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1 tion occurred through the c-Met receptor and PI3 kinase.
2 re sensitive to inhibition of either MAPK or PI3 kinase.
3 nd was insensitive to inhibitors of P2Y12 or PI3 kinase.
4 ransduces BAFFR survival signals via ERK and PI3 kinase.
5 ivation of phospholipase C and, for TLR 2/1, PI3-kinase.
6 n insulin-like receptor, primarily activates PI3-kinase.
7 LRP1 activates cell survival signals such as PI3-kinase.
8 g p110gamma despite the presence of class Ia PI3-kinase.
9 activation of Beclin 1-containing class III PI3-kinase.
10 p110gamma, the catalytic subunit of class Ib PI3-kinase.
11 chemokines, and other agonists that activate PI3-kinase.
12 sing due to blockade of RAS interaction with PI3-Kinase.
13 which is chemotactic and controlled through PI3-kinase.
14 t manner that is reversible and regulated by PI3-kinase.
15 d >500-fold selectivity over closely related PI3 kinases.
16 bind the p85 subunit of phosphoinositide 3 (PI3)-kinase.
17 of the survival kinase, phosphoinositide 3 (PI3)-kinase.
18 y of the other catalytic subunits of class I PI3-kinases.
19 RAS proteins directly activate PI3-kinases.
22 ng a type III PI3 kinase (Vps34), a putative PI3 kinase, a putative mitogen-activated extracellular s
24 critically dependent on phosphoinositide 3 (PI3)-kinase activation, as administration of a PI3 kinas
27 , the role of phosphatidylinositol 3-kinase (PI3-kinase) activation in CD28 function has been highly
29 n, and the prevention of both WW binding and PI3 kinase activity are required for ErbB4 nuclear trans
30 ized phagosomes did not require p40(phox) or PI3 kinase activity, although superoxide production befo
31 minant-negative forms, but not inhibition of PI3 kinase activity, dramatically impaired EpoR internal
36 their native microenvironment when levels of PI3-kinase activity and DE-cadherin are elevated in NBs.
47 gnaling effectors phosphoinositide-3 kinase (PI3 kinase), Akt, Raf-1, mitogen-activated protein kinas
49 ition of the phosphatidylinositide 3-kinase (PI3 kinase)/AKT pathway, as was the tightly bound fracti
53 Accordingly, PM-based motogenic signals (PI3-kinase-Akt and PLCgamma1) are amplified, and cell mi
54 iciency did not alter BAFF activation of the PI3-kinase-Akt or NF-kappaB signaling pathways, which ar
56 rowth factor signaling pathways regulated by PI3 kinase/Akt and MAP kinases with Myc-mediated transcr
57 sure to overcome the defective activation of PI3 kinase/Akt and Raf/MEK/ERK, implicate both Ras effec
58 output of two major oncogenic pathways, the PI3 kinase/AKT and the Rat sarcoma (RAS)/ERK pathways.
61 d site" amino acid substitutions that impair PI3 kinase/Akt or Raf/MEK/ERK activation in bone marrow
64 rative and antiapoptotic effects include the PI3 kinase/Akt pathway, the MAP kinase pathway and the b
68 ssion of Inpp4b and changes in intracellular PI3 Kinase/AKT signaling in follicular granulosa cells.
70 K causes dephosphorylation of members of the PI3 kinase/AKT/mTOR pathway and delays sensitive cells i
71 monstrate activation of macrophage/foam cell PI3-kinase/Akt in atherosclerotic plaques from apolipopr
74 d HO-1 mRNA expression through activation of PI3-kinase/Akt pathway without affecting ERK and p38 MAP
81 rm of atherosclerosis, whereas activation of PI3-kinase/Akt was undetectable in lesions from apoE-nul
82 ellular-signal regulated kinase [ERK] 1/2 or PI3-kinase/Akt) during the early min of reperfusion.
84 ly an additional mechanism through which the PI3-kinase/Akt/FOXO pathway can modulate Myc function.
85 ze and exhibited an elevated activity of the PI3-kinase/Akt/mTOR pathway, which was associated with a
86 al function in the induction of the type III PI3 kinase and autophagy in response to amyloid beta pep
88 pe is mimicked by constitutive activation of PI3 kinase and is rescued by the removal of PDK1 (PDPK1)
91 their downstream effectors suggest that Ras/PI3 kinase and Ras/Raf1 pathways contribute to SF stimul
92 RAS-GTP-driven signaling via MAP kinases and PI3 kinases and mitogen-stress-related kinase-1 for NF-k
94 signal transduction machinery, but involving PI3-kinase and downstream PH domain proteins, CRAC and P
95 anges require activation of the MAP kinases, PI3-kinase and downstream signalling pathways and are ob
96 the Drosophila retina has demonstrated that PI3-kinase and downstream TOR signalling regulate the ti
103 genes, is correlated with activation of both PI3-kinase and Ras signaling in human prostate tumors an
105 er metastasis in response to coactivation of PI3-kinase and Ras signaling pathways in a genetically e
106 s in prostate tumors that have activation of PI3-kinase and Ras signaling, and therefore, ETV4 repres
108 rosophila utilize Phosphoinositide 3-kinase (PI3-kinase) and DE-cadherin to build adhesive contact fo
109 signaling through phosphoinositide 3-kinase (PI3-kinase) and the PI3-kinase-dependent protein serine/
110 confirmed coimmunoprecipitation of erbB2/4, PI3 kinase, and Akt with ET(A), and confocal microscopy
111 The protein powder increased insulinemia, PI3 kinase, and erk phosphorylation but did not affect t
114 aises active Erk, halts receptor editing via PI3 kinase, and promotes differentiation via Erk, breaki
117 h the non-receptor tyrosine kinase c-Src and PI3-kinase, and that treating cells with inhibitors to b
122 ns with switch 2 insertions are impaired for PI3 kinase binding and Akt activation, and are hypersens
123 n of the proximal tyrosine motif interrupted PI3-kinase binding and prevented CD28-dependent phosphor
124 These results suggest that the commonly used PI3 kinase blocker LY 294002 may modulate GlyT1 function
125 egulation of autophagy requires the type III PI3 kinase, but not inhibition of mTORC1, the essential
126 naling pathway, whereas direct activation of PI3-kinase by the proximal tyrosine motif of CD28 is not
128 EA1 and Rab5A (early endosomes), Rab7L1, and PI3-kinase C2gamma and PI4-kinase IIIalpha (phospholipid
130 ts p85alpha and p85beta are dispensable, the PI3-kinase catalytic subunit p110alpha requires interact
131 yeast Candida glabrata Here, we demonstrate PI3-kinase (CgVps34) to be essential for maintenance of
132 tophagy flux by interacting with the Beclin1-PI3 kinase class III protein complex in response to auto
133 n of autophagy molecules such as Beclin1 and PI3 kinase class III resulted in impaired growth of HTLV
135 esion to low-density fibrinogen, whereas PKC/PI3 kinases contribute to platelet spreading on high-den
136 es for both a WW domain and an SH2 domain of PI3 kinase, demonstrated enhanced nuclear translocation
137 ated that LY 294002 and wortmannin inhibited PI3 kinase-dependent Akt phosphorylation in the primary
139 nophil lifespan (via a NF-kappaB and Class I PI3-kinase-dependent mechanism); and (v) complete abroga
141 osphoinositide 3-kinase (PI3-kinase) and the PI3-kinase-dependent protein serine/threonine kinase Akt
146 including Gbetagamma-dependent activation of PI3-kinase gamma and Rac1, could inhibit chemoattractant
147 cule targeting of phosphoinositide 3-kinase (PI3-kinase) gamma catalytic activity is a target of inte
148 onic lethality seen in mice lacking class Ia PI3-kinase, germ-line deletion of p110gamma results in m
149 transport system, organized by agrin through PI3 kinase, GSK3beta, CLASP2, and LL5beta, for precise d
150 totic signaling from its receptor (c-Met) to PI3 kinase --> c-Akt --> Pak1 (p21-activated kinase -1)
151 ignalling through phosphoinositide 3-kinase (PI3-Kinase) has been shown to have an essential role in
152 tein kinase targets and structurally related PI3 kinases, histone deacetylases, poly(ADP-ribose)polym
153 ion of this signaling includes activation of PI3-kinase, IGF1R and Akt, Ca2(+)-sensitive transcriptio
154 esults highlight the importance of the c-Kit-PI3 kinase-IL-6 signaling axis in DCs in regulating T ce
156 iety of protocols used to assess the role of PI3 kinase in biological systems, or for achieving optim
157 ances in understanding the roles of class II PI3 kinases in different pathological contexts is leadin
160 itogen activated protein kinases (MAPK), the PI3-kinase induced signalling network and E3 ubiquitin l
164 mote glucose uptake, as Akt1(-/-) T cells or PI3-kinase inhibition and RNAi of STAT5 led to defective
166 utophagy, treatment of infected cells with a PI3 kinase inhibitor attenuates autophagy in infected ce
168 s not surprising that the presence of a sole PI3 kinase inhibitor does not prevent inevitable host-ce
169 B. xylophilus with long-chain FAEEs, or the PI3 kinase inhibitor LY294002, promotes LIV formation, w
171 was blocked by the Jak2 inhibitor AG490, the PI3 kinase inhibitor wortmannin, and the phospholipase C
173 3)-kinase activation, as administration of a PI3 kinase inhibitor, wortmannin, reduced Gsk3 phosphory
177 )] and a specific phosphoinositide 3 kinase (PI3 kinase) inhibitor (LY294,002 [2-(4-morpholinyl)-8-ph
178 l-2-/- cells was enhanced in the presence of PI3 kinase inhibitors 3-methyladenine and Wortmannin and
179 rview on the current development of class II PI3 kinase inhibitors and outline the potential use for
180 d the effects of the phosphatidylinositol 3 (PI3) kinase inhibitors LY 294002 and wortmannin on GlyT1
183 tween C20 and a lysine in the active site of PI3 kinase is essential to Wm's ability to inhibit this
186 lear, however, which of the three classes of PI3-kinases is required for insulin-stimulated apoB100 d
187 ] products of phosphatidylinositol 3-kinase (PI3-kinase) is an early event in establishing the direct
188 nsulin regulates GLUT4 and FoxO1 through the PI3-kinase isoform p110alpha, although FoxO1 showed high
189 age checkpoint, which is orchestrated by the PI3 kinase-like protein kinases ATR and ATM (Mec1 and Te
190 ponents of the PI3-kinase pathway, including PI3-kinase (LY294002) and mTORC1 (rapamycin), ablated th
191 signaling involvement was determined using a PI3-kinase (LY294002) or Rac1 (NSC23766) inhibitor.
193 regulated by HGF and EGF receptors and that PI3 kinase-mediated signaling independent of AKT is a cr
195 hepatic hepcidin synthesis, in part through PI3 kinase MEK/ERK kinase pathways which may be modulati
196 ortening, cellular senescence, activation of PI3 kinase-mTOR signaling, impaired autophagy, mitochond
198 poptosis and triggered the activation of the PI3-kinase/mTOR Complex 1 (mTORC1)/p70 S6-kinase pathway
199 valuated the therapeutic efficacy of a novel PI3-kinase/mTOR inhibitor, PI-103, in established glioma
200 EpoR cytoplasmic domain bind p85 subunit of PI3 kinase on Epo stimulation and individually are suffi
201 tment of AMkL may be improved by integrating PI3-kinase or Akt inhibitors into the chemotherapy of th
202 p110delta subunit of phosphatidylinositol-3 (PI3) kinase (p110(D910A)) secreted lower amounts of IL-6
203 ence that disruption of RAS interaction with PI3-Kinase p110alpha decreases cell motility and prevent
204 linkage analysis: a homozygous stop codon in PI3-kinase p110delta (PIK3CD) and a homozygous frame shi
205 h a combined deficiency of 2 genes products, PI3-kinase p110delta and SKAP, both of which appear to p
206 p85alpha and p85beta regulatory subunits of PI3'-kinase (p85alpha(-/-)beta(-/-)) to precisely define
207 FR and PDGFR was necessary for abrogation of PI3 kinase pathway activity in the mixed population.
208 olecule kinase inhibitors, inhibitors in the PI3 kinase pathway and in the mitogen-activated ERK kina
210 on of cell cycle and phosphatidylinositol-3 (PI3) kinase pathway genes and can be reactivated through
211 l partly through the phophostidylinositol 3 (PI3) kinase pathway: inhibiting this path was previously
212 complex and also through phosphoinositide-3 (PI3)-kinase pathway-dependent stabilization of CD154 mRN
215 ologic outcome of selectively activating the PI3-kinase pathway in the endometrial epithelium remains
217 trate that cell-autonomous activation of the PI3-kinase pathway is sufficient for the initiation of e
219 tion from neonatal HSCs did not activate the PI3-kinase pathway or promote HSC proliferation, HSC dep
223 downstream of PDK1, the master kinase of the PI3-kinase pathway, exhibit deficient neuron production.
224 inhibitors that inactivate components of the PI3-kinase pathway, including PI3-kinase (LY294002) and
225 dult mouse hematopoietic cells activates the PI3-kinase pathway, inducing hematopoietic stem cell (HS
226 nd negative regulators, respectively, of the PI3-kinase pathway, which regulates growth, survival, an
230 rved activation of nuclear factor-kappaB and PI3-kinase pathways in response to APRIL in both cyclin
232 hosphorylated sites on PKMzeta, we show that PI3-kinase (phosphoinositide 3-kinase), CaMKII (Ca2+/cal
234 the ECM, promoted focal adhesions, enhanced PI3 kinase (PI3K) activity, and induced the invasion of
235 or absence of pharmacological inhibition of PI3 kinase (PI3K) and Akt signalling using wortmannin.
240 bits the Hippo pathway through activation of PI3-kinase (PI3K) and phosphoinositide-dependent kinase
242 that mutations in critical genes within the PI3-kinase (PI3K) pathway are not functionally equivalen
245 associates with G2/M-arrest, inactivation of PI3-kinase (PI3K) signaling, and induction of apoptosis.
246 To test this, we targeted class II and III PI3 kinases (PI3Ks) in an MTM1-deficient mouse model.
247 dentify a new pathway based on the class III PI3-kinase (PIK3C3), ankyrin-B (AnkB), and dynactin, whi
248 r activating mutations of phosphoinositol-3 (PI3) kinase (PIK3CA) may be associated with trastuzumab
249 and MEF2B), NF-kappaB (CARD11 and TNFAIP3), PI3 kinase (PIK3CD, PIK3R1, and MTOR), B-cell lineage (I
252 inhibitor of phosphatidyl inositol 3-kinase (PI3-kinase) prevented induction of ATG5 and activation o
253 phate (PIP(3)), formed by the p110 family of PI3-kinases, promotes cellular growth, proliferation, an
254 lin thus plays a role in restraining RAS and PI3-kinase promotion of cell motility and potentially tu
257 d that Wnt5a stimulates phagocytosis through PI3 kinase-Rac1 and lipid-raft-dependent processes.
258 at CIN translocates to the leading edge in a PI3-kinase-, Rac1-, and cofilin-dependent manner after E
262 ression induces the sequential activation of PI3 kinase, Rho and ROCK, leading to activation of Myc t
264 AIA circuit and AGE-1, an insulin-regulated PI3 kinase, signal to AWC to drive nuclear enrichment of
266 d that GDF10 downregulated PTEN, upregulated PI3 kinase signaling and induced specific axonal guidanc
269 iferation slows because of decreased insulin/PI3 kinase signaling, resulting in nuclear localization
271 val through a novel mechanism that activates PI3-kinase signaling events, thus highlighting tTG as a
272 ding genetic evidence supporting the role of PI3-kinase signaling in these processes in E. histolytic
273 We tested the hypothesis that ErbB3-mediated PI3-kinase signaling is critical for heregulin-induced m
275 ical role for phosphatidylinositol 3-kinase (PI3-kinase) signaling in cell proliferation that is supp
276 t human UCC that have high levels of Wnt and PI3 kinase signalling may be responsive to mTOR inhibiti
282 ipocytes demonstrated that insulin-activated PI3-kinase signals to GLUT4 primarily through Akt2 kinas
284 observed that phosphatidylinositol-3-kinase (PI3 kinase), Src family kinase (SFK), and downstream pro
285 significantly reduced phosphorylation of the PI3 kinase substrate Akt, and have reduced activation of
286 Although the oncogenic potential of the PI3-kinase subunit p110alpha requires its mutational act
288 ctor 3, a subunit of protein phosphatase 2A, PI3 kinase target of rapamycin 1) scaffold of protein ph
290 stradiol triggers a nongenomic activation of PI3 kinase that results in enhanced glutamate release fr
291 rm in liver, we now show that it is class II PI3-kinase that is required for insulin-stimulated apoB1
293 hyperinsulinaemia on the liver, mediated by PI3 kinase, though consensus on the downstream effectors
294 h factors and cytokines inhibit the type III PI3 kinase through multiple pathways, including the MAPK
295 also stimulates an IGF1 receptor (IGF1R) to PI3 kinase to AKT to GSK-3beta pathway required for acti
296 n, and differentiation, including a type III PI3 kinase (Vps34), a putative PI3 kinase, a putative mi
297 fragments but not for parental cells, while PI3 kinase was essential for the direction sensing of wh
298 s upstream of the activation of the type III PI3 kinase, which is critical for the initiation of auto
299 induction of GRP78 and CHOP, suggesting that PI3-kinase, which is known to mediate ER stress-induced
300 ed) and ATR (ATM and Rad3-related) are large PI3 kinases whose human mutations result in complex synd
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