or wortmannin, inhibitors of the endocytic cycle, attenuate

188 ophageal cancer cells with the Akt inhibitor wortmannin inhibits NF-kappaB signaling, induces GSK3bet

189 In addition, we show that wortmannin inhibits Plk3 activity in live cells at conce

190 changes in food intake and body weight when wortmannin injection (into the third ventricle) occurred

191 This wortmannin-insensitive PI4KIIalpha was chosen because ba

192 Wortmannin is a steroid-derived fungal metabolite that c

193 kt activity, although based on inhibition by wortmannin, it is dependent on phosphatidylinositol 3' k

194 rtantly, we found that inhibition of Plk3 by wortmannin lead to a decrease in phosphorylation of p53

195 Wortmannin, LY294002, GDC0941, IC87114, and GS-9820 indu

196 a (PLCgamma) or preincubation with 10 microm wortmannin markedly reduced NMDA currents.

197 Wortmannin-mediated inhibition of lipid presentation ind

198 phosphatidylinositol 3-kinase (PI 3-kinase) (wortmannin), mitogen-activated protein kinase kinase (ME

199 Third, the addition of a PI3K inhibitor, wortmannin, negates the inhibition of mineralization by

200 d by DNA damage, demonstrating the effect of wortmannin on a downstream Plk3 target.

201 itol 3 (PI3) kinase inhibitors LY 294002 and wortmannin on GlyT1- and GlyT2-mediated glycine uptake w

202 phatidylinositol 3-kinase (PI3-kinase) using wortmannin or 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyra

203 PI3K by the non-isoform-selective inhibitors wortmannin or 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran

204 utophagosome formation or acidification with wortmannin or bafilomycin A1, respectively, inhibited th

205 Inhibition of PI3K with wortmannin or blockage of IRS-2/PI3K complex formation w

206 r ezrin small interfering RNA, as well as by Wortmannin or compound C (respectively for phosphatidyli

207 Cell expansion was inhibited by wortmannin or dominant-negative forms of Rac1 or Akt.

208 d by Brefeldin A and tunicamycin, but not by wortmannin or leupeptin.

209 sphatidylinositol 3-kinase (PI3K) inhibitors wortmannin or LY294002 and 50% by rapamycin, a specific

210 Pharmacologic inhibitors of PI3K (wortmannin or LY294002) were administered 1 h before myo

211 his increase was blocked by PI3K inhibitors, wortmannin or LY294002, as was the effect of FcgammaR li

212 s by blocking phosphoinositide-3 kinase with wortmannin or LY294002, or by blocking phospholipase C w

213 horylation is blocked upstream by PD98059 or Wortmannin or LY294002, respectively.

214 ylinositol 3-kinase (PI3K) was blocked using wortmannin or LY294002, the difference in disruption of

215 is effect was abrogated by pretreatment with wortmannin or LY294002.

216 ither of the well-known chemical inhibitors, wortmannin or LY294002.

217 bition of phosphatidylinositol 3-kinase with wortmannin or mTORC1 with rapamycin effectively inhibits

218 ned in cultured acinar cells pretreated with wortmannin or p85alpha siRNA.

219 Pretreatment with either wortmannin or PD 098059 heightened these apoptotic respo

220 inhibition of PI 4-kinase III beta either by wortmannin or PIK93 inhibited the conversion of [3H]seri

221 sphorylation of eNOS that was inhibitable by wortmannin or PP2 (but not by MEK inhibitor PD98059).

222 Inhibition of PI3K with wortmannin or suppression of Akt activation with dominan

223 The PI3-K inhibitor LY294002 or wortmannin or the p38 inhibitor BIRB796 blocked resolvin

224 nt with the vesicular trafficking inhibitors Wortmannin or Tyrphostin A23 impaired flg22-elicited rea

225 IF-1alpha activation, which was prevented by Wortmannin or YC-1 treatment.

226 is following hypoxemia was also prevented by Wortmannin or YC-1 treatment.

227 or antagonist (ICI 182,780), PI3K inhibitor (Wortmannin), or vehicle was injected intravenously durin

228 antagonist (ICI 182,780), a PI3K inhibitor (Wortmannin), or vehicle, was injected during resuscitati

229 t dye DAF-2) that was inhibitable by l-NAME, wortmannin, or PP2.

230 nd reproduced by a dominant negative mutant, wortmannin, or PTEN.

231 response to T3 was not blocked by LY294002, wortmannin, or rapamycin, thus supporting a T3-activated

232 Reducing PIP2 production using wortmannin, or sequestration of PIP2 using a palmitoylat

233 Compared with rapamycin and wortmannin, P529 also significantly (P < 0.05) reduced k

234 ral hemisphere weight at 22d after HI, while wortmannin partially reversed these effects.

235 kinase-beta (CaMKKbeta) using the inhibitors wortmannin, PD98059, PP2, and STO-609, respectively.

236 isrupting endomembrane trafficking by BFA or wortmannin perturbed actin polymerization at the apical

237 hibitable by L-NAME (NO synthase inhibitor), wortmannin (phosphatidylinositol 3-kinase inhibitor), or

238 D98059 (MEK1 inhibitor, 0.1 micromol/L), and wortmannin (phosphatidylinositol 3-kinase inhibitor, 1 n

239 ostin AG538 (IGF-IR inhibitor), LY294002, or Wortmannin (phosphoinositide-3-kinase inhibitor).

240 KKalphaT23 is inhibited both by LY294002 and wortmannin, phosphorylation of Ser(176)/Ser(180) is not.

241 was inhibited by pretreatment of cells with wortmannin (PI 3-kinase inhibitor) or H89 (protein kinas

242 inhibited by Gallein (betagamma inhibitor), Wortmannin (PI 3-kinase inhibitor), SecinH3 (cytohesin A

243 this was prevented by dominant negative Akt, wortmannin (PI3K inhibitor), and U0126 (MEK inhibitor).

244 rauma-hemorrhage and hypoxia groups received Wortmannin (PI3K inhibitor), YC-1 (HIF-1alpha inhibitor)

245 We previously reported that wortmannin potently inhibits Polo-like kinase 1 (Plk1).

246 Inhibition of p110 PI3-kinases by wortmannin prevents IPMK phosphorylation and activation.

247 We found that wortmannin reduced [Ca(2+) ]i increase induced by spike

248 Wortmannin reduced Ang II-evoked TRPC6 activity by over

249 The PI3K inhibitor wortmannin reduced phospholipid substitution, suggesting

250 ectin or ICAM-1 or treating neutrophils with wortmannin reduced rolling, adhesion, and migration of n

251 Pre-treatment with Ang II, OAG and wortmannin reduced TRPC6 association with PIP(2).

252 as administration of a PI3 kinase inhibitor, wortmannin, reduced Gsk3 phosphorylation and augmented l

253 tidylinositol 3-kinase (PtdInsI3K) inhibitor wortmannin, rescued the multiple-apical domain phenotype

254 Likewise, wortmannin restored bradykinin-induced M-current inhibit

255 Blockade of PI3K with wortmannin resulted in marked enhancement of flagellin-i

256 phatidylinositol 3-kinase (PI-3K) inhibitor, wortmannin reversed the ANG II-dependent repression of N

257 rated that inhibition of PIP2 synthesis with wortmannin robustly blocked both the medium and slow AHP

258 mAHP or IsAHP in OT neurons, consistent with wortmannin's effects not being due to reducing diacylgly

259 rons, which in OT neurons not only prevented wortmannin's inhibitory effect, but slowed rundown of th

260 Finally, wortmannin selectively reduced whole cell Ca(2+) current

261 This effect was wortmannin sensitive.

262 ells revealed that hyperoxia also stimulates wortmannin-sensitive degradation of p21.

263 king changes in cell morphology, including a wortmannin-sensitive increase in cell filopodia and cell

264 Processing of noncompatible ends required wortmannin-sensitive kinase activity.

265 that BiP is transported to the vacuole in a wortmannin-sensitive manner in tobacco (Nicotiana tabacu

266 In sperm, the CIL-1 5-phosphatase and a wortmannin-sensitive PI 3-kinase act antagonistically to

267 on of the mTORC1 pathway, as revealed by the wortmannin-sensitive sequential phosphorylation of tuber

268 4KIIIbeta enzyme that showed greatly reduced wortmannin sensitivity and was catalytically still activ

269 ct of insulin on KL shedding is inhibited by wortmannin, showing that insulin acts through a PI3K-dep

270 sphatidylinositol 3-kinase (PI3-K) inhibitor wortmannin, suggesting a critical regulation by PI3-K.

271 e effects could be reversed with LY294002 or wortmannin, suggesting phosphatidylinositol-3-phosphate

272 ellular Ca(2+) or pretreated with EGTA-AM or wortmannin, suggesting that the entry of Ca(2+) through

273 h sensitivity to multiple drugs (amiodarone, wortmannin, sulfometuron methyl, and tunicamycin) and io

274 ed to inhibit the more well known targets of wortmannin, the phosphoinositide 3-kinases.

275 ine, the phosphoinositide 3-kinase inhibitor wortmannin, the protein kinase C blocker chelerythrine,

276 ition of EC insulin uptake caused by L-NAME, wortmannin, the Src inhibitor PP1, and tumor necrosis fa

277 phosphoinositide 3-kinase [PI3K] inhibitor [wortmannin], the phospholipase C inhibitor [U73122] and

278 ecific enlargement of GRV2:YFP structures by Wortmannin, together with biochemical data showing that

279 ed muscle than in unstimulated muscle before wortmannin treatment and no different in stimulated and

280 tivation is confirmed with latrunculin A and wortmannin treatment as well as IPMK or SF1 depletion.

281 Combined AMPK alpha2 and Akt inhibition by wortmannin treatment of AMPK alpha2 transgenic mice did

282 ion at S1177 increased during exercise after wortmannin treatment relative to values obtained from se

283 Before wortmannin treatment, stimulation reduced thick-filament

284 Wortmannin treatment, which induces the fusion of late e

285 fferent from those of relaxed muscle without wortmannin treatment.

286 Wortmannin/U0126 or AG490 was used for pharmacological R

287 Such effect of inhibiting PI3K with wortmannin was mimicked by the PI3K inhibitor LY294002,

288 phosphoinositide 3-kinase (PI3K) activity by wortmannin was sufficient to block insulin-dependent sig

289 tor of phosphatidylinositol-3 kinase (PI3K) (wortmannin) was administered, and EX-4 or vehicle was ad

290 intake, the "anti-binge" effects of MPEP and wortmannin were not additive, nor were they observed in

291 hed by the phosphoinositide 3-kinase blocker wortmannin, whereas the low-voltage component is not.

292 the phosphatidylinositol 3-kinase inhibitor wortmannin, whereas the novel and conventional protein k

293 ts are greatly reduced by the PI3K inhibitor wortmannin, whereas this attenuation is largely PI3K ind

294 Caffeine and wortmannin, which are broad-spectrum inhibitors of ATM a

295 tion by trachealis muscle was inhibited with wortmannin, which inhibits myosin light-chain phosphoryl

296 The interference of BFA/wortmannin with actin polymerization was progressive rat

297 of PI3K activity by 3-methyl adenine (3-MA), Wortmannin (WM) and LY294002 (LY) increased viral titers

298 When the viridin wortmannin (Wm) is modified by reaction with certain nuc

299 sphoinositol-3-OH kinase (PI3K) by producing wortmannin (Wm) through an intramolecular attack.

300 nical potential of abandoned compounds using wortmannin (Wtmn) as a model drug.