ライフサイエンスコーパス: PI3K

1 PI3K isoform-selective inhibitors are in development for

2 PI3K lipid kinases signal through the PI3K/Akt pathway,

3 PI3K-related kinases (PIKKs) are large Serine/Threonine

4 PI3K/AKT activation stabilizes G6PD, the rate-limiting e

5 PI3K/AKT signaling is known to regulate cancer metabolis

6 PI3K/mTOR pathway inhibitors (PI3K/mTORi) showed supra-a

7 PI3K/mTORi also augmented CHK1i-induced DNA damage by at

8 PI3Ks activate critical signaling cascades and have mult

9 The opto-RTKs efficiently trigger ERK1/2, PI3K/Akt, and PLCgamma signaling.

10 ation of HIF-1alpha, but not Notch, ERK1/2, (PI3K)AKT, and P38 pathways.

11 ositide 3-kinase/glycogen synthase kinase 3 (PI3K/GSK3) signaling, with serum-glucocorticoid kinase 1

12 A PI3K inhibitor, BKM120, was tested in our patient-derive

13 I3K signaling, promoting cell migration in a PI3K-dependent manner, this did not fully recapitulate t

14 e activation of Rev-ErbA-alpha and induced a PI3K/PDK1/PKA-dependent signaling cascade.

15 y incorporating an HDAC pharmacophore into a PI3K inhibitor (Idelalisib) via an optimized linker.

16 ase-independent role for Rac1 in mediating a PI3K-independent MET-to-mTOR pathway and suggest alterna

17 However, the addition of a PI3K inhibitor to the BMP7v-based combination potentiate

18 tiviral effector functions in endosomes to a PI3K amplification loop at the cell surface.

19 of copanlisib in advanced MCC with aberrant PI3K activation for which immunotherapy is insufficient,

20 a single strong driver cannot fully activate PI3K, and two weak drivers may or may not do so.

21 r traits of cell proliferation and activated PI3K signaling, whereas during vascular remodeling, peri

22 n the presence of a constitutively activated PI3K pathway.

23 Using the growth factor-activated PI3K-Akt signaling pathway, we develop here computationa

24 tudy reveals an important role for activated PI3K signaling in regulating arachidonic acid metabolism

25 Although overexpression of IRS2 activated PI3K signaling, promoting cell migration in a PI3K-depen

26 t of multiple oncogenic mutations activating PI3K and RAS signaling.

27 ons of the PTEN locus, which promotes active PI3K signaling, were among the most significant copy-num

28 cell viability through regulation of the Akt/PI3K pathway.

29 a), duvelisib (PI3K-gamma/delta), alpelisib (PI3K-alpha), and AZD8186 (PI3K-beta/delta).

30 ctory of early T-cell activation by altering PI3K activity and PtdIns levels.

31 3-dependent signalling complexes and amplify PI3K signalling for malignant transformation.

32 rsed to different extents by p38, Erk1/2 and PI3K-Akt pathway inhibition, suggesting p38, Erk1/2 and

33 thway inhibition, suggesting p38, Erk1/2 and PI3K-Akt pathways as signaling pathways downstream of ch

34 /dopaminergic synaptic function, calcium and PI3K-AKT signaling.

35 The Wnt-beta-catenin and PI3K-Akt pathways cooperate to promote tumorigenesis and

36 CD2AP and PI3K are both upstream and downstream of actin polymeriz

37 Dual inhibition of CHK1 and PI3K/mTOR pathways yields potent synthetic lethality by

38 enabling anchorage independence via ERK and PI3K bypass cascades activated in a non-IL6-dependent ma

39 ce the activation of downstream MAPK/ERK and PI3K/Akt signaling as well as the neurite outgrowth of P

40 nhibition markedly inhibited Raf/MEK/ERK and PI3K/AKT signaling.

41 -like ALL cells have activated SRC, ERK, and PI3K signaling consistent with activated B cell receptor

42 e show that TGF-beta, via AhR induction, and PI3K signaling promotes IL-22 production in Th17 cells.

43 sus the structurally related PI3 (lipid) and PI3K-related protein kinases.

44 2 collaborated with both E-cadherin loss and PI3K pathway activation via PTEN loss in ILC development

45 This binary switching between MAPK and PI3K signaling, modulated by EGFR palmitoylation, was on

46 se but requires, in addition to p38 MAPK and PI3K, a serine protease activity, whereby FAP-alpha is t

47 expression dependent on Erk1/2, p38 MAPK and PI3K-Akt signaling pathway activation, thereby regulatin

48 verely impaired, and activation of MAPKs and PI3K signaling pathways are delayed in P2-deficient mous

49 degradation linked to ROS-mitochondrial and PI3K/Akt/mTOR signaling pathways.

50 rs that merge the pharmacophores of PARP and PI3K inhibitors.

51 PIM and PI3K/mTOR pathways are often dysregulated in prostate ca

52 Moreover, we identify the WNT, MAPK/RAS and PI3K pathways as good candidate targets for molecular th

53 ownstream of G protein-coupled receptors and PI3K.

54 nt functions supporting proper RhoGTPase and PI3K/mTOR signaling.

55 EGFR-dependent activation of RhoA/Rock and PI3K-Akt signals and their reciprocal interaction were u

56 tivity in the canonical RAF/MAPK/ERK/RSK and PI3K/AKT/PDK/mTOR/S6K pathways are identified.

57 hypersensitizes parasites to heat shock and PI3K inhibitors.

58 ition, as well as by the downstream SHP2 and PI3K/AKT pathways.

59 ling pathways, including MAPK, JAK-STAT, and PI3K-Akt.

60 particles requiring actin dynamics, Syk, and PI3K, but not phagocytosis, elicits both NLRP3-dependent

61 sulin/IGF/MAPKK, FGF, Hedgehog, TGFbeta, and PI3K signaling pathways.

62 late the phenotype seen with loss of PTEN as PI3K signaling is not as robust as observed in the setti

63 delta), alpelisib (PI3K-alpha), and AZD8186 (PI3K-beta/delta).

64 over-expression in Lrrc8a KO myotubes boosts PI3K-AKT-mTOR signaling to supra-normal levels and fully

65 GDC-0941 (GDC) to simultaneously block both PI3K and RAS signaling, thereby exerting synergistic ant

66 Here, we found that both PI3K-alpha and -delta isoforms are abundantly expressed

67 phagic cell death in bladder cancer cells by PI3K/AKT/HIF-1alpha-mediated glycolysis promotion.

68 is lost are also resistant to eradication by PI3K inhibitors.

69 s, we find that the dual regulation of GR by PI3K and PTEN functions as a rheostat that can be exploi

70 lyze Abeta42 toxicity and its suppression by PI3K activation in in vitro assays with SH-SY5Y human ne

71 Insight into how cellular PI3K signaling is encoded or decoded may open new avenue

72 Our findings indicate that combined PI3K/mTORi and CHK1i induces greater cell death in HGSOC

73 suggesting that PRR11 amplification confers PI3K dependence.

74 intrinsic mechanisms that cause constitutive PI3K/AKT/MTOR pathway activation, secreted factors from

75 ding defects as compared to normal controls, PI3K/mTOR hyperactivation interfered with primary cilia

76 cluding idelalisib (PI3K-delta), copanlisib (PI3K-alpha/delta), duvelisib (PI3K-gamma/delta), alpelis

77 tivated phosphatidylinositol 3-kinase-delta (PI3K-delta) syndrome (APDS) is a rare primary combined i

78 ne (12%) involved in lymphocyte development, PI3K-AKT/mTOR (6%), and loss-of-function mutations in TP

79 ng of the relative contribution of different PI3K isoforms under homeostatic and inflammatory conditi

80 to aberrant Akt activation, as SHIP1 diverts PI3K signaling toward a noncanonical pathway.

81 ocytes and fly fat bodies with downregulated PI3K, which were confirmed by biochemical assays in mamm

82 , shRNA COASY knockdown disrupted downstream PI3K pathway activation and also hindered DNA double-str

83 nally designed and synthesized as novel dual PI3K/HDAC inhibitors by incorporating an HDAC pharmacoph

84 ), copanlisib (PI3K-alpha/delta), duvelisib (PI3K-gamma/delta), alpelisib (PI3K-alpha), and AZD8186 (

85 ory to inhibition of the downstream effector PI3K but instead require active MEK (mitogen-activated p

86 elopment of DHHC20 inhibitors to reduce EGFR-PI3K signaling could be beneficial to patients with KRAS

87 c studies show that SDCBP activates the EGFR-PI3K-Akt signaling pathway by binding to EGFR and preven

88 promotes ESCC tumor growth through the EGFR-PI3K-Akt signaling pathway.

89 buting to the protective cascade, endogenous PI3K was immunoprecipitated from neuronal cells exposed

90 conditioning in animals, including the ERK, PI3K, and PKC pathways.

91 These hits included expected PI3K interactors, such as the platelet-derived growth fa

92 through inhibition of Rho-ROCK-MLC- and FAK-PI3K-dependent signaling pathways.

93 nent role of hypothalamic alpha-klotho/FGFR1/PI3K signaling in the modulation of NPY/AgRP neuron acti

94 ed antitumor efficacy across a panel of five PI3K inhibitors with distinctive isoform-specificities,

95 These results show a key role for PI3K signaling in Treg cell-mediated protection against

96 We previously found PI3K pathway activation in human MCC cell lines and tumo

97 PS/IL-1-mediated inhibition of RXR Function, PI3K in B lymphocytes, iCOS-iCOSL in T helper cells, and

98 Mechanistically, KDM5B governed PI3K/AKT signaling in prostate cancer in vitro and in vi

99 "hijacked" p110 from p85:p110 heterodimeric PI3K, thereby abating BCR tonic signaling, resulting in

100 Class I PI3K enzymes are critical for the maintenance of effecti

101 important first step in repurposing class I PI3K inhibitors to modulate CMA in vivo.

102 th either of two orally bioavailable class I PI3K inhibitors, pictilisib or buparlisib, display eleva

103 he high sequence homology across the class I PI3K isoforms.

104 nd glioblastoma cells, we found that class I PI3K mediated oncogenic MET-induced cell migration but n

105 Here, we report that inhibition of class I PI3K or PDPK1 activates CMA.

106 Class I PI3Ks are obligate heterodimers with catalytic and regul

107 pik3r5 and pik3r1 genes indicating class IA PI3K as the responsible signaling pathway.

108 d catalytic scenarios are shared by class IA PI3Ks; the activation is mimicked by oncogenic mutations

109 isoform-specificities, including idelalisib (PI3K-delta), copanlisib (PI3K-alpha/delta), duvelisib (P

110 isoform-selective PI3K inhibitors identified PI3K-delta as required for tumor proliferation.

111 contrast, selective inhibition of class III PI3Ks does not activate CMA.

112 ins disrupts homodimer formation and impacts PI3K signalling.

113 Importantly, PI3K/Akt inhibition by Rictor/mTORC2 deletion blocks dis

114 tion, together with a remarkable decrease in PI3K signaling.

115 both loss- and gain-of-function mutations in PI3K can cause immunodeficiency in humans.

116 include the downregulation of 25 proteins in PI3K-Akt signaling pathway (such as GRB2, EGFR, EPHA2, G

117 To this end, we inactivated PI3K by genetic means in the fly fat body and by pharmac

118 modified in more than one tissue, including PI3K (phosphatidylinositol 3-kinase/protein kinase-B) si

119 , KDM5B overexpression resulted in increased PI3K/AKT signaling.

120 brane protein that has been shown to inhibit PI3K in T cells.

121 a mutant (R649W) previously shown to inhibit PI3K, exhibit decreased activation of IRE1alpha and PERK

122 PI3K/mTOR pathway inhibitors (PI3K/mTORi) showed supra-additive cytotoxicity with CHK1

123 The INS-PI3K-PDPK1 pathway regulates Akt, but its role in CMA is

124 eal that the LRRC8 complex regulates insulin-PI3K-AKT-mTOR signaling in skeletal muscle to influence

125 Here, we discuss the insulin-PI3K signalling cascade and emphasize its roles in norma

126 ogen binding, whereas P2Y(12) and the kinase PI3K were also required for alpha(IIb)beta(3) activation

127 ts, including phosphatidylinositol 3-kinase (PI3K) and cyclin-dependent kinases.

128 hibitors revealed phosphoinositide 3-kinase (PI3K) as a central player transducing ACM-mediated neuro

129 Phosphoinositide 3-kinase (PI3K) comprised of the p110beta catalytic subunit was re

130 t in the P85-P110 phosphoinositide 3-kinase (PI3K) heterodimer, which reduced PI3K activity and down-

131 etion of CD2AP or phosphoinositide 3-kinase (PI3K) inhibition results in loss of F-actin and expansio

132 Phosphoinositide 3-kinase (PI3K) inhibitor LY-294002 abolished SPARC-induced down-r

133 activation of the phosphoinositide 3-kinase (PI3K) pathway.

134 y used downstream phosphoinositide 3-kinase (PI3K) pathways, whereas FGFR2b relied on downstream mito

135 study the role of phosphoinositide 3-kinase (PI3K) signaling in pericyte biology during angiogenesis,

136 Class IA phosphoinositide 3-kinase (PI3K) signaling is critical for normal growth and develo

137 lytic activity of phosphoinositide 3-kinase (PI3K), a lipid kinase that coordinates the intake and ut

138 ospholipase C and phosphoinositide 3-kinase (PI3K), also attenuated HMWH-induced antihyperalgesia.

139 factor-regulated phosphoinositide 3-kinase (PI3K)-AKT signalling network has diverse downstream effe

140 cal class III phosphatidylinositol-3-kinase (PI3K).

141 ics, Syk, and phosphatidylinositol 3-kinase (PI3K).

142 Hyperactivated phosphoinositide 3-kinase (PI3K)/Akt serine/threonine kinase (Akt) and mitogen-acti

143 naling pathway of phosphoinositide 3-kinase (PI3K)/Akt, which plays a critical role in angiogenesis.

144 ctivation of phosphatidylinositide-3-kinase (PI3K)/AKT/mTOR pathway is frequently detected in MCC, ma

145 o identify active phosphoinositide 3-kinase (PI3K)/AKT/mTOR signalling in early human embryos, and in

146 The phosphoinositide 3-kinase (PI3K)beta isoform is uniquely coupled to both RTK and GP

147 stimulated phosphatidylinositol-3-OH kinase (PI3K)-Akt signalling proposes that PI3K is activated at

148 Class Ia phosphoinositide 3-kinases (PI3K) are critical mediators of insulin and growth facto

149 omotes extrafollicular responses by limiting PI3K signaling during initial interactions between B and

150 olism, glycolysis/gluconeogenesis, and MAPK, PI3K-AKT, HIPPO and calcium signaling pathways.

151 ence of inhibitors of RIPK3, MLKL, p38 MAPK, PI3K, and FAP-alpha.

152 Mechanistically, PI3K/Akt-mediated SRF activation promotes nuclear transl

153 Moreover, PI3K activation induces a significant increase of 6E10 a

154 deleted on chromosome 10 (PTEN), a negative PI3K regulator that tau controls, as a plausible mechani

155 multiple pathways including STAT3, NFkappaB, PI3K/Akt, beta-catenin, and Notch signaling, which are c

156 ion of TAZ was mediated through RAF, but not PI3K, signaling.

157 g RAS-inhibitor or PTPN11-inhibitor, but not PI3K/JAK-inhibitors, suggesting a unified treatment targ

158 romoter sites with concomitant activation of PI3K and MAPK pathways.

159 alpha heterodimers to IRS1 and activation of PI3K.

160 was upregulated to trigger the activation of PI3K/Akt/NF-kappaB pathway and elevated expression of pr

161 unction of BRD4 and the kinase activities of PI3K and CDK4/6 by the TP inhibitor improves efficacy in

162 IFITM3-dependent amplification of PI3K signalling, which in part acts downstream of the BC

163 The amplification of PI3K signals depends on IFITM3 using two lysine residues

164 as a PIP3 scaffold and central amplifier of PI3K signalling.

165 ighlight the development and applications of PI3K inhibitors and summarize data supporting the concep

166 wever, are suppressed by the coexpression of PI3K.

167 studies showed a synergistic combination of PI3K-alpha/delta inhibitors with histone deacetylase inh

168 Despite decades of PI3K research, understanding of context-dependent regula

169 ese studies support a role for disruption of PI3K/GSK3 signaling as a risk factor for SCZ.

170 me includes the transcriptional shut down of PI3K expression.

171 ontrolling cellular metabolism downstream of PI3K and AKT and of how these events couple two major ha

172 of glucose, and mTOR, a kinase downstream of PI3K that stimulates transcription and translation.

173 Downstream of PI3K, Rac1 mediated cell migration through its GTPase ac

174 tide to assay the neuroprotective effects of PI3K in adult Drosophila melanogaster.

175 ieved through pharmacological enhancement of PI3K/AKT signaling and PIK3CD inhibition.

176 ts GTPase activity, whereas independently of PI3K, Rac1 mediated anchorage-independent growth in a GT

177 C and IDC cell lines identified induction of PI3K/Akt and p90-RSK pathways specifically in ULA cultur

178 Pharmacological inhibition of PI3K in cells blunts the ER stress-dependent phosphoryla

179 ctivity on PtdIns(3,4,5)P3 and inhibition of PI3K pathway is well characterized, the biological relev

180 ver, they engender much higher inhibition of PI3K signaling and stimulation of apoptosis in an ovaria

181 y, genetic and pharmacological inhibition of PI3K suppresses PRR11-mediated, estrogen-independent gro

182 n of SMAD2 or SMAD3 as well as inhibition of PI3K, mTORC2, and PDGFR abrogated the induction of GLS1

183 Pharmacological inhibition of PI3K, overexpression of a mutant of p85alpha that lacks

184 Furthermore, both inhibition of PI3K/AKT/HIF-1alpha and attenuation of glycolysis signif

185 s was confirmed using specific inhibitors of PI3K and actin polymerization.

186 ent of CBD-targeted cells with inhibitors of PI3K-AKT-NF-kappaB, IKK-NF-kappaB or JAK2-STAT3 pathways

187 did not extend cPFS in mCRPC irrespective of PI3K/AKT/PTEN pathway activation status.

188 d OS results were consistent irrespective of PI3K/AKT/PTEN pathway activation status.

189 c-Myc, increased Bim expression, and loss of PI3K signaling mediated apoptosis downstream of BCR sign

190 the loss of PI3Kalpha targeting and loss of PI3K-Akt signalling downstream of multiple agonists.

191 Pre-inhibition of RAS or PTPN11, but not of PI3K or JAK-signaling, prevented TSLP-induced RAS-GTP bo

192 encoding the catalytic subunit p110delta of PI3K-delta (referred to as type 1 APDS) or dominant loss

193 The principles of PI3K context-dependent signal encoding and decoding desc

194 inst this disease through the restoration of PI3K activity.

195 Despite the controversial role of PI3K-Akt in CD8(+) T cell mTORC1 activation, a link betw

196 These data show that the strength of PI3K signaling is a key regulator of pregerminal center

197 A encodes the p110alpha catalytic subunit of PI3K and is frequently mutated in human cancers, includi

198 ated that the p85alpha regulatory subunit of PI3K modulates the unfolded protein response (UPR) by in

199 RR11 with the p85alpha regulatory subunit of PI3K suppresses p85 homodimerization, thus enhancing ins

200 Moreover, suppression of PI3K/AKT and HIF-1alpha attenuated Vitamin K2-increased

201 es for rational pharmacological targeting of PI3K-associated diseases.

202 imetic IFITM3(Y20E) mutant induced oncogenic PI3K signalling and initiated the transformation of prem

203 rs PTEN and RIG-I to enhance proto-oncogenic PI3K-AKT signaling.

204 osphatase function cooperates with oncogenic PI3K to promote rapid mammary tumorigenesis, the additio

205 , preclinical studies have shown that JAK or PI3K pathway inhibition is insufficient to eradicate the

206 e or in combination with standard therapy or PI3K inhibitors.

207 bitor and an AKT inhibitor, as well as other PI3K pathway inhibitors, could overcome the therapeutic

208 athogenesis strongly relies on overactivated PI3K/Akt/mTOR and VEGFR2 pathways in endothelial cells (

209 ers of response to combined MEK and p110beta/PI3K inhibition.

210 Combined inhibition of MEK and p110beta/PI3K reduced mouse tumor cell growth in vitro.

211 le KRAS (siKRAS) in combination with the pan-PI3K inhibitor GDC-0941 (GDC) to simultaneously block bo

212 Herein, we report the discovery of dual PARP/PI3K inhibitors that merge the pharmacophores of PARP an

213 or cancer, such as lipid metabolism pathway, PI3K/AKT and MAPK signaling pathways.

214 : Pathways in cancer, Ras signaling pathway, PI3K-Akt signaling pathway, and Rap1 signaling pathway,

215 nd associated oncogenic signalling pathways (PI3K-AKT/ERK), which may also involve the distinct alter

216 We investigated the novel multikinase PIM/PI3K/mTOR inhibitor, AUM302, versus a combination of the

217 complex despite p110delta being the primary PI3K isoform found within monocytes.

218 ion stalls vesicle fast recycling to promote PI3K-Akt immunological responses.

219 th PI3K components and its deletion promotes PI3K-AKT-mTOR signaling in NPCs of mouse cortex and cere

220 eration, indicating that Vitamin K2 promotes PI3K/AKT and HIF-1alpha-mediated glycolysis in bladder c

221 tify a putative Wnt/heterotrimeric G protein/PI3K pathway for PCP regulation.

222 shift to a lower threshold of excitable Ras/PI3K/ERK network, caused by various combinations of gene

223 plied driver mutations targeting the RTK/RAS/PI3K and p53 pathways to induce the formation of high-gr

224 tory cascades such as the androgen receptor, PI3K-AKT or GATA2-dependent pathways, as well as initiat

225 -citrate lyase (ACLY) in a TGF-beta receptor/PI3K/protein kinase B-dependent manner, to regulate hepa

226 e 3-kinase (PI3K) heterodimer, which reduced PI3K activity and down-regulated the activation of prote

227 se modulator in rectal cancer that regulates PI3K activation and DNA repair.

228 swell-activated anion channel that regulates PI3K-AKT, ERK1/2, mTOR signaling, muscle differentiation

229 Here, we show that oncogenic ERG repressed PI3K signaling through direct transcriptional suppressio

230 Isoform-selective PI3K inhibitors are used clinically but intrinsic and ac

231 rfering RNA knockdowns and isoform-selective PI3K inhibitors identified PI3K-delta as required for tu

232 while variants affecting Hedgehog signaling, PI3K signaling, TRAF7, KLF4, and POLR2A result in mening

233 (including; focal adhesion, MAPK signaling, PI3K-Akt-mTOR signaling, p53 signaling, Jak-STAT signali

234 Combinatorial targeting of JAK/STAT, PI3K, and "BCR-like" signaling with multiple TKIs and/or

235 mme driven by IL-5 is dependent on the STAT5/PI3K/Akt signalling axis and that nicotinamide adenine d

236 STAT6, PI3K-Akt-NF-kappaB, and Src signaling mediated the cellu

237 sm for spatial control of agonist-stimulated PI3K-Akt signalling at internal membrane compartments li

238 d via the NPY2 receptor (NPY2R), stimulating PI3K, MAPK, and NFAT activation.

239 interacted with the PI3K regulatory subunit PI3K-P85alpha, which increased AKT and mTOR phosphorylat

240 n, survival, and tumor growth by suppressing PI3K/mTOR/Akt activities in mouse models generated from

241 ile partially downregulated the pro-survival PI3K-AKT cascade, thereby changing a balance between cel

242 enefit of blocking MEK compared to targeting PI3K.

243 Prior studies demonstrated that PI3K/Akt signaling is important in thyroid hormone recep

244 H kinase (PI3K)-Akt signalling proposes that PI3K is activated at the plasma membrane, where receptor

245 In validation studies, we show that PI3K recruitment of ZC3H14 is necessary for PDGF-induced

246 These data suggest that PI3K inactivation has a conserved effect of upregulating

247 These data suggest that PI3K pathway dysfunction causes ER stress that may drive

248 ics and drug-targeting studies revealed that PI3Ks act to reduce glucocorticoid receptor (GR) levels,

249 The PI3K/AKT-TBL1XR1-ERK1/2-Sox2 axis may represent a target

250 When chronically activated, the PI3K pathway can drive malignant transformation.

251 ion and omental metastasis by activating the PI3K/AKT/mTOR pathway and its downstream effectors HIF-1

252 r withdrawal of the stress condition and the PI3K inhibitor.

253 tion of the PIM inhibitor, AZD-1208, and the PI3K/mTOR inhibitor BEZ235 (Dactolisib) to determine the

254 ty converts PIP3 to PIP2 and antagonizes the PI3K-Akt pathway.

255 In types 1 and 2 APDS, the PI3K-delta hyperactivity resulting from the gene mutatio

256 e important reciprocal crosstalk between the PI3K/AKT signal and pentose phosphate pathway (PPP) bran

257 nctions as an upstream activator of both the PI3K/Akt and MAPK/ERK pathways in liver cancer cells, an

258 This process is mediated by the PI3K/Akt pathway.

259 sequencing broadly implicates TrkB.T1 in the PI3K signaling cascades in a ligand-independent fashion.

260 Patients with mutations in the PI3K/MTOR pathway had significantly shorter PFS than tho

261 bstrate 1 (IRS1), which in turn inhibits the PI3K-PKB/Akt-mTORC1 pathway and promotes TFEB/TFE3 nucle

262 1 (p85) and increased the recruitment of the PI3K heterodimer to the plasma membrane.

263 nding of context-dependent regulation of the PI3K pathway and of the underlying signaling code remain

264 ndicate that pharmacologic inhibition of the PI3K pathway could potentially be effective in limiting

265 Increased activation of the PI3K pathway was observed in PIK3IP1-deficient B cells i

266 which lead to constitutive activation of the PI3K pathway.

267 almitoylated EGFR, reducing formation of the PI3K signaling complex.

268 be modulated by additional inhibition of the PI3K signalling cascade, there is no apparent benefit of

269 ied to be involved in the enhancement of the PI3K-AKT signaling pathway in the undifferentiated cells

270 A, which operates at the intersection of the PI3K/Akt and MAPK/ERK pathways and dephosphorylates and

271 ion triggered simultaneous inhibition of the PI3K/Akt and MAPK/ERK pathways, suppressed the expressio

272 characteristics and found activation of the PI3K/AKT pathway in sphere-forming cells.

273 mutations in TP53 and the activation of the PI3K/AKT pathway, two events crucial for cancer progress

274 al program that sustains the activity of the PI3K/AKT/mTOR pathway and glycolysis in B-cell lymphomas

275 Dysregulation of the PI3K/Akt/mTOR pathway has become a point of convergence

276 tic proteins and sustained activation of the PI3K/AKT/MTOR pathway, despite inhibition of the HER2 an

277 ptosis or depletion via dysregulation of the PI3K/ATM pathways.

278 al inhibition of downstream effectors of the PI3K/GSK3 pathway, SGK1 and GSK3, induced alterations in

279 umours dependent upon mutant TP53 and/or the PI3K/AKT pathway.

280 but whether metabolic feedback regulates the PI3K/AKT pathway is unclear.

281 rly to our previous study, we found that the PI3K-Akt signaling pathway was upregulated in the CSCs.

282 PI3K lipid kinases signal through the PI3K/Akt pathway, regulating cell growth and proliferati

283 ound to influence glucose uptake through the PI3K/AKT pathway.

284 , COASY protein directly interacted with the PI3K regulatory subunit PI3K-P85alpha, which increased A

285 Palmitoylated EGFR interacted with the PI3K regulatory subunit PIK3R1 (p85) and increased the r

286 r from an oncogenic gain of function through PI3K-mediated C-terminal p27 phosphorylation, which disr

287 rotective signaling cascade mediated through PI3K that requires recruitment of ZC3H14 and may present

288 ly response and FOXM1-mediated resistance to PI3K inhibition in estrogen-receptor-positive breast can

289 h laminin and hypoxia to drive resistance to PI3K inhibitors.

290 s rely on PIK3CA and are highly sensitive to PI3K inhibitors, suggesting that PRR11 amplification con

291 remain uncharacterized, their sensitivity to PI3K inhibitors unknown.

292 Thus, the disruption of CD133 signal to PI3K pathway is essential to overcome Melanoma resistanc

293 Conversely, unleashing PI3K signaling by means of PTEN deletion delayed pericyt

294 signaling and was dependent on signaling via PI3K/AKT, in GC stem-like cells distinguished by CD44 ex

295 IgA-mediated programmed neutrophil death was PI3K-, p38 MAPK-, and JNK-dependent and evoked anti-infl

296 eases in Gq/11 coupling and association with PI3K and Homer compared to controls (p < 0.01 for all).

297 but can regain lethality when combined with PI3K pathway inhibitors.

298 ic studies reveal that RAB39b interacts with PI3K components and its deletion promotes PI3K-AKT-mTOR

299 ponse in a Stage IV MCC patient treated with PI3K inhibitor idelalisib.

300 tumors that may benefit from treatment with PI3K inhibitors and antiestrogens.