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1 horylation and impaired binding to GSK3beta (glycogen synthase kinase 3beta).
2 ) transcriptional activity via inhibition of glycogen synthase kinase 3beta.
3 7, p38 mitogen-activated protein kinase, and glycogen synthase kinase 3beta.
4 ociated with activated AKT and inhibition of glycogen synthase kinase 3beta.
5 r export, which however, were independent of glycogen synthase kinase 3beta.
6 x ratio, phosphorylation of Akt, ERK1/2, and glycogen synthase kinase 3beta.
7 on of 4E-binding protein 1 and activation of glycogen synthase kinase 3beta.
8 pstream signaling pathways known to regulate glycogen synthase kinase-3beta.
9 n E2 expression and independently of p53 and glycogen synthase kinase-3beta.
10 ed by application of a specific inhibitor of glycogen synthase kinase 3beta (6-bromoindirubin-3'-oxim
11 increase in phospho-beta-catenin and active glycogen synthase kinase 3beta, a kinase known to target
12 cortical and hippocampal phosphorylation of glycogen synthase kinase-3beta, a constitutively active
13 marked reduction of inactive phosphorylated glycogen synthase kinase-3beta, a negative regulator of
14 orylation of the inhibitory Ser-9 residue of glycogen synthase kinase-3beta, a primary Tau kinase inv
15 atty acids, and this suppression depended on glycogen synthase kinase 3beta activation and induction
17 NF-kappaB activation by sorafenib requires glycogen synthase kinase 3beta activation, subsequent to
18 au phosphorylation and solubility, increased glycogen synthase kinase 3beta activity, compromised lon
19 protein that plays a key role in attenuating glycogen synthase kinase 3beta activity, leading to aber
20 post-translational mechanism, independent of glycogen synthase kinase-3beta activity regulating beta-
21 ronic inflammation, we found that inhibiting glycogen synthase kinase-3beta activity with lithium red
22 sed p38 mitogen-activated protein kinase and glycogen synthase kinase-3beta activity, which are belie
24 gnaling cascade, including phospho-GSK3beta (glycogen synthase kinase-3beta), also show significant d
26 2A and recruits protein phosphatase 2A with glycogen synthase kinase 3beta and beta-catenin, inducin
27 ls (P<0.05), and expressions of proapoptotic glycogen synthase kinase 3beta and caspase 3 were lower
29 isms involved demonstrate that ASPH binds to glycogen synthase kinase 3beta and inhibits its subseque
30 ibition of ASPH activity, phosphorylation of glycogen synthase kinase 3beta and p16 expression were i
31 king M(1)R were attributed to changes in the glycogen synthase kinase 3beta and protein kinase C acti
32 f kinases including protein kinase B/Akt and glycogen synthase kinase 3beta and regulates cell prolif
33 activation of Akt, leading to inhibition of glycogen synthase kinase-3beta and activation of beta-ca
34 on occurred secondary to the inactivation of glycogen synthase kinase-3beta and an increase in levels
35 attenuated basal phosphorylation of Akt and glycogen synthase kinase-3beta and blocked cardiac prote
36 ulin signaling may lead to overactivation of glycogen synthase kinase-3beta and down-regulation of O-
37 re was an increase in the level of activated glycogen synthase kinase-3beta and enhanced expression o
38 panied by hyperphosphorylation of substrates glycogen synthase kinase-3beta and mammalian target of r
39 at Ser-473 and other ILK targets, including glycogen synthase kinase-3beta and myosin light chain.
40 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa
41 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa
42 Wnt/beta-catenin signaling is independent of glycogen synthase kinase-3beta and of the proteasome- an
43 ac1 activation, redox phosphorylation of AKT/glycogen synthase kinase 3beta, and consequent smooth mu
44 t3a (the canonical activator), inhibitors of glycogen synthase kinase 3beta, and small-interfering RN
45 endent kinase 1, protein kinase C theta, and glycogen synthase kinase 3beta, as well as contributing
46 d beta-TrCP and decreased phosphorylation of glycogen synthase kinase 3beta associated with decreased
49 ollowed by phosphorylation (inactivation) of glycogen synthase kinase-3beta, at least in part via STA
50 cyclin D1, E-cadherin, beta-catenin, Dvl-1, glycogen synthase kinase-3beta, axin-1, and adenomatous
51 3-kinase, Akt, and Bcl.xL and inhibition of glycogen synthase kinase 3beta besides release of SDF-1a
52 establishing a mechanistic role for the ERK/glycogen synthase kinase 3beta/beta-catenin pathway in t
53 ial-mesenchymal transition by repressing AKT/glycogen synthase kinase-3beta/beta-catenin signaling.
54 reasing Ser9 phosphorylation-inactivation of glycogen synthase kinase 3beta by RBMY, thereby impeding
55 of stable MT subsets through inactivation of glycogen synthase kinase 3beta by the viral Ser/Thr kina
56 Akt murine thymoma viral oncogene homolog-1, glycogen synthase kinase 3beta, cyclin-dependent kinase
58 mylation by Taxol treatment or inhibition of glycogen synthase kinase 3beta decreased the selectivity
59 mpaired insulin signaling, overactivation of glycogen synthase kinase-3beta, decreased levels of majo
60 e kinase 3beta by RBMY, thereby impeding the glycogen synthase kinase 3beta-dependent degradation of
65 ver, inhibition of protein phosphatase 1 and glycogen synthase kinase 3beta, downstream targets of Ca
66 ced tumor growth, induced phosphorylation of glycogen synthase kinase 3beta, enhanced p16 expression
68 ogated insulin-stimulated phosphorylation of glycogen synthase kinase-3beta, forkhead box O1, and mTO
69 sion of insulin receptor, IRS-1, IRS-2, Akt, glycogen synthase kinase-3beta, forkhead box O1, protein
70 ted with release of the inhibitory effect of glycogen synthase kinase 3beta function by decreasing Se
72 eta-catenin signaling cascades, which switch glycogen synthase kinase 3beta (GSK-3beta) activation on
74 Ser215, a consensus phosphorylation site for glycogen synthase kinase 3beta (GSK-3beta) and its primi
76 ction in thrombin-induced phosphorylation of glycogen synthase kinase 3beta (GSK-3beta) at Ser9, whic
78 ase A (PKA) activation by cAMP analogues and glycogen synthase kinase 3beta (GSK-3beta) inhibition de
84 ected T cells and reduces phosphorylation of glycogen synthase kinase 3beta (GSK-3beta), a downstream
85 phorylation of PHLPP1 by casein kinase I and glycogen synthase kinase 3beta (GSK-3beta), and activati
86 ylation of Ser-389, a key inhibitory site of glycogen synthase kinase 3beta (GSK-3beta), and this eff
87 olved and show that the Tau-specific kinase, glycogen synthase kinase 3beta (GSK-3beta), is robustly
88 of cyclin B1, cyclin D3, and phosphorylated glycogen synthase kinase 3beta (GSK-3beta), while infect
93 Akt/mammalian target of rapamycin (mTOR) and glycogen synthase kinase 3beta (GSK-3beta)/adenomatous p
94 rom AD patients exhibited elevated levels of glycogen synthase kinase 3beta (GSK-3beta, an enzyme kno
96 arrest in G1/S phase, mAb16D10 triggering of glycogen synthase kinase-3beta (GSK-3beta) activation, d
97 DA receptors was involved in the increase of glycogen synthase kinase-3beta (GSK-3beta) activity, whi
98 is revealed that leptin and DEX converged on glycogen synthase kinase-3beta (GSK-3beta) and beta-cate
99 Treatment with NO donor led to activation of glycogen synthase kinase-3beta (GSK-3beta) and c-Jun N-t
100 events include the proline-directed kinases glycogen synthase kinase-3beta (GSK-3beta) and cyclin-de
101 rexpression of TDP-43 leads to activation of glycogen synthase kinase-3beta (GSK-3beta) and that GSK-
103 c entry in Xenopus oocytes, we characterized glycogen synthase kinase-3beta (GSK-3beta) as a dampener
105 on of downstream signaling molecules Akt and glycogen synthase kinase-3beta (GSK-3beta) at Ser9, and
106 inked to phosphorylation and inactivation of glycogen synthase kinase-3beta (GSK-3beta) at serine 9,
107 dated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3beta (GSK-3beta) by attacking
108 regulation of galectin-3 resulted in AKT and glycogen synthase kinase-3beta (GSK-3beta) dephosphoryla
112 etin, reactivation of beta-catenin using the glycogen synthase kinase-3beta (GSK-3beta) inhibitor LiC
117 as a putative molecular recognition site for glycogen synthase kinase-3beta (GSK-3beta) phosphorylati
119 decreased by POX in that phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) was decreased
122 osphorylation (and hence, the activation) of glycogen synthase kinase-3beta (GSK-3beta) with a declin
124 neurin, apoptosis-stimulated kinase (ASK-1), glycogen synthase kinase-3beta (GSK-3beta), GATA4, and c
125 sis coli tumor suppressor protein (APC), and glycogen synthase kinase-3beta (GSK-3beta), which could
126 atocytes, which led to a delayed increase in glycogen synthase kinase-3beta (GSK-3beta)-mediated hepa
127 demonstrate that alcohol intake also blocks glycogen synthase kinase-3beta (GSK-3beta)-phosphorylati
137 ), agonists of the Wnt/beta-catenin pathway (glycogen synthase kinase 3beta [GSK-3beta] inhibitors),
138 udy phosphorylated PKC zeta (p-PKC zeta) and Glycogen Synthase Kinase 3beta (GSK3 beta) were found to
139 lizes PRLr via inhibitory phosphorylation of glycogen synthase kinase-3beta (GSK3 beta) on Ser(9).
140 Consequently, GRbeta-Ad mice had increased glycogen synthase kinase 3beta (GSK3beta) activity and r
141 the c-Jun N-terminal kinase (JNK)-dependent glycogen synthase kinase 3beta (GSK3beta) activity on do
142 , N-methyl-d-aspartate receptor function, or glycogen synthase kinase 3beta (GSK3beta) activity or ex
143 ver, hypoinsulinemia leads to an increase in glycogen synthase kinase 3beta (GSK3beta) activity that,
144 ssociated with insulin resistance, decreased glycogen synthase kinase 3beta (GSK3beta) activity, acti
145 (NF-kappaB) pathway and in the induction of glycogen synthase kinase 3beta (GSK3beta) activity, resu
146 uroprotective factor that acts by modulating glycogen synthase kinase 3beta (GSK3beta) activity.
147 of beta-catenin by enhancing binding between glycogen synthase kinase 3beta (GSK3beta) and beta-caten
148 phosphorylation-mediated interaction between glycogen synthase kinase 3beta (GSK3beta) and c-Myc.
149 degradation of beta-catenin mediated by the glycogen synthase kinase 3beta (GSK3beta) and destructio
150 tcome on different molecular targets such as glycogen synthase kinase 3beta (GSK3beta) and Forkhead b
152 tion of downstream effectors of Akt, such as glycogen synthase kinase 3beta (GSK3beta) and mammalian
153 factors combined with LIF and inhibitors of glycogen synthase kinase 3beta (GSK3beta) and mitogen-ac
154 egrons that bind Cdc4 when phosphorylated by Glycogen Synthase Kinase 3beta (GSK3beta) and p38 MAPK,
155 Unexpectedly, RNAi-mediated silencing of glycogen synthase kinase 3beta (GSK3beta) and phosphoino
156 oteasomal degradation via phosphorylation by glycogen synthase kinase 3beta (GSK3beta) and recognitio
157 ted protein kinase kinase 4 (MKK4), JNK, and glycogen synthase kinase 3beta (GSK3beta) and thereby de
158 (APC), casein kinase 1alpha (CK1alpha), and glycogen synthase kinase 3beta (GSK3beta) and undergoes
160 TGF-beta1 expression and hyperacetylation of glycogen synthase kinase 3beta (GSK3beta) at residue K15
161 tein, HSC70) and causes dephosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser 9 by re
162 ects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing s
163 e tested the hypothesis that inactivation of glycogen synthase kinase 3beta (GSK3beta) by high glucos
164 n this issue, Wu et al. demonstrate that the glycogen synthase kinase 3beta (GSK3beta) controls micro
169 phosphorylation by casein kinase 1 (CK1) and glycogen synthase kinase 3beta (GSK3beta) in a phosphode
170 quent signaling, causing overt activation of glycogen synthase kinase 3beta (GSK3beta) in nerves of m
171 synthesis is associated with inactivation of glycogen synthase kinase 3beta (GSK3beta) in renal cells
172 y, we provide evidence to support a role for glycogen synthase kinase 3beta (GSK3beta) in such regula
173 In this study, we investigated the role of glycogen synthase kinase 3beta (GSK3beta) in the surviva
183 ar carcinoma-derived KLF6 mutations affect a glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
184 inked kinase (ILK), leading to modulation of glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
185 ates beta-TrCP recognition and encompasses a glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
186 of TGF-beta receptors and p38 MAPK increased glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
187 This was associated with decreased levels of glycogen synthase kinase 3beta (GSK3beta) protein and mR
190 d by the core clock oscillator BMAL1 and AKT/glycogen synthase kinase 3beta (GSK3beta) signaling path
192 ically, leptin stimulates phosphorylation of glycogen synthase kinase 3beta (GSK3beta) via Akt activa
193 [e.g., strong bias toward phosphorylation of glycogen synthase kinase 3beta (GSK3beta) via the full-l
197 5-HT levels is accompanied by activation of glycogen synthase kinase 3beta (GSK3beta), a signaling m
198 kt, mammalian target of rapamycin complex 1, glycogen synthase kinase 3beta (GSK3beta), and CREB.
199 e IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta), as one major
201 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p
202 kt pathway, leading to the downregulation of glycogen synthase kinase 3beta (GSK3beta), in wild type
203 compelling evidence supporting key roles for glycogen synthase kinase 3beta (GSK3beta), mitochondrial
206 fate through the translational regulation of glycogen synthase kinase 3beta (GSK3beta), we investigat
207 hic signaling intermediates, such as Akt and glycogen synthase kinase 3beta (GSK3beta), were dephosph
208 y sites in the N-terminus of beta-catenin as glycogen synthase kinase 3beta (GSK3beta), which are rec
209 dent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase 3beta (GSK3beta), which is medi
210 APC also induced phosphorylation of Ser-9 in glycogen synthase kinase 3beta (GSK3beta), which was blo
211 s strictly regulated in normal cells via the glycogen synthase kinase 3beta (GSK3beta)- adenomatous p
212 n this paper, we show a critical role of the glycogen synthase kinase 3beta (GSK3beta)-cyclin D3 path
216 1 interacts with Nrf2 and stabilizes it from glycogen synthase kinase 3beta (GSK3beta)-mediated phosp
217 FN signaling pathways occurs at the point of glycogen synthase kinase 3beta (GSK3beta)-TANK-binding k
231 nted pre-synaptic protein deficit, decreased glycogen synthase kinase-3beta (GSK3beta) activity, and
232 chanism by which the serine-threonine kinase glycogen synthase kinase-3beta (GSK3beta) affects surviv
234 of signaling proteins, including fyn kinase; glycogen synthase kinase-3beta (GSK3beta) and cyclin-dep
235 global ischemia promotes early activation of glycogen synthase kinase-3beta (GSK3beta) and forkhead t
236 finding is the pronounced downregulation of glycogen synthase kinase-3beta (Gsk3beta) and upregulati
239 Here we demonstrate that hyperactivity of glycogen synthase kinase-3beta (GSK3beta) in the atrium
243 uclear Nrf2 export/degradation machinery via glycogen synthase kinase-3beta (Gsk3beta) signaling was
245 at PAD4 recognizes, binds, and citrullinates glycogen synthase kinase-3beta (GSK3beta), both in vitro
246 lted in increased phosphorylation of Akt and glycogen synthase kinase-3beta (GSK3beta), leading to en
247 ase activity of the serine/threonine kinase, glycogen synthase kinase-3beta (GSK3beta), via its Ser9
252 s (ankyrin G, EB1) were knocked down or when glycogen synthase kinase-3beta (GSK3beta; an AD-associat
253 cogene/protein kinase B [AKT], inhibition of glycogen synthase kinase-3beta [GSK3beta], a 20-fold up-
254 x and is required for phosphorylation of the glycogen synthase kinase-3beta homologue Zeste-white 3 k
255 tion of Akt and increased phosphorylation of glycogen synthase kinase 3beta in an arrestin signalsome
256 elet activating factor-induced activation of glycogen synthase kinase 3beta in platelets in a manner
257 Overexpression of Snail1 and inhibition of glycogen synthase kinase-3beta in colorectal tumor cells
259 nalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3beta, in maternal liver (P < 0
263 in, and that beta-catenin activation through glycogen synthase kinase 3beta inhibition leads to FANCC
264 cin complex 1 (TORC1) activity, resulting in glycogen synthase kinase 3beta inhibition, beta-Catenin
265 -beta stimulation of human keratinocytes, by glycogen synthase kinase-3beta inhibition in several epi
266 d human T cells by treatment either with the glycogen synthase kinase 3beta inhibitor TWS119 or the p
267 igated, and we demonstrate that VPA, a known glycogen synthase kinase 3beta inhibitor, blocks platele
268 erentiated hPSCs into mesoderm cells using a glycogen synthase kinase-3beta inhibitor for 3 days, the
269 mbinant Wnt3a protein or CHIR-99021 (CHIR, a glycogen synthase kinase-3beta inhibitor) caused a dose-
270 naling pathway involving caspase-3, Akt1 and glycogen synthase kinase-3beta is an important mediator
272 ha/wrd pathway in the motoneuron antagonizes glycogen synthase kinase-3beta kinase activity to preven
273 no changes in Ctnnb1 expression, activity of glycogen synthase kinase-3beta, known to phosphorylate a
274 involves activation of ERK and inhibition of glycogen synthase kinase 3beta leading to cytoprotection
275 decreased DJ-1 and increased phosphorylated glycogen synthase kinase 3beta levels may account for im
277 hosphorylation, downstream phosphosubstrates glycogen synthase kinase 3beta, mammalian target of rapa
279 G-132 but was independent of the activity of glycogen synthase kinase 3beta or MALT-1, both of which
281 in endothelial cells as reflected in Akt and glycogen synthase kinase 3beta phosphorylation, Ras-rela
284 OE mouse hearts had increased basal Akt and glycogen synthase kinase-3beta phosphorylation comparabl
285 of cyclin-dependent protein kinase 5 (Cdk5), glycogen synthase kinase 3beta, protein phosphatase 1, o
286 f the endogenous MTA1s or ERK, or its target glycogen synthase kinase 3beta resulted in a substantial
287 activator of beta-catenin via inhibition of glycogen synthase kinase-3beta, reversed the inhibition
288 te-mediated phosphoinositide 3-kinase (PI3K)/glycogen synthase kinase 3beta signaling and decreased a
289 on of GABAergic transmission via D2 receptor-glycogen synthase kinase-3beta signaling dramatically re
290 oxygen species and restored dysregulated Akt-glycogen synthase kinase-3beta signaling in the hippocam
291 egradation can be triggered by inhibitors of glycogen synthase kinase 3beta, such as lithium, and als
292 TGF-beta1-induced phosphorylation of Akt and glycogen synthase kinase-3beta, suppressed cyclin D1 exp
293 ll as the cyclin-dependent kinase family and glycogen synthase kinase 3beta that also utilize the C-t
294 tube formation, whereas knockdown of RhoA or glycogen synthase kinase 3beta that are inactivated afte
295 on, and increased phosphorylation of Akt and glycogen synthase kinase-3beta, ultimately resulting in
296 in total and phosphorylated Akt, as well as glycogen synthase kinase 3beta, via a caspase-dependent
297 The phosphorylation and inactivation of glycogen synthase kinase-3beta was dependent on mammalia
298 ization of Nmyc is mediated by activation of glycogen synthase kinase 3beta, which targets Nmyc for p
300 d to the phosphorylation and inactivation of glycogen synthase kinase-3beta, which resulted in inhibi
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