ライフサイエンスコーパス: protein kinase B

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

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

3 tein, as well as total and activated ERK and protein kinase B.

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

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

6 he protein kinase B pathway by injecting the protein kinase B activator SC79 in Lgr4(-/-) mice can ef

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

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

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

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

11 tide-dependent kinase 1 (PDK1 or PDPK1), and protein kinase B (Akt or PKB) in the follicular epitheli

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

13 1(-/-) ) mice were traced to a deficiency in protein kinase B (Akt) activation in hepatocytes, which

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

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

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

17 rized resting membrane potentials and higher protein kinase B (Akt) activity than wild-type VSMCs in

18 Protein kinase B (Akt) and downstream transcription fact

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

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

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

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

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

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

25 through mechanisms involving suppression of protein kinase B (AKT) and Notch-1 pathways.

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

27 ective effect of GPR35 activation depends on protein kinase B (Akt) and p38 MAPK.

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

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

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

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

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

33 Furthermore, PI3K inhibitor LY294002 and protein kinase B (Akt) inhibitor IV blocked the effects

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

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

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

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

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

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

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

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

42 2 impairs the signaling function of the PI3K/protein kinase B (AKT) pathway, leading to functional de

43 reasing extracellular ATP and activating the protein kinase B (Akt) pathway, ultimately leading to gl

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

45 r (IGF-1R), and subsequent activation of the protein kinase B (Akt) pathway.

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

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

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

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

50 feration and death, but aberrantly increased protein kinase B (AKT) phosphorylation, elevated Vcan tr

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

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

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

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

55 ry fibrosis through the inactivation of PI3K/protein kinase B (AKT) signaling in fibroblast cells.

56 mmalian target of rapamycin (mTOR)-dependent protein kinase B (AKT) signaling mediates HCC cell survi

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

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

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

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

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

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

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

64 MC3T3-E1 cells transfected with scrambled or protein kinase B (Akt) small interfering RNA following A

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

66 ed by small GTPases of the Ras subfamily and protein kinase B (Akt) to advance the development of fil

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

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

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

70 lular signal-regulated kinase (ERK) 1/2, and protein kinase B (AKT), but only inhibition of ERK1/2 ph

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

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

73 extracellular signal-related kinases (ERKs), protein kinase B (Akt), Janus kinases (JAKs), and signal

74 n-induced autophagy concomitant with reduced protein kinase B (AKT), mammalian target of rapamycin (m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 1 suppressed fMLP-induced phosphorylation of protein kinase-B (AKT) in dHL-60 cells.

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

101 es, impacting insulin receptor signaling via protein kinase B/AKT (AKT).

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

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

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

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

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

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

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

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

110 INS1) cells impaired calcium homeostasis and protein kinase B/Akt signaling and, subsequently, decrea

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

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

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

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

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

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

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

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

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

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

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

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

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

124 Isoforms of protein kinase B (also known as AKT) play important role

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

126 ivating expression of Myc, via activation of protein kinase B, also known as (AKT), nuclear factor ka

127 PGE(2) (via protein kinase A) and FGF-2 (via protein kinase B, also known as AKT) depended on activat

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

129 ditionally, we identified that both the PI3K/protein kinase B and ERK pathways are activated downstre

130 y ET1 was mediated through activation of the protein kinase B and ERK1/2 signaling pathways.

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

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

133 ancies in the phosphatidylinositol-3'-kinase/protein kinase B and KRAS/extracellular-signal-regulated

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

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

136 extracellular signal-regulated kinase (ERK), protein kinase B and p53, and MIF may also reverse immun

137 Protein kinase B and pantothenate synthetase are examine

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

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

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

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

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

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

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

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

146 nscription) activation was reduced, and Akt (protein kinase B) and mTOR (mammalian target of rapamyci

147 extracellular signal-regulated kinase), AKT (protein kinase B), and JNK (c-Jun N-terminal kinase) pat

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

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

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

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

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

153 time- and dose-dependent activation of ERK, protein kinase B, and mTORC1 signaling in wild-type PC-3

154 transducer and activator of transcription 3, protein kinase B, and NF-kappaB.

155 50% (of phosphorylated IGF1R, phosphorylated protein kinase B, and phosphorylated MAPK kinase), sugge

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

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

158 abolic rates, and reduced phosphorylation of protein kinase B compared with RAPA-treated cells.

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

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

161 ate lyase (ACLY) in a TGF-beta receptor/PI3K/protein kinase B-dependent manner, to regulate hepatic a

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

163 192 protein kinases and discovered that Akt/protein kinase B dramatically accelerates and amplifies

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

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

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

167 thway, including key signaling intermediates protein kinase B, extracellular signal-regulated kinase

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

169 eration and tube formation, possibly through protein kinase B, extracellular signal-regulated kinase,

170 indings reveal that the dysregulation of the protein kinase B-FOXO1 pathway may be a critical cause o

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

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

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

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

175 nses 1 (REDD1), a negative regulator of mTOR/protein kinase B, is poorly understood.

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

177 he phosphatidylinositol 3-kinase (PI3K)/Akt (protein kinase B)/ mammalian target of rapamycin (mTOR)

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

179 g through IGF receptor (IGF1R) activated the protein kinase B-mammalian target of rapamycin (AKT-mTOR

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

181 oted EMT in NPC cells by activating the PI3K-protein kinase B-mammalian target of rapamycin signaling

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

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

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

185 phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling

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

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

188 ects of E2 via the phosphoinositide 3-kinase-protein kinase B-mechanistic target of rapamycin pathway

189 However, an increase in protein kinase B-mediated phosphorylation of FOXO1 was o

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

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

192 ith psoriatic serum led to the activation of protein kinase B, nuclear exclusion of FOXO1, and the lo

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

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

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

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

197 ogen-activated protein kinase kinase (pMEK), protein kinase B (pAkt), or phosphoinositide-4,5-bisphos

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

199 Importantly, the reactivation of the protein kinase B pathway by injecting the protein kinase

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

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

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

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

204 This was associated with increased protein kinase B phosphorylation and increased hepatic g

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

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

207 etylase 8 led to the inhibition of EphA2 and protein kinase B phosphorylation, reduced invasion, and

208 ce and insulin resistance by increasing AKT (protein kinase B) phosphorylation in endothelial cells a

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

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

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

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

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

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

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

216 gnaling, as well as DA D2 receptor (D2R) and protein kinase B (PKB or Akt)/glycogen synthase kinase 3

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

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

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

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

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

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

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

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

225 orylated on Ser(2461)/Ser(2462)/Thr(2463) by protein kinase B (PKB) in response to insulin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 ed phosphorylation of the activation loop of protein kinase B (PknB) and of the essential PknB substr

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

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

264 range of regulatory proteins, including the protein kinase B (PknB) which controls peptidoglycan bio

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

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

267 While targeted serine/threonine-protein kinase B-Raf (BRAF) and immune checkpoint inhibi

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

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

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

271 ed with vehicle or combined serine/threonine-protein kinase B-Raf (BRAF) kinase inhibitor (BRAFi) and

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

273 Serine/threonine-protein kinase B-Raf inhibitor and anti-programmed death

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

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

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

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

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

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

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

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

282 1 activation along with activated downstream protein kinase B signaling cascades.

283 impaired insulin action at the level of Akt/protein kinase B signaling in mouse adipose tissue.

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

285 Even though mTOR/protein kinase B signaling is important for adipogenesis

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

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

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

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

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

291 ifferentiation through receptor-induced AKT (protein kinase B) signaling and phosphorylation of FOXO1

292 ncluding PI3K (phosphatidylinositol 3-kinase/protein kinase-B) signaling pathway, cytokine-cytokine r

293 Nevertheless, there is evidence that Akt (protein kinase B) signalling and FOXO transcription fact

294 acellular signal-regulated kinase1-/2), AKT (protein kinase B), SRC, and overexpression of HIF1-alpha

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

296 signaling pathway phosphoinositide-3-kinase/protein kinase B that regulates inflammation (suppressor

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