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1 on of its two downstream targets, p21Cip and S6 kinase.
2 activity of its direct downstream target p70 S6 kinase.
3 1 pathway components AMPK, RAGA-1 and RSKS-1/S6 kinase.
4 educed phospho-IRS-1(S302) through AMPKalpha-S6 Kinase.
5 tion depended on activation of p90 ribosomal S6 kinase.
6 uggesting a downstream pathway distinct from S6 kinase.
7 ed phosphorylation of MET, AKT and ribosomal S6 kinase.
8 he protein kinase AKT, protein kinase C, and S6 kinase.
9 tion of the ribosomal regulatory protein p70-S6 kinase.
10 processing is blocked by an inhibitor of p70 S6-kinase.
11 phosphorylates the 70-kDa ribosomal protein S6 kinase 1 (p70S6K1), which subsequently phosphorylates
12 FNlambda activates the p90 ribosomal protein S6 kinase 1 (RSK1) and its downstream effector, initiati
13 dependent kinase 1 target kinases, ribosomal S6 kinase 1 (Rsk1) and Rsk2, produced a striking perturb
15 owed that the inactive form of p90 ribosomal S6 kinase 1 (RSK1) interacts with the regulatory subunit
17 ells, interacts with mammalian p90 ribosomal S6 kinase 1 (RSK1), and causes a decrease in NK cell pop
21 hat curcumin inhibits phosphorylation of p70 S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E (
23 ignificantly induced phosphorylation of both S6 kinase 1 (S6K1) and S6 ribosomal protein (S6) in the
25 downstream effectors, the ribosomal protein S6 kinase 1 (S6K1) and the translation initiation factor
28 active and rapamycin-resistant mutant of p70 S6 kinase 1 (S6K1) conferred to resistance to rapamycin.
29 We found that targeting ribosomal protein S6 kinase 1 (S6K1) in Pten-deficient cells suppressed gl
30 ycin complex 1 (mTORC1) and its effector p70 S6 kinase 1 (S6K1) in the extinction of auditory threat
32 ve shown that loss of ribosomal protein (RP) S6 kinase 1 (S6K1) increases systemic insulin sensitivit
36 n complex 1 (mTORC1) and its effector kinase S6 kinase 1 (S6K1) is known to trigger multisite seryl p
38 1 (mTORC1)short right arrowribosomal protein S6 kinase 1 (S6K1) pathway decreases tumor suppressor pr
39 Leucine alone stimulated ribosomal protein s6 kinase 1 (S6K1) phosphorylation approximately 280% mo
43 identified PKD3 to trigger the activation of S6 kinase 1 (S6K1), a main downstream target of the mamm
44 on mTOR signaling, the ribosomal protein S6, S6 kinase 1 (S6K1), and eukaryotic translation initiatio
45 tein (4E-BP) and activates ribosomal protein S6 kinase 1 (S6K1), both of which stimulate translation.
46 wnstream of mTORC1 include ribosomal protein S6 kinase 1 (S6K1), eukaryotic translation initiation fa
47 via its downstream target ribosomal protein S6 kinase 1 (S6K1), which directly phosphorylates S1859
49 o the inhibitory effects of rapamycin and an S6 kinase 1 (S6K1)-specific inhibitor on T cell activati
54 rate-1 (Tyr-608), Akt (Thr-308 and Ser-473), S6 kinase 1 (Thr-389), eukaryotic initiation factor 4E b
55 phosphorylation (e.g., p70 ribosomal protein S6 kinase 1 [S6K1] and eukaryotic initiation factor 4E b
57 ciated with an increase in ribosomal protein S6 kinase 1 and eukaryotic initiation factor 4E-binding
58 itor implicated a role for ribosomal protein S6 kinase 1 in IL-33-induced mTOR-dependent cytokine pro
60 1-dependent manner in NIH 3T3 cells, whereas S6 kinase 1 is the dominant regulator in hepatocellular
61 orylation of their substrates phosphorylated S6 kinase 1 or phosphorylated S6 ribosomal protein and p
62 the mammalian target of rapamycin complex 1/S6 kinase 1 pathway downstream of nutrient signaling.
63 r signal-regulated kinase 1/2, and ribosomal S6 kinase 1 signal transduction pathways and subsequent
66 lysis of divergent signaling through ERK1/2, S6 kinase 1, and 4E binding protein 1 provides insights
67 et of rapamycin complex 1, ribosomal protein S6 kinase 1, and eukaryotic translation initiation facto
68 lular signal-regulated kinase 1/2, ribosomal S6 kinase 1, or cAMP responsive element binding protein
70 tes (mammalian target of rapamycin complex-1/S6 kinase 1/HIF-1alpha) were detected in LPS-stimulated
71 ing protein 1 (4E-BP1) and ribosomal protein S6 kinase-1 (S6K1), whereas HIF-1alpha degradation remai
74 alpha II (the 70-kDa 40 S ribosomal protein S6 kinase-1 alpha II isoform), and Thr-229 phosphorylati
78 l regulatory mechanism whereby p90 ribosomal S6 kinase 2 (RSK2) interacts with 5-hydroxytryptamine(2A
81 red that the ERK/MAPK effector p90 ribosomal S6 kinase 2 (RSK2) phosphorylates the 5-HT(2A) receptor
84 otably, we showed that EGF induces ribosomal S6 kinase 2 (RSK2) ubiquitination, and knocking down TRA
85 neurons cultured from mice lacking ribosomal S6 kinase 2 (Rsk2), a model for the Coffin-Lowry syndrom
87 t growth factor 2 (FGF-2) signalling-induced S6 kinase 2 (S6K2) activation is necessary, but the down
88 is study, we evaluated p70 ribosomal protein S6 Kinase 2 (S6K2), a downstream effector of mTORC1, for
90 The RPS6KA6 gene encodes the p90 ribosomal S6 kinase-4 (RSK4) that is still largely uncharacterized
91 malian target of rapamycin/ribosomal protein S6 kinase, 70 kDa, pathway and thereby stimulate protein
92 malian target of rapamycin/ribosomal protein S6 kinase, 70 kDa, pathway, and the importance of this C
96 re hypertrophied, and the phosphorylation of S6 kinase, a target of mammalian target of rapamycin (mT
100 d in TLR-4-mediated 70-kDa ribosomal protein S6 kinase activation and enhanced TNF-alpha release, whe
101 oxidative stress) that are also positive for S6-kinase activation (a marker associated with aging).
102 ty of glucocorticoids to inhibit Akt and p70 S6 kinase activity and reduced glucocorticoid induction
103 tion leads to reduced mTOR activity, reduced S6 kinase activity, and activation of autophagy to reduc
104 /mammalian target of rapamycin/p70 ribosomal S6 kinase (Akt/mTOR/p70S6K) in the kidney were measured
105 ) phosphorylation of mTOR downstream targets S6 kinase and 4E-binding protein; and (4) formation of e
108 d that UCH-L1 impairs mTORC1 activity toward S6 kinase and 4EBP1 while increasing mTORC2 activity tow
112 ced phosphorylation of Akt, MAP kinases, and S6 kinase and Fos expression in the absence of Crk and C
113 is, including IFN-induced phosphorylation of S6 kinase and its effector rpS6, as well as phosphorylat
115 AKT/mammalian target of rapamycin/ribosomal S6 kinase and MEK/ERK/RSK pathways because it was resist
116 1/2 and of two downstream targets (ribosomal S6 kinase and mitogen- and stress-activated protein kina
117 ase (AMPK) and upstream of ribosomal protein S6 kinase and mTOR complex 1 (TORC1), by its direct asso
121 es ordered C-terminal phosphorylation by p70 S6 kinases and p90 ribosomal S6 kinases on four conserve
123 uding mTOR, raptor, rictor, 70-kDa ribosomal S6 kinase, and 4E-binding protein 1 in the mTOR axis by
124 amatically inhibited insulin-stimulated Akt, S6 kinase, and 4E-BP1 phosphorylation but had little eff
125 ed IGF-1R-induced phosphorylation of PRAS40, S6 kinase, and 4EBP-1, indicating inhibition of mTORC1 a
126 ownregulation of germline targets, including S6 kinase, and by the activation of an intestinal transc
127 n-activated protein kinase kinase, ribosomal S6 kinase, and cyclin-dependent kinase 1/2 in combinatio
128 sociated with reduced activation of Akt, p70 S6 kinase, and extracellular regulated kinase signaling
129 owed increased nuclear levels of phospho-p70 S6 kinase, and neurons protected with DRB and flavopirid
130 r signal-regulated kinase, ribosomal protein S6 kinase, and protein kinase D (PKD) that increase cAMP
131 s of p70 S6 protein kinase and p90 ribosomal S6 kinase, and there is good evidence that it plays a po
132 orylation of ERK1/2, CREB, and p90 ribosomal S6 kinase, as well as a decreased level of pore formatio
133 obic motif, on the AGC kinases Akt, PKC, and S6 kinase, as well as an inhibitory site on the kinase M
135 her involving the RPS6KB1 (Ribosomal protein S6 kinase beta-1) were recurrently expressed in a number
137 the proteasome (by MG-132) or p90 ribosomal S6 kinases (by BI-D1870) is further increased by knockdo
138 inase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun, and cAMP response element binding prot
141 as regulated by an ERK1/2- and p90 ribosomal S6 kinase-dependent mechanism, unlike in macrophages in
143 for inhibition of Thr-389 phosphorylation on S6 kinases (EC(50) = 2 nM) relative to other inhibitors.
145 , in daf-16/FOXO, sir-2.1, rsks-1 (ribosomal S6 kinase), gcn-2, and aak-2 (AMPK) longevity pathway mu
146 in addition to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6 kina
149 ling molecules forkhead box O (FOXO) and p70 S6 kinase in a tissue and blood meal-specific manner.
150 revealed increased phosphorylation of p70S6/S6 kinases in SB-, but not in rhTpo-, treated cells.
152 erevisiae homologue of the mammalian Akt and S6 kinase, in DNA damage and genomic instability during
156 of phosphorylation of ERK-1/2, p90 ribosomal S6 kinase-l and Akt, although phosphorylations occur mor
157 Upon feeding, dietary cholesterol stimulates S6 kinase-mediated phosphorylation of the Boi cytoplasmi
160 mammalian target of rapamycin complex 1 and S6 kinase (mTORC1--> S6K) attenuates insulin-stimulated
161 rylation by p70 S6 kinases and p90 ribosomal S6 kinases on four conserved Ser residues (Ser-235, Ser-
162 tations in the predicted CeTOR target rsks-1/S6 kinase or in ife-2/eIF4E also reduce protein biosynth
164 stream of mTOR, persistent inhibition of p70 S6 kinase or S6K1 can activate Akt via a negative feedba
165 uced decreases in mTOR-regulated phospho-p70 S6 kinase (P-p70) and the p62 protein, as well as increa
169 ally induced signaling through the ribosomal S6 kinase [p70(389)] is not strain rate sensitive, but i
170 f two mTOR targets, 70-kDa ribosomal protein S6 kinase (p70S6K) and eukaryote initiation factor 4E bi
171 of ERK2, activation of the ribosomal protein S6 kinase (p70S6K) and its downstream target, ribosomal
173 ion required phosphorylation of TRIB2 by p70 S6 kinase (p70S6K) via another domain (amino acids 69-85
174 its downstream target, ribosomal protein p70 S6 kinase (p70S6K), and concomitant inhibition of cell g
175 of the downstream pathways of p70 ribosomal S6 kinase (p70S6K), eukaryotic initiation factor 4E-bind
176 S6 is regulated by ERK via the "alternative" S6 kinase p90-ribosomal S6 kinase (RSK), as evidenced by
177 s have identified p90 subfamily of ribosomal S6 kinase (p90RSK) family kinases as key factors for gro
178 se 2 (RSK2) is a member of the p90 ribosomal S6 kinase (p90RSK) family of proteins and plays a critic
180 (EGFR) that is coupled to MAPK/p90 ribosomal S6 kinase (p90RSK), but not phosphatidylinositol 3-kinas
182 eport the critical role of the p90 ribosomal S6 kinase (p90RSK)/ERK5 complex in EC dysfunction in dia
184 to prevent phosphorylation of the ribosomal S6 kinase partially alleviated the E4orf1 restriction to
185 of the mammalian target of rapamycin (mTOR)/S6 kinase pathway in a PLD- and endocytosis-dependent ma
186 mammalian target of rapamycin complex 1-p70 S6 kinase pathway, a known growth regulatory pathway.
188 K3) and mammalian target of rapamycin (mTOR) S6 kinase pathways, protein kinase Czeta (PKCzeta) pathw
189 -3s also reduces the level of phosphorylated S6 kinase, phosphorylated Thor/4E-BP and cyclin E (CycE)
191 SV treatment also partially blocked mTOR and S6 kinase phosphorylation in TSC1/2-deficient mouse embr
192 not neuroprogenitor cells, ribosomal S6 and S6 kinase phosphorylation increased over time, despite a
193 GDC-0941, targeted the downstream ribosomal S6 kinase phosphorylation to significantly suppress 5-FU
194 rgin stimulated mTORC1 activity (measured as S6 kinase phosphorylation) to a greater extent in wild-t
195 ytes enhanced insulin-stimulated Akt and p70 S6 kinase phosphorylation, as well as GLUT4 translocatio
202 horylation of AMPK and p70 ribosomal protein S6 kinase, respectively) and IL-6/IL-6 receptor signalin
203 mammalian target of rapamycin, p70 ribosomal S6 kinase, ribosomal protein S6, and mitogen activated p
209 o exhibited decreased levels of phospho-Akt, S6 kinase (RPS6KB1), and phosphorylated S6 protein (RPS6
210 ed that WFA activated phosphorylation of the S6 kinase RSK (ribosomal S6 kinase) in breast cancer cel
211 ORF45, mediates sustained ERK-p90 ribosomal S6 kinase (RSK) activation during KSHV lytic replication
212 mall interfering RNA inhibition of ribosomal S6 kinase (RSK) activity induced death of the FGFR1-tran
213 o increased phosphorylation of p90-ribosomal S6 kinase (RSK) and a concomitant activation of ETS-like
220 tudy evaluated the function of p90 ribosomal S6 kinase (RSK) in the Drosophila circadian system.
222 mediated by either the p90 ribosomal protein S6 kinase (RSK) or p70 S6 kinase (S6K1), in a cell type-
223 lar regulated kinase (ERK) and p90 ribosomal S6 kinase (RSK) proteins, we found several other copurif
225 ia the "alternative" S6 kinase p90-ribosomal S6 kinase (RSK), as evidenced by the site of elevated ph
227 causes sustained activation of p90 ribosomal S6 kinase (RSK), which is crucial for KSHV lytic replica
228 ent study has revealed a novel ERK/ribosomal S6 kinase (RSK)-dependent mechanism that regulates DR5 e
232 of the MEK kinase (MEKK)1/ERK/p90 ribosomal S6 kinase (RSK)1-dependent C/EBPbeta signaling pathway i
234 5 is a robust activator of the p90 ribosomal S6 kinases (RSK), and we found that this activity is nec
236 g pathways, we have identified the ribosomal S6 kinase RSKS-1 as a new cell-autonomous inhibitor of a
237 causes sustained activation of p90 ribosomal S6 kinases (RSKs) and extracellular regulated kinase (ER
238 ted herpesvirus interacts with p90 ribosomal S6 kinases (RSKs) and strongly stimulates their kinase a
239 use model of liver-specific knockdown of p70 S6 kinase (S6K) (L-S6K-KD) by systemic delivery of an ad
241 urther increased phosphorylation of ribosome S6 kinase (S6K) and BAD (Bcl-2-associated death promoter
242 ATRA suppressed phosphorylation of ribosomal S6 kinase (S6K) and its downstream targets S6 and eIF4B.
243 sion with increased levels of phosphorylated S6 kinase (S6K) and S6 was observed, consistent with con
245 hat mammalian target of rapamycin (mTOR) and S6 kinase (S6K) are highly expressed in the undifferenti
246 e investigated the role of ribosomal protein S6 kinase (S6K) at the intersection of nutrition and the
251 cell type-specific manner, by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RSK) a
252 hosphorylation is mediated by either the p70 S6 kinase (S6K) or the p90 ribosomal protein S6K (RSK) i
253 The mammalian target of rapamycin (mTOR) and S6 kinase (S6K) pathway is essential for cell differenti
254 rations activated the PI3K/mTORC2/PKB/mTORC1/S6 kinase (S6K) pathway, but pathophysiologically high a
258 igration an additional pathway that involves S6 kinase (S6K) through PLD2-Y(296), known to be phospho
259 d oral Mf demonstrated greater inhibition of S6 kinase (S6K), a downstream effector of mTOR complex 1
261 iated protein kinases (ROCK1 and ROCK2), p70 S6 kinase (S6K), and mammalian target of rapamycin (mTOR
263 ion of eIF4E-binding protein (4E-BP) and p70 S6 kinase (S6K), which is important for maintaining tran
269 ivation of the translation regulatory kinase S6-Kinase (S6K) through modulation of Rictor expression.
270 o, decreased basal Akt and ribosomal protein S6 kinase (S6K1) activation, and decreased transformatio
271 tly PMT induces phosphorylation of ribosomal S6 kinase (S6K1) and its substrate, ribosomal S6 protein
272 we identify a role for the ribosome protein S6 kinase (S6K1) and its upstream regulator mTOR in the
273 gnaling pathway, activation of p70 ribosomal S6 kinase (S6K1) through mTORC1, is also triggered by PK
274 rget of rapamycin (mTOR) downstream effector S6 kinase (S6K1) was confirmed to be activated in immort
278 unction analysis of Drosophila p90 ribosomal S6 kinase (S6KII) or its mammalian homolog RSK has not b
280 ncreased activation of the intracellular Akt/S6 kinase signaling pathway upon BCR and CD40 stimulatio
281 ession as a sensitive reporter of tonic mTOR-S6 kinase signaling through a novel mouse strain, chino,
282 ian target of rapamycin (mTOR)/p70 ribosomal S6 kinase signaling was activated by A53T but not WT alp
283 racellular signal-regulated kinase-ribosomal s6 kinase signaling was downstream of YAP for cell survi
285 PKD3 potentiates MEK/ERK/RSK (RSK, ribosomal S6 kinase) signaling and significantly enhances cholecys
287 subunit of protein kinase A (PKAc), ribosmal S6 kinase that controls RelA Ser 276 phosphorylation.
288 gulates the phosphorylation of p70 ribosomal S6 kinase, the major downstream target of mTOR complex 1
289 rylation of tau can be regulated through p70 S6 kinase, the well characterized immediate downstream t
290 vity (Akt; +113 +/- 31%), p70S6K1 (ribosomal S6 kinase Thr389; 25 +/- 5%), 4E binding protein 1 (4EBP
295 known Phlpp1 substrates, Akt2, PKC, and p70 S6 kinase, were enhanced in ex vivo cultured Phlpp1(-/-)
296 substrate mTOR, and the mTOR substrate, p70 S6 kinase, were indeed reduced in Hdac3-deficient primar
297 of processing requires the mTORC1 target p70 S6-kinase, whereas induction of mRNA bypasses this enzym
298 unique developmental functions for eIF4E and S6 kinase wherein their activity is specifically uncoupl
299 rol subjects was found for ribosomal protein S6 kinase, which did not change after CBT and did not co
300 reased phosphorylation and activation of p70 S6 kinase, which was inhibited by both DRB and flavopiri
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