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2 a-catenin pathway through phosphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this
6 ignalling pathway or dual inhibition (2i) of glycogen synthase kinase 3 (Gsk3) and mitogen-activated
8 cells due to its constant phosphorylation by glycogen synthase kinase 3 (GSK3) and subsequent proteas
11 ition of protein kinase C-beta (PKCbeta) and glycogen synthase kinase 3 (GSK3) causes synergistic apo
12 ng approaches, we show how the activation of glycogen synthase kinase 3 (GSK3) contributes to neurona
21 phosphodegron (CPD) signal, a target site of glycogen synthase kinase 3 (GSK3) kinase and Fbw7 ubiqui
25 we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm
26 lt gastric epithelium via deletion of either glycogen synthase kinase 3 (GSK3) or APC or via expressi
31 itor pools and plays a key role in mediating glycogen synthase kinase 3 (GSK3) signaling during brain
34 clock proteins by casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3), appear conserved amon
42 We show that this process is dependent on glycogen synthase kinase 3 (GSK3): GSK3 was associated w
43 : it increases Akt phosphorylation, inhibits glycogen synthase kinase 3 activity, reduces IkappaB pho
44 hatidylinositol-dependent kinase 1 regulates glycogen synthase kinase 3 activity: a novel mechanism o
46 evealed increased phosphorylation of AKT and glycogen synthase kinase 3 beta (GSK-3beta) in both the
51 We identify an interaction of BMP and Wnt/glycogen synthase kinase 3 beta (GSK3beta) pathways via
52 dulate the activity of Tankyrase enzymes and glycogen synthase kinase 3 beta (GSK3beta), additional t
53 activator of smoothened, and phosphorylated glycogen synthase kinase 3 beta (pGSK-3B), an inactive f
54 on on Ser(552), a site that differs from the glycogen synthase kinase 3 beta phosphorylation site.
55 ibition of the pro-apoptotic molecules, JNK, glycogen synthase kinase 3 beta, or caspases, toxicity i
56 evealed a role for heat shock protein 90 and glycogen synthase kinase 3 but not casein kinase 1 nor L
57 blocked cardiomyocyte specification, whereas glycogen synthase kinase 3 inhibition at this point enha
59 thermore, sequential treatment of hPSCs with glycogen synthase kinase 3 inhibitors followed by induci
61 way seems to occur from Dishevelleds to axin/glycogen synthase kinase 3(GSK3)/beta-catenin complexes
62 an be phosphorylated and stabilized by GSK3 (GLYCOGEN SYNTHASE KINASE 3)-like kinase BIN2 (BRASSINOST
63 (+) NPCs with a pharmacological inhibitor of glycogen synthase kinase 3, a known regulator of WNT sig
64 in sensitivity likely through increased Akt, glycogen synthase kinase 3, and AMPK phosphorylation; an
65 in kinase and the Akt-mediated inhibition of glycogen synthase kinase 3, critical inhibitors of Smad
66 inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3, or addition of NRG1 signific
67 y treating SH-SY5Y cells with inhibitors for glycogen synthase kinase 3-beta (GSK3beta) and cyclin-de
69 TA accelerated beta-catenin degradation by a glycogen synthase kinase 3-beta-dependent mechanism.
71 s of the brassinosteroid (BR) signaling, the glycogen synthase kinase 3/Arabidopsis SHAGGY-like kinas
83 de et al. uses phosphoproteomics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse e
85 together with inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3), which relieves its i
87 ling events that result in the inhibition of glycogen synthase kinase-3 (GSK-3)beta represent an adap
89 ositol-3 kinase/Akt (IRS-PI3K-Akt) pathways, glycogen synthase kinase-3 (GSK3) and mammalian target o
90 T3 signaling, and simultaneous inhibition of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kin
92 haracterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids p
96 ia containing fetal bovine serum (FBS) and a glycogen synthase kinase-3 (GSK3) inhibitor, and in seru
99 gated the effect of inhibitors targeting the glycogen synthase kinase-3 (GSK3) on the expression of N
102 rrent study, we tested whether inhibitors of glycogen synthase kinase-3 (GSK3), previously reported t
104 lian target of rapamycin signaling, glucose, glycogen synthase kinase-3 and liver kinase B1, protein
105 ardiomyocytes in early developmental stages, glycogen synthase kinase-3 and p38 mitogen-activated pro
106 (G6P) and reversible phosphorylation through glycogen synthase kinase-3 and the glycogen-associated f
108 drogenase kinase-1, or its downstream target glycogen synthase kinase-3 did not prevent CCR9 expressi
109 phosphorylated by recombinant GSK3beta; and glycogen synthase kinase-3 inhibitors effectively reduce
111 enhanced risk for SZ and/or BD can activate glycogen synthase kinase-3 isozymes (GSK3alpha and beta)
114 , while application of Bikinin (inhibitor of glycogen synthase kinase-3), which activated BR signalin
115 lations of AMPK, acetyl CoA carboxylase, and glycogen synthase kinase-3, decreased glycogen synthase
116 ed 4 chemical compound groups: inhibitors of glycogen synthase kinase-3, p38 mitogen-activated protei
117 to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun,
118 hium chloride, a reversible inhibitor of the glycogen synthase kinase-3, that rescued NMJ defects in
120 E-cadherin, and CD44-mediated signaling and glycogen synthase kinase-3/adenomatous polyposis coli-me
122 y phosphorylated at Thr(714) and Ser(727) by glycogen synthase kinase 3alpha and -beta (GSK-3alpha/be
123 m of this study was to determine the role of glycogen synthase kinase-3alpha (GSK-3alpha) in post-MI
125 ed by application of a specific inhibitor of glycogen synthase kinase 3beta (6-bromoindirubin-3'-oxim
126 eta-catenin signaling cascades, which switch glycogen synthase kinase 3beta (GSK-3beta) activation on
131 ected T cells and reduces phosphorylation of glycogen synthase kinase 3beta (GSK-3beta), a downstream
132 of cyclin B1, cyclin D3, and phosphorylated glycogen synthase kinase 3beta (GSK-3beta), while infect
135 Akt/mammalian target of rapamycin (mTOR) and glycogen synthase kinase 3beta (GSK-3beta)/adenomatous p
136 Consequently, GRbeta-Ad mice had increased glycogen synthase kinase 3beta (GSK3beta) activity and r
137 the c-Jun N-terminal kinase (JNK)-dependent glycogen synthase kinase 3beta (GSK3beta) activity on do
138 , N-methyl-d-aspartate receptor function, or glycogen synthase kinase 3beta (GSK3beta) activity or ex
139 ver, hypoinsulinemia leads to an increase in glycogen synthase kinase 3beta (GSK3beta) activity that,
140 ssociated with insulin resistance, decreased glycogen synthase kinase 3beta (GSK3beta) activity, acti
141 (NF-kappaB) pathway and in the induction of glycogen synthase kinase 3beta (GSK3beta) activity, resu
142 of beta-catenin by enhancing binding between glycogen synthase kinase 3beta (GSK3beta) and beta-caten
143 tcome on different molecular targets such as glycogen synthase kinase 3beta (GSK3beta) and Forkhead b
145 Unexpectedly, RNAi-mediated silencing of glycogen synthase kinase 3beta (GSK3beta) and phosphoino
146 oteasomal degradation via phosphorylation by glycogen synthase kinase 3beta (GSK3beta) and recognitio
147 ted protein kinase kinase 4 (MKK4), JNK, and glycogen synthase kinase 3beta (GSK3beta) and thereby de
148 (APC), casein kinase 1alpha (CK1alpha), and glycogen synthase kinase 3beta (GSK3beta) and undergoes
150 TGF-beta1 expression and hyperacetylation of glycogen synthase kinase 3beta (GSK3beta) at residue K15
151 tein, HSC70) and causes dephosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser 9 by re
152 ects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing s
154 quent signaling, causing overt activation of glycogen synthase kinase 3beta (GSK3beta) in nerves of m
155 synthesis is associated with inactivation of glycogen synthase kinase 3beta (GSK3beta) in renal cells
163 of TGF-beta receptors and p38 MAPK increased glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
164 ar carcinoma-derived KLF6 mutations affect a glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
167 d by the core clock oscillator BMAL1 and AKT/glycogen synthase kinase 3beta (GSK3beta) signaling path
169 [e.g., strong bias toward phosphorylation of glycogen synthase kinase 3beta (GSK3beta) via the full-l
170 kt, mammalian target of rapamycin complex 1, glycogen synthase kinase 3beta (GSK3beta), and CREB.
171 e IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta), as one major
173 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p
174 kt pathway, leading to the downregulation of glycogen synthase kinase 3beta (GSK3beta), in wild type
176 hic signaling intermediates, such as Akt and glycogen synthase kinase 3beta (GSK3beta), were dephosph
177 y sites in the N-terminus of beta-catenin as glycogen synthase kinase 3beta (GSK3beta), which are rec
178 dent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase 3beta (GSK3beta), which is medi
180 1 interacts with Nrf2 and stabilizes it from glycogen synthase kinase 3beta (GSK3beta)-mediated phosp
181 FN signaling pathways occurs at the point of glycogen synthase kinase 3beta (GSK3beta)-TANK-binding k
189 atty acids, and this suppression depended on glycogen synthase kinase 3beta activation and induction
191 au phosphorylation and solubility, increased glycogen synthase kinase 3beta activity, compromised lon
192 protein that plays a key role in attenuating glycogen synthase kinase 3beta activity, leading to aber
193 2A and recruits protein phosphatase 2A with glycogen synthase kinase 3beta and beta-catenin, inducin
195 isms involved demonstrate that ASPH binds to glycogen synthase kinase 3beta and inhibits its subseque
196 ibition of ASPH activity, phosphorylation of glycogen synthase kinase 3beta and p16 expression were i
197 reasing Ser9 phosphorylation-inactivation of glycogen synthase kinase 3beta by RBMY, thereby impeding
198 of stable MT subsets through inactivation of glycogen synthase kinase 3beta by the viral Ser/Thr kina
199 ted with release of the inhibitory effect of glycogen synthase kinase 3beta function by decreasing Se
200 in, and that beta-catenin activation through glycogen synthase kinase 3beta inhibition leads to FANCC
201 decreased DJ-1 and increased phosphorylated glycogen synthase kinase 3beta levels may account for im
203 in endothelial cells as reflected in Akt and glycogen synthase kinase 3beta phosphorylation, Ras-rela
205 te-mediated phosphoinositide 3-kinase (PI3K)/glycogen synthase kinase 3beta signaling and decreased a
207 increase in phospho-beta-catenin and active glycogen synthase kinase 3beta, a kinase known to target
208 t3a (the canonical activator), inhibitors of glycogen synthase kinase 3beta, and small-interfering RN
209 Akt murine thymoma viral oncogene homolog-1, glycogen synthase kinase 3beta, cyclin-dependent kinase
211 ver, inhibition of protein phosphatase 1 and glycogen synthase kinase 3beta, downstream targets of Ca
212 ced tumor growth, induced phosphorylation of glycogen synthase kinase 3beta, enhanced p16 expression
214 hosphorylation, downstream phosphosubstrates glycogen synthase kinase 3beta, mammalian target of rapa
215 of cyclin-dependent protein kinase 5 (Cdk5), glycogen synthase kinase 3beta, protein phosphatase 1, o
216 e kinase 3beta by RBMY, thereby impeding the glycogen synthase kinase 3beta-dependent degradation of
221 nalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3beta, in maternal liver (P < 0
223 rexpression of TDP-43 leads to activation of glycogen synthase kinase-3beta (GSK-3beta) and that GSK-
224 dated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3beta (GSK-3beta) by attacking
226 etin, reactivation of beta-catenin using the glycogen synthase kinase-3beta (GSK-3beta) inhibitor LiC
230 sis coli tumor suppressor protein (APC), and glycogen synthase kinase-3beta (GSK-3beta), which could
231 atocytes, which led to a delayed increase in glycogen synthase kinase-3beta (GSK-3beta)-mediated hepa
232 demonstrate that alcohol intake also blocks glycogen synthase kinase-3beta (GSK-3beta)-phosphorylati
238 nted pre-synaptic protein deficit, decreased glycogen synthase kinase-3beta (GSK3beta) activity, and
239 finding is the pronounced downregulation of glycogen synthase kinase-3beta (Gsk3beta) and upregulati
241 Here we demonstrate that hyperactivity of glycogen synthase kinase-3beta (GSK3beta) in the atrium
244 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
248 s (ankyrin G, EB1) were knocked down or when glycogen synthase kinase-3beta (GSK3beta; an AD-associat
249 sed p38 mitogen-activated protein kinase and glycogen synthase kinase-3beta activity, which are belie
250 panied by hyperphosphorylation of substrates glycogen synthase kinase-3beta and mammalian target of r
251 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa
252 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa
254 Overexpression of Snail1 and inhibition of glycogen synthase kinase-3beta in colorectal tumor cells
256 -beta stimulation of human keratinocytes, by glycogen synthase kinase-3beta inhibition in several epi
257 erentiated hPSCs into mesoderm cells using a glycogen synthase kinase-3beta inhibitor for 3 days, the
258 mbinant Wnt3a protein or CHIR-99021 (CHIR, a glycogen synthase kinase-3beta inhibitor) caused a dose-
260 ha/wrd pathway in the motoneuron antagonizes glycogen synthase kinase-3beta kinase activity to preven
261 on of GABAergic transmission via D2 receptor-glycogen synthase kinase-3beta signaling dramatically re
262 The phosphorylation and inactivation of glycogen synthase kinase-3beta was dependent on mammalia
264 orylation of the inhibitory Ser-9 residue of glycogen synthase kinase-3beta, a primary Tau kinase inv
265 ollowed by phosphorylation (inactivation) of glycogen synthase kinase-3beta, at least in part via STA
266 cyclin D1, E-cadherin, beta-catenin, Dvl-1, glycogen synthase kinase-3beta, axin-1, and adenomatous
267 no changes in Ctnnb1 expression, activity of glycogen synthase kinase-3beta, known to phosphorylate a
268 activator of beta-catenin via inhibition of glycogen synthase kinase-3beta, reversed the inhibition
269 on, and increased phosphorylation of Akt and glycogen synthase kinase-3beta, ultimately resulting in
270 d to the phosphorylation and inactivation of glycogen synthase kinase-3beta, which resulted in inhibi
271 inding (CREB) protein levels to decreaseviaa glycogen synthase kinase-3beta-dependent mechanism.
273 ial-mesenchymal transition by repressing AKT/glycogen synthase kinase-3beta/beta-catenin signaling.
275 Apc participates in a complex that includes glycogen synthase kinase beta (Gsk3beta) and betacatenin
279 Studies have implicated signaling through glycogen synthase kinase (GSK) 3alpha/beta in the activa
280 work, we demonstrate that overexpression of glycogen synthase kinase (GSK) 3beta in neural precursor
284 CRMP-2 and ROCK II is partially regulated by glycogen synthase kinase (GSK)-3 phosphorylation of CRMP
290 eptor is modulated, here, we have found that glycogen synthase kinase (GSK)-3beta phosphorylation of
293 show that the dual phosphodiesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15, a het
294 Mechanistically, Tanshinone IIA blunted glycogen synthase kinase (GSK)3beta overactivity and hyp
295 used to deliver low doses of small molecule glycogen synthase kinase (GSK-3) antagonists that promot
296 sly showed that the serine/threonine kinase, glycogen synthase kinase, GSK-3alpha/beta, is a central
297 exerted its positive effect by inhibition of glycogen synthase kinase (GSK3) activity and enhancement
300 f lithium, in which fine-tuned regulation of glycogen synthase kinase type 3, a prime target for lith
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