ライフサイエンスコーパス: protein kinase B

1 a peptidase-resistant substrate peptide for protein kinase B.

2 kt, a serine/threonine kinase, also known as protein kinase B.

3 y caused by an inhibitory phosphorylation by protein kinase B.

4 of protein phosphatase 2A, which inactivates protein kinase B.

5 HlyA can potently inhibit activation of Akt (protein kinase B), a key regulator of host cell survival

6 ulation of optimal level and duration of Akt/protein kinase B activation (a molecule important for ef

7 ation repair of DNA double-strand breaks and protein kinase B activation, leading to increased apopto

8 (H2O2), p38 activation did not inhibit AKT (protein kinase B) activation by IGF-I, which is in contr

9 dhesion kinase (FAK Tyr576/577; +28 +/- 6%), protein kinase B activity (Akt; +113 +/- 31%), p70S6K1 (

10 Both agents lowered protein kinase B activity, but this was not mediated by

11 nant negative constructs, we found that Akt (protein kinase B) activity controlled gap junction stabi

12 bitor, suppresses protein kinase C (PKC) and protein kinase B/AK transforming (AKT) signaling, induce

13 primary keratinocytes and the activation of protein kinase B Akt and MAPKp42/44 The QHREDGS peptide,

14 droxidopa effect on the Rho kinase (RhoK) / protein kinase B (AKT) / endothelial nitric oxide syntha

15 1(-/-) ) mice were traced to a deficiency in protein kinase B (Akt) activation in hepatocytes, which

16 Finally, blocking downstream Protein kinase B (AKT) activation with Phosphatidylinosi

17 AF also induced protein kinase B (Akt) activation, which was reduced wit

18 leted on chromosome 10 (PTEN) loss regulated protein kinase B (AKT) activation.

19 ffects are mediated via a novel mechanism of protein kinase B (Akt) activation.

20 oitin sulfate proteoglycans could inactivate protein kinase B (Akt) and activate GSK-3beta signals in

21 Protein kinase B (Akt) and downstream transcription fact

22 enhanced the phosphorylation (activation) of Protein kinase B (Akt) and endothelial nitric oxide synt

23 enhanced the phosphorylation (activation) of Protein kinase B (Akt) and endothelial nitric oxide synt

24 ng residues that persists downstream through protein kinase B (AKT) and FOXO1 (forkhead box protein O

25 rylation of the insulin-signalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3bet

26 d >50% reduction in levels of phosphorylated protein kinase B (Akt) and H3K36me3 in bones of NO66-TG

27 lls resulted in increased phosphorylation of protein kinase B (Akt) and inhibitory phosphorylation of

28 The activity of PI3K/protein kinase B (AKT) and insulin receptor substrate-1

29 There were elevated activities of protein kinase B (Akt) and mitogen-activated protein kin

30 Protein kinase B (Akt) and nuclear factor (NF)-kappa B (

31 extracellular regulated kinase (ERK)1/2 and protein kinase B (AKT) as well as the G-protein-coupled

32 rus expressing a dominant-negative mutant of protein kinase B (Akt) compared with cells infected with

33 rough phosphatidylinositol-3-kinase (PI 3-K)/protein kinase B (Akt) dependent activation of mTOR sign

34 ignaling by phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) has previously been shown to regu

35 extracellular signal regulated kinase (ERK), protein kinase B (Akt) in HL60 cells differentiated to n

36 ked potency in ABC DLBCL models, whereas the protein kinase B (AKT) inhibitor AZD5363 induced apoptos

37 Protein kinase B (Akt) is a key effector of multiple cel

38 Protein kinase B (AKT) is a major target in this disease

39 xpressed GTPase, which binds to and enhances protein kinase B (Akt) kinase activity in a guanine nucl

40 g pathway, such as phosphorylation of either protein kinase B (Akt) or of the insulin receptor.

41 pts the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway and shows high proapoptot

42 these, the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway appears to be pivotal to

43 The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway has been identified as an

44 elated with activation of the oncogenic PI3K/protein kinase B (AKT) pathway in both DLBCL cell lines

45 of the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) pathway in the regulation of LPS

46 vity in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway, as being critical events

47 2 impairs the signaling function of the PI3K/protein kinase B (AKT) pathway, leading to functional de

48 ibition of the phosphatidylinositol 3 kinase/protein kinase B (Akt) pathway.

49 of the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) pathway.

50 ugh the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway.

51 -containing inositol 5-phosphatase 1 (SHIP1)/protein kinase B (Akt) pathway.

52 smalogen insufficiency resulted in defective protein kinase B (AKT) phosphorylation and subsequent si

53 ty of integrin-linked kinase (ILK), level of protein kinase B (Akt) phosphorylation at serine 473 and

54 racellular signal regulated kinase (ERK) and protein kinase B (AKT) phosphorylation resulting in diff

55 of insulin resistance through inhibition of protein kinase B (Akt) phosphorylation.

56 p between mitochondrial alterations and PI3K/protein kinase B (AKT) signaling activation using hepato

57 cts via the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling cascade to protect CA1

58 Disrupted neuronal protein kinase B (Akt) signaling has been associated wit

59 the phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) signaling pathway and a potent tu

60 The phosphatidylinositol 3-kinase (PI3K)-protein kinase B (Akt) signaling pathway is one of the m

61 protein and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways in the epiderm

62 cogenic phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathways.

63 eration, affected the magnitude of c-Src and protein kinase B (AKT) signaling, and reduced tumorigeni

64 eptor (EGFR) and focal adhesion kinase (FAK)/protein kinase B (AKT) signaling.

65 of Rac1, p21-activated kinase (PAK) and AKT/protein kinase B (AKT) signaling.

66 he phosphatidylinositol-3-OH kinase (PI(3)K)-protein kinase B (Akt) signalling cascade, leads to the

67 ing the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signalling pathway.

68 The protein kinase B (Akt) substrate cAMP response-binding p

69 extracellular signal-related kinase (ERK) or protein kinase B (Akt) was also blunted by bexarotene.

70 ic inhibition of TGF-beta receptor, PI3K, or protein kinase B (AKT) was found to block hypoxia-induce

71 in mTOR phosphorylation, levels of activated protein kinase B (Akt) were also reduced.

72 ts inhibitory phosphorylation on serine 9 by protein kinase B (Akt), a major effector of the canonica

73 ion of several signaling pathways, including protein kinase B (Akt), extracellular signal-regulated k

74 , such as hypoxia-inducible factor (HIF) and protein kinase B (AKT), in addition to pathways independ

75 ivation of autophagy, measures were taken of protein kinase B (AKT), mTORC1, and AMPK pathway activat

76 ts of GLUT1, GLUT4, total and phosphorylated protein kinase B (Akt), phosphorylated AMP-activated pro

77 glycogen synthase kinase 3-beta (GSK-3beta), protein kinase B (Akt), phosphorylated tau (phospho-tau)

78 The intracellular signalling kinases Akt/protein kinase B (Akt), protein kinase A (PKA) and adeno

79 lin treatment, through the downstream kinase protein kinase B (Akt), significantly decreases NET surf

80 The activity of protein kinase B (Akt)--a major kinase promoting cell pr

81 dylinositol-4,5-bisphosphate-3-kinase (PI3K)-protein kinase B (AKT)-mammalian target of rapamycin (mT

82 lecular level, we observed activation of the protein kinase B (Akt)-mechanistic target of rapamycin g

83 vation of protein kinase A and inhibition of Protein kinase B (AKT).

84 ant decrease in PTEN and increased activated protein kinase B (AKT).

85 eta through phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt).

86 hoinositide 3-kinase-dependent activation of protein kinase B (Akt).

87 ugh phosphatidylinositol-3 kinase (PI3K) and protein kinase B (Akt).

88 togen-activated protein (MAP) kinase Erk and protein kinase B (Akt).

89 tion of both focal adhesion kinase (Fak) and protein kinase B (Akt).

90 the potential involvement of the protective protein kinase B (AKT)/extracellular signal-related kina

91 ing the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mT

92 of intrinsic cellular programs regulated by protein kinase B (Akt)/mammalian target of rapamycin (mT

93 d is associated with the inactivation of the Protein kinase B (Akt)/mammalian target of Rapamycin/p70

94 The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (

95 through the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/p53 axis in the intestinal stem c

96 ng pathways, including the TGF-beta pathway, protein kinase B (AKT)/PI3K pathway, RAS, etc.

97 iation and progression in vivo by abrogating protein kinase B (AKT)1 activation, and that Id1 interac

98 anisms including polo-like kinase 1 (Plk-1), protein kinase B (Akt-1), and/or p53 pathways leading to

99 v-akt murine thymoma viral oncogene homolog/protein kinase B (AKT/PKB) is shown to modulate PGC1alph

100 pamycin complex (mTORC1), is known to induce Protein kinase B (Akt/PKB) Ser-473 phosphorylation in a

101 alciparum merozoites is mediated through Akt/protein kinase B (Akt/PKB), the mitogen-activated protei

102 n, we found that KSHV reactivation activates protein kinase B (AKT/PKB), which promotes cell survival

103 phosphorylation status of the Ser/Thr kinase protein kinase B (Akt/PKB), while Thr(308) phosphorylati

104 ation of v-akt murine thymoma viral oncogene/protein kinase B [AKT], inhibition of glycogen synthase

105 ork showed that p27 can be phosphorylated by protein kinase B/Akt (PKB/Akt) at T157 and T198.

106 role in the activation of kinases including protein kinase B/Akt and glycogen synthase kinase 3beta

107 ulation, and this binding was independent of protein kinase B/Akt and protein kinase C kinase activit

108 ibited insulin-stimulated phosphorylation of protein kinase B/Akt and reduced glycogen content.

109 is required for the sustained activation of protein kinase B/AKT but not for the activation of mitog

110 (PI3K), but inhibition of phosphorylation of protein kinase B/Akt does not entirely abolish expressio

111 of the p38alpha/beta and ERK1/2 MAPKs and of protein kinase B/Akt increased in IL-18Ralpha ko MEF, wh

112 Furthermore, protein kinase B/Akt inhibition induced by ONOO- or high

113 are ATP-competitive, selective inhibitors of protein kinase B/Akt is reported.

114 EGF activation of the Erk and protein kinase B/Akt pathways is enhanced, both in ampli

115 Protein kinase B/Akt protein kinases control an array of

116 with an impairment of the insulin-stimulated protein kinase B/Akt serine 473 phosphorylation but not

117 to increased PI3K activity and activation of protein kinase B/Akt survival pathways.

118 while inhibiting Fas expression, activating protein kinase B/AKT, and inducing Faim 3.

119 ly the various isoforms of protein kinase A, protein kinase B/Akt, and protein kinase C, PKD family m

120 in upstream of the phosphoinositide 3-kinase-protein kinase B/AKT-mammalian target of rapamycin (PI3K

121 event requires p27 Ser-10 phosphorylation by protein kinase B/Akt.

122 ged by CD97 in cancer cells, such as ERK and protein kinase B/Akt.

123 itors stabilize the phosphorylation state of protein kinases B/Akt and C.

124 Th2 cells displayed reduced activity of PKB (protein kinase B; Akt), and constitutively active Akt re

125 ression in wild-type but not in eNOS(-/-) or protein kinase B (Akt1)(-/-) mice.

126 Phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT1), and c-myc have well-established

127 led a defective prosurvival pathway via PI3K/protein kinase B (Akt1)/Bcl-2-associated death promoter

128 er with reduced muscle GLUT4, hexokinase II, protein kinase B/Akt1, and Akt2 protein level, and a ten

129 owth factor beta (TGFbeta) signaling through protein kinase B (Akt2) induces phosphorylation of heter

130 Protein kinase B (also known as AKT) and the mechanistic

131 p85 regulatory subunit of PI(3)K and induced protein kinase B (also known as Akt) phosphorylation, si

132 ay via a caspase-3-dependent cleavage of the protein kinase B (also known as Akt).

133 o oppose activation of the key PI3K effector protein kinase B (also known as Akt).

134 The activity of protein kinase B, also known as Akt, is commonly elevate

135 sis and hepatic tumors with up-regulation of protein kinase B and extracellular signal-related kinase

136 Specifically, CXCL10 induced long-term protein kinase B and Jun N-terminal kinase activation, l

137 phoinositide 3-kinase and phosphorylation of protein kinase B and mitogen-activated protein kinases.

138 nd inhibits its subsequent interactions with protein kinase B and p38 upstream kinases as shown by co

139 FTY720 altered the phosphorylation state of protein kinase B and p38, our data refuted the role of t

140 Protein kinase B and pantothenate synthetase are examine

141 ction of human biliverdin reductase with Akt/protein kinase B and phosphatidylinositol-dependent kina

142 wo of these, the serine/threonine kinase Akt/protein kinase B and the PH domain-containing protein Ph

143 phorylation of 14 phosphoproteins (including protein kinases B and C) after 5 and 15 minutes.

144 Akt (also known as protein kinase B) and extracellular signal-regulated pro

145 d with attenuated insulin/Akt (also known as protein kinase B) and extracellular signal-related kinas

146 gamma membrane recruitment, and reduced Akt (protein kinase B) and glycogen synthase kinase 3beta pho

147 increased phosphorylation/activation of Akt (protein kinase B) and increased phosphorylation/inhibiti

148 rin involves activation of the JAK/PI3K/AKT (protein kinase B) and MAPK/ERK pathways.

149 AMPK phosphorylation, and increased Akt/PKB (protein kinase B) and mTOR phosphorylation (P<0.05).

150 fluorescent substrate for Akt, also known as protein kinase B, and a method to quantitatively report

151 l inhibition implicated the calcineurin, Akt/protein kinase B, and Ca(2+)/calmodulin-dependent protei

152 ogen-activated protein kinase as well as AKT protein kinase B, and caused cyclin B-dependent G(2)-M c

153 h factor homology domains-2 (TIE2) receptor, protein kinase B, and Erk1,2 phosphorylation detectable

154 Rac1, insulin-like growth factor 1 receptor, protein kinase B, and extracellular signal-regulated kin

155 racellular signal-regulated protein kinases, protein kinase B, and Janus kinase, which are activated

156 significantly inhibited ROS generation, Akt/protein kinase B, and tuberin phosphorylation and result

157 potential and self-renewal of MM cells in a protein kinase B- and SRY (sex-determining region Y)-box

158 d through mTORC2-mediated phosphorylation of protein kinase B at Ser(473) and that this mechanism is

159 omain, and leucine zipper motif 1) is an Akt/protein kinase B-binding protein involved in signal tran

160 Akt/protein kinase B controls cell growth, proliferation, an

161 ere modulated by a phosphoinositide 3-kinase-protein kinase B-cycle-dependent kinase 7 pathway as rev

162 roliferation via a phosphoinositide 3-kinase-protein kinase B-cycle-dependent kinase 7 pathway.

163 For disseminated tumors, protein kinase B disruption in itself had no effect on t

164 192 protein kinases and discovered that Akt/protein kinase B dramatically accelerates and amplifies

165 iption factor signaling through enhanced Akt/protein kinase B expression, in glycolytic muscles, PGC-

166 showed restoration of wild-type (WT) AKT or protein kinase B, extracellular signal-regulated kinase

167 Phosphorylation of protein kinase B, extracellular signal-regulated kinase

168 ein kinase, stress-activated protein kinase, protein kinase B, extracellular signal-regulated kinase,

169 ted phosphorylation of IR, IRS proteins, Akt/protein kinase B, glycogen synthase kinase 3beta, and p7

170 The Akt serine/threonine kinase (also called protein kinase B) has emerged as a critical signaling mo

171 horylation of IRS1 leads to its degradation, protein kinase B inhibition, and the loss of insulin-med

172 -based screening identified 7-azaindole as a protein kinase B inhibitor scaffold.

173 t the identification of a small molecule Akt/protein kinase B inhibitor, API-1.

174 The protein kinase Akt (also known as protein kinase B) is a critical signaling hub downstream

175 AKT kinase, also known as protein kinase B, is a key regulator of cell growth, pro

176 cytotoxic T cells (CTL), Akt, also known as protein kinase B, is activated by the T cell antigen rec

177 linositol 3-kinase (PI3K)-AKT (also known as protein kinase B)-mammalian target of rapamycin (mTOR) p

178 o blunted the increase in phosphorylation of protein kinase B, mammalian target of rapamycin, p70 rib

179 e phosphatidylinositide 3-kinase (PI3K) -AKT/protein kinase B-mammalian target of rapamycin (mTOR) ca

180 AR) and the phosphoinositide 3-kinase (PI3K)/protein kinase B/mammalian target of rapamycin (mTOR) si

181 ibitors of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT

182 sin homolog (PTEN) is a key inhibitor of the protein kinase B/mammalian target of rapamycin axis that

183 xample, PKA (protein kinase A) and AKT/mTOR (protein kinase B/mammalian target of rapamycin) pathway

184 apoptosis, autophagy and phosphorylation of protein kinase B/mammalian target of rapamycin/p70 ribos

185 Here we show that Protein Kinase B-mechanistic Target of Rapamycin (PKB/AK

186 protein kinase C, phosphoinositide 3-kinase/protein kinase B, mitogen-activated protein kinases [MAP

187 mutation in Akt3 (encoding one of three AKT/protein kinase B molecules), leading to a non-synonymous

188 e plasma membrane and suppression of the Akt/protein kinase-B oncogene pathway, to which KM12C cells

189 etyl-CoA carboxylase, glycogen synthase, and protein kinase B or insulin receptor substrate-1 level w

190 The silencing of GSK-3beta, but not Akt-2 (protein kinase B) or glycogen synthase kinase-3alpha (GS

191 ence in part by up-regulating phosphorylated protein kinase B (p-AKT) and decreasing phosphorylated e

192 the expression of NGF, phospho-TrkA, phospho-protein kinase B (p-AKT), NF-kappaB, and B-cell lymphoma

193 TNNB1), and immunohistochemical (phosphor[p]-protein kinase B, p-insulin growth factor-IR, p-S6, p-ep

194 cells through the phosphoinositide 3-kinase/protein kinase B pathway and is markedly elevated with a

195 stimulation of the phosphoinositide 3-kinase/protein kinase B pathway leading to cyclin D1 nuclear ac

196 nt signaling pathways such as the AKT kinase/protein kinase B pathway.

197 s of Pten resulted in activation of the AKT (protein kinase B) pathway components from P28 onward, wh

198 The phosphoinositide 3-kinase (PI3K)/AKT (protein kinase B) pathway is a pivotal signaling corrido

199 ular signal-regulated kinase, phosphorylated protein kinase B, phosphorylated mammalian target of rap

200 same extent as mutation of Thr-246, the Akt/protein kinase B-phosphorylated site.

201 he enhanced ability of insulin to induce Akt/protein kinase B phosphorylation in liver, muscle, and a

202 iated with an increase in insulin-stimulated protein kinase B phosphorylation in the liver and muscle

203 oinositide-dependent protein kinase or alter protein kinase B phosphorylation.

204 effects on the Phosphatidylinositol 3 kinase/Protein kinase B (PI3K/Akt) apoptotic pathway.

205 rtantly, phosphoinositide 3-kinase inhibitor/protein kinase B (PI3K/AKT) pathway plays a key role in

206 ated and triggered phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway, which subsequently

207 kinase (MAPK) and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathways.

208 ugs, cells become sensitive to drugs against protein kinase B (PKB or AKT) and rapidly accelerated fi

209 Protein kinase B (PKB or Akt) is an important component

210 sults in significantly reduced activation of protein kinase B (PKB or Akt) leading to decreased Akt p

211 rated that GSK3beta through a beta-arrestin2/protein kinase B (PKB or Akt)/protein phosphatase 2A (PP

212 Akt/protein kinase B (PKB) activation/phosphorylation by ang

213 el-18 is accompanied by the reduction of Akt/protein kinase B (PKB) activity in breast cancer cells.

214 imized peptide substrate was used to measure protein kinase B (PKB) activity in single cells.

215 Cellular protein kinase B (PKB) activity, as measured by immunofl

216 distinct pathways from IR to GLUT4: (i) via protein kinase B (PKB) and Akt substrate of 160 kDa (AS1

217 The activity of protein kinase B (PKB) and phosphorylation of eukaryotic

218 pase (LPL) activity, involving activation of protein kinase B (PKB) and reduced phosphorylation of li

219 t the temporal and spatial activation of two protein kinase B (PKB) homologues, PkbA and PkbR1, in Di

220 ol 3-kinase (PI3K) inhibitor LY294002 or Akt/protein kinase B (PKB) inhibitor IV, on the regulation o

221 )-mediated phosphorylation and activation of protein kinase B (PKB) is essential for the phosphorylat

222 Protein kinase B (PKB) is implicated in this action of i

223 urine thymoma viral oncogene homolog 1 (AKT)/protein kinase B (PKB) kinase (pAKT) is localized to the

224 oststimulus phosphorylation of Dictyostelium protein kinase B (PKB) kinase family member PKBR1 and PK

225 is transient and precedes phosphorylation of protein kinase B (PKB) on Ser473.

226 nd survival signals imparted through the Akt/protein kinase B (PKB) pathway in activated or effector

227 am target of rapamycin complex 2 (TORC2)-Akt/protein kinase B (PKB) pathway.

228 a reduction in GTPase activity and increased protein kinase B (PKB) phosphorylation.

229 ol) or downstream constitutive activation of protein kinase B (PKB) significantly decreased IRS-2 exp

230 lity of this system, a peptide substrate for protein kinase B (PKB) was designed, synthesized, and lo

231 determine whether NHE1 is phosphorylated by protein kinase B (PKB), identify any pertinent phosphory

232 e serine/threonine kinase Akt, also known as protein kinase B (PKB), is a central node in cell signal

233 vates multiple AGC serine kinases, including protein kinase B (PKB), p70Ribosomal S6 kinase (S6K) and

234 The Ser and Thr kinase AKT, also known as protein kinase B (PKB), was discovered 25 years ago and

235 through the intermediary protein kinase Akt2/protein kinase B (PKB)-beta, elicits the phosphorylation

236 R via a phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB)-dependent mechanism.

237 of the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (PKB)-mammalian target of rapamycin (mT

238 GF) receptor 2 and its downstream target Akt/protein kinase B (PKB).

239 the CD103 intracellular domain, resulting in protein kinase B (PKB)/AKT activation, thereby initiatin

240 tion of the phosphoinositide 3-kinase (PI3K)-protein kinase B (PKB)/Akt pathway markedly reduced endo

241 se), Src family kinase (SFK), and downstream protein kinase B (PKB)/AKT pathways were constitutively

242 lper (Th)1 differentiation and increased Th1 protein kinase B (PKB)/AKT phosphorylation while silenci

243 e 3-kinase pathway and its downstream kinase protein kinase B (PKB)/Akt prevented both insulin-mediat

244 ted phosphatidylinositol 3-kinase (PI3K) and protein kinase B (PKB)/AKT via SEMA 7A-dependent mechani

245 eir trafficking and downstream signaling via protein kinase B (PKB)/Akt, which, in turn, promotes inv

246 naling includes activation of PI3 kinase and protein kinase B (PKB)/Akt.

247 prevented CD28-dependent phosphorylation of protein kinase B (PKB)/Akt; however, there was no detect

248 ing the phosphoinositide 3-kinase (PI3K) and protein kinase B (PKB); however, this hypothesis has not

249 The serine/threonine protein kinase B (PKB, also known as Akt) plays a pivota

250 mTORC2 promoted phosphorylation of protein kinase B (PKB, or Akt) and PKC, Akt activity, an

251 ation of short-term growth factor signaling (protein kinase B (PKB/Akt) activity) and longer-term pro

252 y of human tumors and triggers activation of protein kinase B (PKB/Akt) and mammalian target of rapam

253 Protein kinase B (PKB/Akt) is an important mediator of s

254 Protein kinase B (PKB/Akt) plays a critical role in cell

255 e (ERK)/mitogen-activated protein kinase and protein kinase B (PKB/AKT) signaling.

256 a), which activates the cell-survival factor protein kinase B (PKB/Akt) via the G protein-coupled rec

257 n may serve a role in the brain by measuring protein kinase B (PKB/Akt), pGSK3 and the mitogen activa

258 eptor complexes activates the oncogenic PI3K-protein kinase B (PKB/AKT)-mammalian target of rapamycin

259 Down-regulation of protein kinase B (PKB/Akt)-mammalian target of rapamycin

260 d in regulation of hematopoiesis is the PI3K/protein kinase B (PKB/c-Akt) signaling module.

261 The PI3K-protein kinase B (PKB; also known as Akt) signaling path

262 our growth, only PI3K, through activation of protein kinase B (PKB; also known as AKT), must remain a

263 olving phosphatidylinositol 3 kinase (PI3K), protein kinase B (PKB; here referred to as Akt), and the

264 normal, and phosphoinositide 3-kinase (PI3K)-protein kinase B (PKB; or Akt) signaling is compromised

265 ex 2)-mediated activation of a myristoylated protein kinase B (PKB; PKBR1) and the phosphorylation of

266 proliferation is triggered, and Akt (a.k.a. protein kinase B, PKB) activation is impaired downstream

267 crystal structure of the anti-cancer target protein kinase B (PKBbeta/Akt-2) has been useful in guid

268 d chemotaxis, possibly through activation of protein kinase Bs (PKBs).

269 The Mycobacterium tuberculosis protein kinase B (PknB) comprises an intracellular kinas

270 Protein kinase B (PknB) is a transmembrane serine/threon

271 Akt, also known as protein kinase B, plays key roles in cell proliferation,

272 in-dependent kinase kinase, serine/threonine protein kinase B, protein kinase A, extracellular signal

273 Activating mutations in serine-threonine protein kinase B-RAF (BRAF) are found in 50% of patients

274 ns in the gene encoding the serine-threonine protein kinase B-RAF (BRAF) in the majority of melanomas

275 ome melanoma cells adapt to Serine/threonine-protein kinase B-Raf (BRAF) inhibitor therapy are incomp

276 ing (V600) mutations in the serine-threonine protein kinase B-RAF (BRAF).

277 The protein kinase B-Raf is a critical component of the Ras/

278 The protein kinase B-Raf proto-oncogene, serine/threonine ki

279 er cancers harbor oncogenic mutations in the protein kinase B-Raf, which leads to constitutive activa

280 Moreover, we identified an Akt/protein kinase B recognition sequence in the PML-binding

281 Because Akt (also known as protein kinase B) resides primarily in the cytosol, it i

282 Remarkably, inhibition of Akt/PKB (protein kinase B) restores DNA damage processing and Chk

283 rowth factor-1-phosphotidylinositol 3-kinase-protein kinase B serine threonine kinase (IGF-1-PI3K-Akt

284 ssion of the TYRO3/phosphoinositide 3-kinase/protein kinase B signal transduction pathway, and that c

285 ogen-activated protein kinase (MAPK) and AKT/protein kinase B signaling cascades, the major intracell

286 constitutively active Akt by a specific Akt/protein kinase B signaling inhibitor-2 (API-2) significa

287 e activation of the potent antiapoptotic Akt/protein kinase B signaling pathway in lymphocytes both r

288 ates activation of the host cell prosurvival protein kinase B signaling pathway, which results in the

289 xtracellular signal-regulated kinase 1/2 and protein kinase B signaling pathways are involved in the

290 gh phosphorylation by p38 MAP kinase and Akt/protein kinase B signaling pathways has been extensively

291 , with changes in components of the MAPK and protein kinase B signaling pathways, components of the a

292 the mitogen-activated protein kinase and Akt/protein kinase B signaling pathways, demonstrated by pho

293 molog (PTEN) negatively regulates downstream protein kinase B signaling, resulting in decreased cellu

294 de 3-kinase (PI3K) and Akt (serine/threonine protein kinase B) survival pathway in rod photoreceptor

295 ia leads to FOXO3a phosphorylation at an Akt/protein kinase B target site and subsequent nuclear expo

296 tidylinositol 3-kinase-activated protein Akt/protein kinase B) that are required for long term potent

297 The basal levels of phosphorylated mTOR and protein kinase B, the signaling proteins downstream of m

298 neurotrophic factor (BDNF) and its tyrosine protein kinase B (TrkB) receptors are known to potentiat

299 Insulin-stimulated phosphorylation of protein kinase B was increased in hIRECO EC as was Nox2

300 pathways, such as phosphoinositide 3-kinase/protein kinase B, which are critical in cell proliferati