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1 ase) and mammalian target of rapamydn (mTOR)-p70 S6 kinase .
2 not by rapamycin, which blocks activation of p70(S6 kinase).
3 te cross-regulated by rapamycin and IL-7 was p70 S6 kinase.
4 nd enhances the ability of Tiam1 to activate p70 S6 kinase.
5 PI3-kinase downstream effectors PKB/Akt and p70 S6 kinase.
6 n and regulate a growth checkpoint involving p70 S6 kinase.
7 e NEK6 interferes with insulin activation of p70 S6 kinase.
8 enous EDG-1 required G(i) activation but not p70 S6 kinase.
9 ovel candidate physiologic regulators of the p70 S6 kinase.
10 t not by a kinase-inactive mTOR mutant or by p70 S6 kinase.
11 mediates that link cell surface receptors to p70 S6 kinase.
12 ression of rat SGK, but not mouse PKB or rat p70 S6 kinase.
13 the activity of its direct downstream target p70 S6 kinase.
14 ositide 3-kinase with IRS-1 or activation of p70 S6 kinase.
15 uced regulation, thus suggesting the role of p70 S6 kinase.
16 eukin-2 receptor, the protooncogene PKB, and p70 S6 kinase.
17 enic potential, but did activate p21 RAS and p70 S6 kinase.
18 apamycin (mTOR) and downstream activation of p70 S6 kinase.
19 ivated downstream of PI 3'-kinase, involving p70 S6 kinase.
20 ld be blocked by inhibitors of PI3-kinase or p70 S6-kinase.
21 -1c processing is blocked by an inhibitor of p70 S6-kinase.
22 rylation of the ribosomal regulatory protein p70-S6 kinase.
23 tion of BAD on serine(112), or activation of p70(S6) kinase.
24 wn that curcumin inhibits phosphorylation of p70 S6 kinase 1 (S6K1) and eukaryotic initiation factor
25 ely active and rapamycin-resistant mutant of p70 S6 kinase 1 (S6K1) conferred to resistance to rapamy
26 apamycin complex 1 (mTORC1) and its effector p70 S6 kinase 1 (S6K1) in the extinction of auditory thr
28 tes the mammalian target of rapamycin (mTOR)/p70 S6 kinase 1 (S6K1) signaling pathway and promotes ne
35 erfering RNA knockdown of the mTOR substrate p70 S6 kinase abrogated PAK1 phosphorylation and enhance
38 annot bind to Tiam1 suppresses serum-induced p70 S6 kinase activation in cells, suggesting that a Tia
39 ed receptor on PI 3-kinase/Akt signaling and p70 S6 kinase activation using Rat-1 fibroblasts stably
41 tussis toxin treatment inhibited S1P-induced p70 S6 kinase activation, cyclin D1 expression and proli
44 ectomy induced a transient increase in liver p70 S6 kinase activity and 4E-BP1 phosphorylation as com
45 g protein 1 (4E-BP1), resulting in decreased p70 S6 kinase activity and an increase in 4E-BP1 binding
47 bility of glucocorticoids to inhibit Akt and p70 S6 kinase activity and reduced glucocorticoid induct
48 zing radiation caused a 2-3-fold increase in p70 S6 kinase activity that was blocked pharmacologicall
49 pendent Erb-B3 signaling also contributed to p70 S6 kinase activity through recruitment and activatio
50 DQA*03011 (DQ 65-79), and rapamycin inhibit p70 S6 kinase activity, but only DQ 65-79 blocks Akt kin
51 ffects of IFNs, imatinib mesylate suppressed p70 S6 kinase activity, consistent with inhibition of BC
58 ed neoplastic proliferation, tumor size, and p70/S6 kinase activity, but did not affect the status of
59 ycin.FKBP12 complex in vitro can protect the p70 S6 kinase against rapamycin-induced dephosphorylatio
60 kinase activity, p110(CAAX) fully stimulated p70 S6 kinase, Akt, 2-deoxyglucose uptake, and Ras, wher
64 of eIF4F assembly and the phosphorylation of p70 S6 kinase and 4E-BP1 and that basal MEK activity is
65 rotein synthesis, and the phosphorylation of p70 S6 kinase and 4E-BP1 independently of both phosphati
67 by phosphorylation of the downstream targets p70 S6 kinase and 4E-BP1, and mTOR inhibition with rapam
70 ine kinase network stimulates cytoprotective p70 S6 kinase and Akt activity in response to clinically
71 cts of low dose ionizing radiation (2 Gy) on p70 S6 kinase and Akt signaling with respect to Erb-B re
73 -IR cells results in a rapid deactivation of p70 S6 kinase and dephosphorylation of eIF-4E BP1, which
75 ycin-induced dephosphorylation, and for both p70 S6 kinase and eIF-4E BP1, such protection requires t
77 oposide led to the dephosphorylation of both p70 S6 kinase and eukaryotic initiation factor (eIF) 4E-
78 osphorylation of two translation modulators, p70 S6 kinase and eukaryotic initiation factor 4E-bindin
79 3'-kinase pathway mediates activation of the p70 S6 kinase and inactivation of 4E-BP1, to regulate mR
81 t in healthy kidney, whereas, phosphorylated p70 S6 kinase and p56 were present only in angiomyolipom
84 ), and the p70 and p90 ribosomal S6 kinases (p70 S6 kinase and p90 Rsk, respectively), are activated
85 glutathione S-transferase fusion proteins of p70 S6 kinase and PAK3 each isolated PP2A; and 3) PAK3 a
90 to be accompanied by a strong activation of p70 S6 kinase and the mitogen-activated protein kinase (
92 two other downstream effectors of PI3K, the p70 S6 kinase and the repressors of mRNA translation, 4E
93 ases revealed that PP2A co-precipitated with p70 S6 kinase and the two PAK isoforms; 2) glutathione S
94 cross-linked PP2A revealed an enrichment of p70 S6 kinase and two p21-activated kinases (PAK1 and PA
95 en stimulates translation by phosphorylating p70 S6 kinase and, consequently, the 40 S ribosomal prot
97 ergoes ordered C-terminal phosphorylation by p70 S6 kinases and p90 ribosomal S6 kinases on four cons
99 ere it could activate its substrates such as p70 S6-kinase and p90 ribosomal S6 kinase that do not in
100 ing of the actin cytoskeleton, activation of p70(S6) kinase and c-jun N-terminal kinase (JNK), and re
101 eukaryotic translation regulators, including p70-S6 kinase and the eukaryotic translation initiation
102 he translational regulatory proteins 4E-BP1, p70 S6 kinase, and eIF-4E, thus providing a mechanism fo
103 o associated with reduced activation of Akt, p70 S6 kinase, and extracellular regulated kinase signal
104 l showed increased nuclear levels of phospho-p70 S6 kinase, and neurons protected with DRB and flavop
107 creases in protein synthesis, phosphorylated p70 S6 kinase, and ribosomal S6 protein levels as well a
108 gulation of CYP2E1 and implicate PI3-kinase, p70 S6 kinase, and Src kinase in mediating these effects
109 s to see whether there is phosphorylation of p70 S6 kinase, and the ribosomal S6 protein in angiomyol
110 k1/2, insulin-like growth factor receptor-1, p70 S6 kinase, and transforming growth factor alpha comp
113 BrdU incorporation, coinjection with an anti-p70 S6 kinase antibody effectively blocked anti-NSH2-sti
114 c initiation factor 4E binding protein-1 and p70 S6 kinase are early events that control the translat
116 its downstream signaling molecules, Akt and p70 S6 kinase, are required, albeit to varying degrees.
117 r-308, and concurrently activated downstream p70 S6 kinase as well as glycogen synthase kinase-3beta.
118 cruited by Pl 3-kinase for the activation of p70 S6 kinase as well as of PKB, and serves as a multifu
119 otently inhibited PDGF-induced activation of p70 S6 kinase as well as proliferation of smooth muscle
120 d levels of phosphorylated Akt and activated p70/S6 kinase associated with an increase in proliferati
125 and PAK3 each isolated PP2A; and 3) PAK3 and p70 S6 kinase bound to microcystin-Sepharose (an affinit
126 in, VacA did not suppress phosphorylation of p70 S6 kinase but caused mitochondrial depolarization an
127 ha(1)-adrenergic receptor agonist, activated p70 S6 kinase but did not activate PI 3-kinase or any of
128 nsulin-like growth factor 1, which activates p70 S6 kinase but not Erk, regulation of eEF2 is blocked
129 ar or lower levels and activity of ribosomal p70 S6 kinase, but c-Myc levels were elevated in both re
132 These results demonstrate that activation of p70 S6 kinase by the alpha(1A)-adrenergic receptor in Ra
133 with Shc and activation of MAPK, but not the p70 S6 kinase, could be stimulated by epidermal growth f
134 nases activated by IL-2, MAP kinase/ERK2 and p70 S6 kinase, do not appear to be involved in STAT5 reg
137 creases in the phosphorylation of 4E-BP1 and p70 S6 kinase, eIF4F assembly, and protein synthesis.
138 PDK1 phosphorylates the hydrophobic motif of p70 S6 kinase either directly or by activation of anothe
140 rterial wall also stimulated the activity of p70 S6 kinase from 30 minutes to 12 hours, suggesting an
141 SCs in addition to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6
142 ile inhibitors of MEK, protein kinase C, and p70 S6 kinase had a modest effect or no effect on NF-kap
144 e major protein kinase that is active on the p70 S6 kinase hydrophobic regulatory site, Thr412, was p
146 horylation of mTOR and its downstream target p70 S6 kinase in a PKC-delta- and PI3K/Akt-dependent man
147 ignaling molecules forkhead box O (FOXO) and p70 S6 kinase in a tissue and blood meal-specific manner
151 at Thr412 and other sites and activates the p70 S6 kinase in vitro and in vivo, in a manner synergis
153 eveals a prominent role of neural Drosophila p70/S6 kinase in the modulation of hunger response by in
157 proliferation, suggesting that activation of p70 S6 kinase is critical in EDG-1/G(i)-mediated cell pr
160 the LKB1/AMPK/TSC1/2 pathway alleviates the p70 S6 kinase-mediated negative regulation of insulin si
161 tream regulator of eIF-4E BP1 as well as the p70 S6 kinase; moreover, these two mTOR targets are regu
162 and increased ribosomal antigen and phospho-p70 S6 kinase, occurred early in the course of acute vas
163 e whether inhibition of either the ribosomal p70 S6 kinase or eukaryotic initiation factor (eIF) 4E p
164 t upstream of mTOR, persistent inhibition of p70 S6 kinase or S6K1 can activate Akt via a negative fe
165 does not require the activation of PAK, JNK, p70 S6 kinase, or Rho, but instead requires phosphatidyl
166 -induced decreases in mTOR-regulated phospho-p70 S6 kinase (P-p70) and the p62 protein, as well as in
170 de that modulates translation initiation via p70 S6 kinase (p70(s6k)) and eIF-4E binding protein 1 (4
171 icated by the FK1012-dependent activation of p70 S6 kinase (p70(S6k)) and mitogen-activated protein (
172 he increased phosphorylation in dendrites of p70 S6 kinase (p70(S6K)) at Thr3889, a major regulator o
176 racellular signal-regulated kinase (ERK) and p70 S6 kinase (p70(S6k)) in the NO-induced increase in p
177 r growth factor-dependent phosphorylation of p70 S6 kinase (p70(S6K)) in vitro, and we demonstrate th
180 pathways to investigate the contribution of p70 S6 kinase (p70(S6K)) to Rac1 transformation and to d
181 rapamycin, an inhibitor of the activation of p70 S6 kinase (p70(S6k)), completely abolished IGF stimu
182 luding rapamycin, which blocks activation of p70 S6 kinase (p70(S6k)), PD98059, which inhibits the ac
183 kinases downstream from PI-3 kinase, Akt and p70 S6 kinase (p70(S6K)), was decreased in cells express
188 ivates phosphoinositide 3-kinase (PI3-K) and p70 S6 kinase (p70S6K) and that rapamycin, a FRAP/mammal
194 ination required phosphorylation of TRIB2 by p70 S6 kinase (p70S6K) via another domain (amino acids 6
195 crease of the TPA-induced phosphorylation of p70 S6 kinase (p70S6K), a protein kinase involved in the
196 of its downstream target, ribosomal protein p70 S6 kinase (p70S6K), and concomitant inhibition of ce
197 rphosphorylation, constitutive activation of p70 S6 kinase (p70S6K), and increased basal DNA synthesi
198 the protein-serine/threonine kinases Akt and p70 S6 kinase (p70S6K), are crucial effectors in oncogen
199 le protein regulated by insulin (PHAS-I) and p70 S6 kinase (p70S6k), in an insulin-independent and ra
200 ond, we observed that Thr-389-phosphorylated p70 S6 kinase (p70S6K), the main active phosphoform of t
205 rovide evidence for association of PP2A with p70 S6 kinase, PAK1, and PAK3 in the context of the cell
206 was unaffected by rapamycin, an inhibitor of p70 S6 kinase pathway but abolished by the PI3K inhibito
208 the mammalian target of rapamycin complex 1-p70 S6 kinase pathway, a known growth regulatory pathway
212 , the most downstream target of the Akt-mTOR-p70-S6 kinase pathway, is a frequent event in clinical s
214 t phosphorylation, concurrently with reduced p70 S6 kinase phosphorylation at Thr389 as well as IRS-1
216 n or LY294002 and rapamycin, an inhibitor of p70 S6 kinase phosphorylation, ameliorated the insulin-m
217 ipocytes enhanced insulin-stimulated Akt and p70 S6 kinase phosphorylation, as well as GLUT4 transloc
220 ses, including protein kinase B (PKB)/c-Akt, p70 S6 kinase, PKC isoforms, and serum- and glucocortico
221 ion factor 4E (eIF4E)-eIF4G interactions and p70 S6 kinase polypeptide 1 (S6K1) in reconsolidation.
222 or rapamycin (which blocks the activation of p70 S6 kinase) prevented the formation of multinucleated
224 though H(2)O(2) increased phosphorylation of p70 S6 kinase, rapamycin failed to inhibit H(2)O(2) from
225 inase family; we show that two such kinases, p70 S6 kinase (regulated via mTOR) and p90(RSK1) (activa
228 and rapamycin, which inhibit MAP kinase and P70 S6 kinase, respectively, had little effect on the in
229 diators of PI 3-kinase, the serine/threonine p70 S6-kinase (S6-kinase) and the antiapoptotic protein
230 a mouse model of liver-specific knockdown of p70 S6 kinase (S6K) (L-S6K-KD) by systemic delivery of a
233 nt phosphorylation is mediated by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RS
234 n a cell type-specific manner, by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RS
237 ssociated protein kinases (ROCK1 and ROCK2), p70 S6 kinase (S6K), and mammalian target of rapamycin (
238 ylation of eIF4E-binding protein (4E-BP) and p70 S6 kinase (S6K), which is important for maintaining
241 Phosphorylation of this motif (FLGFT389Y) in p70 S6 kinase (S6K1) is both rapamycin- and wortmannin-s
243 the p90 ribosomal protein S6 kinase (RSK) or p70 S6 kinase (S6K1), in a cell type-specific manner.
244 RNA interference-mediated knockdown of TSC2, p70 S6 kinase (S6K1), raptor, or rictor demonstrates tha
246 ble knock-out cells for both isoforms of the p70 S6 kinase (S6k1/S6k2), a downstream effector of Akt
248 stimulate the phosphorylation of PHAS-I and p70(s6) kinase, suggesting that the mammalian target of
249 sphorylation of tau can be regulated through p70 S6 kinase, the well characterized immediate downstre
250 nt led to decreased levels of phosphorylated p70 S6 kinase (Thr(389)) in gallbladder tissue as assess
251 (Ser-2448 and Ser-2481), phosphorylation of p70 S6 kinase (Thr-389), and ribosomal protein S6 (Ser-2
252 mplex acts to dephosphorylate/deactivate the p70 S6 kinase; thus, some mTOR mutants that have lost th
253 tiation factor 4E-binding protein (4EBP) and p70 S6 kinase to promote protein synthesis and cell size
254 ch as the translational regulators 4E-BP and p70 S6 kinase, to the TOR catalytic domain is essential
255 parallel insulin response pathways including p70 S6 kinase, ubiquitin ligase Cbl, or mitogen-activate
258 ated, its ability to cause activation of the p70 S6 kinase was also controlled by the p70 carboxy-ter
260 th this, thrombin-induced phosphorylation of p70 S6 kinase was defective in embryonic fibroblasts fro
266 tion with Shc and activation of MAPK and the p70 S6 kinase were insensitive to insulin stimulation.
267 n of known Phlpp1 substrates, Akt2, PKC, and p70 S6 kinase, were enhanced in ex vivo cultured Phlpp1(
268 its substrate mTOR, and the mTOR substrate, p70 S6 kinase, were indeed reduced in Hdac3-deficient pr
269 eukaryotic translation initiation factor and p70 S6 kinase, were up-regulated following NO treatment,
270 reviously to engender some activation of the p70 S6 kinase, whereas both modifications together produ
271 ibited the c-Kit signaling events of Akt and p70 S6 kinase, whereas SDF-1alpha-mediated activation of
272 ion of processing requires the mTORC1 target p70 S6-kinase, whereas induction of mRNA bypasses this e
273 y a dose-dependent activation of Akt/PKB and p70(S6) kinase, whereas the MAP kinase pathway was unaff
274 increased phosphorylation and activation of p70 S6 kinase, which was inhibited by both DRB and flavo
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