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2 a-catenin pathway through phosphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this
5 but REDD1-mediated Nrf2 degradation required glycogen synthase kinase 3 (GSK3) activity and Ser-351/S
7 maller receptor-mediated vesicles containing glycogen synthase kinase 3 (GSK3) and protein arginine e
9 ion in p-AKT (S473), which in turn activated glycogen synthase kinase 3 (GSK3) and reduced beta-caten
10 cells due to its constant phosphorylation by glycogen synthase kinase 3 (GSK3) and subsequent proteas
12 ition of protein kinase C-beta (PKCbeta) and glycogen synthase kinase 3 (GSK3) causes synergistic apo
13 ng approaches, we show how the activation of glycogen synthase kinase 3 (GSK3) contributes to neurona
14 rt the evolutionary importance of the enzyme Glycogen Synthase Kinase 3 (GSK3) for maintaining podocy
17 in collagen I 3D cultures in the absence of glycogen synthase kinase 3 (GSK3) inhibition, hPSC-deriv
24 phosphodegron (CPD) signal, a target site of glycogen synthase kinase 3 (GSK3) kinase and Fbw7 ubiqui
28 we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm
33 itor pools and plays a key role in mediating glycogen synthase kinase 3 (GSK3) signaling during brain
35 ptor (D2R) and protein kinase B (PKB or Akt)/glycogen synthase kinase 3 (GSK3) signaling in the ventr
36 sites and secondary casein kinase 1 (CK1) or glycogen synthase kinase 3 (GSK3) sites was carefully ev
37 here show a novel mode of eIF6 regulation by glycogen synthase kinase 3 (GSK3) that is predominantly
40 clock proteins by casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3), appear conserved amon
42 ation of proteins (Wnt/STOP), which inhibits glycogen synthase kinase 3 (GSK3)-dependent protein ubiq
50 We show that this process is dependent on glycogen synthase kinase 3 (GSK3): GSK3 was associated w
51 pathways including phosphoinositide 3-kinase/glycogen synthase kinase 3 (PI3K/GSK3) signaling, with s
52 : it increases Akt phosphorylation, inhibits glycogen synthase kinase 3 activity, reduces IkappaB pho
53 hatidylinositol-dependent kinase 1 regulates glycogen synthase kinase 3 activity: a novel mechanism o
55 atenin was required for BRB restoration, but glycogen synthase kinase 3 alpha/beta (GSK-3alpha/beta)
57 ing protein, p53, which is phosphorylated by glycogen synthase kinase 3 at serine 33 and then ubiquit
58 evealed increased phosphorylation of AKT and glycogen synthase kinase 3 beta (GSK-3beta) in both the
60 through a kinome-wide screen, we found that glycogen synthase kinase 3 beta (GSK-3beta) was robustly
61 he virulence of P. gingivalis (Pg) affecting glycogen synthase kinase 3 beta (GSK-3beta)/nuclear fact
65 We identify an interaction of BMP and Wnt/glycogen synthase kinase 3 beta (GSK3beta) pathways via
66 activator of smoothened, and phosphorylated glycogen synthase kinase 3 beta (pGSK-3B), an inactive f
67 we found that CAMK4 phosphorylates GSK3beta (glycogen synthase kinase 3 beta), activates the Wnt path
68 ibition of the pro-apoptotic molecules, JNK, glycogen synthase kinase 3 beta, or caspases, toxicity i
69 evealed a role for heat shock protein 90 and glycogen synthase kinase 3 but not casein kinase 1 nor L
72 way seems to occur from Dishevelleds to axin/glycogen synthase kinase 3(GSK3)/beta-catenin complexes
73 d THC-induced downregulation of local GSK-3 (glycogen synthase kinase 3) and Akt signaling pathways d
74 cked cortical downregulation of local GSK-3 (glycogen synthase kinase 3) and Akt signaling pathways,
75 an be phosphorylated and stabilized by GSK3 (GLYCOGEN SYNTHASE KINASE 3)-like kinase BIN2 (BRASSINOST
76 (+) NPCs with a pharmacological inhibitor of glycogen synthase kinase 3, a known regulator of WNT sig
77 in sensitivity likely through increased Akt, glycogen synthase kinase 3, and AMPK phosphorylation; an
78 an inhibitor of cyclin-dependent kinases and glycogen synthase kinase 3, as a modulator of parkin rec
79 inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3, or addition of NRG1 signific
80 screen for anti-fibrotic compounds targeting glycogen synthase kinase 3, which has a consistent role
81 y treating SH-SY5Y cells with inhibitors for glycogen synthase kinase 3-beta (GSK3beta) and cyclin-de
83 TA accelerated beta-catenin degradation by a glycogen synthase kinase 3-beta-dependent mechanism.
85 s of the brassinosteroid (BR) signaling, the glycogen synthase kinase 3/Arabidopsis SHAGGY-like kinas
89 plex 1 (mTORC1) inhibitor rapamycin, and the glycogen synthase kinase-3 (GSK-3) inhibitor lithium act
96 bition of the histone deacetylase (HDAC) and glycogen synthase kinase-3 (GSK-3) pathways, which cause
98 de et al. uses phosphoproteomics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse e
100 together with inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3), which relieves its i
103 ling events that result in the inhibition of glycogen synthase kinase-3 (GSK-3)beta represent an adap
104 ositol-3 kinase/Akt (IRS-PI3K-Akt) pathways, glycogen synthase kinase-3 (GSK3) and mammalian target o
105 T3 signaling, and simultaneous inhibition of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kin
107 haracterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids p
110 ia containing fetal bovine serum (FBS) and a glycogen synthase kinase-3 (GSK3) inhibitor, and in seru
111 e describe a cell-engineering strategy using glycogen synthase kinase-3 (GSK3) inhibitor-loaded nanop
116 gated the effect of inhibitors targeting the glycogen synthase kinase-3 (GSK3) on the expression of N
120 rrent study, we tested whether inhibitors of glycogen synthase kinase-3 (GSK3), previously reported t
122 lian target of rapamycin signaling, glucose, glycogen synthase kinase-3 and liver kinase B1, protein
123 ardiomyocytes in early developmental stages, glycogen synthase kinase-3 and p38 mitogen-activated pro
126 drogenase kinase-1, or its downstream target glycogen synthase kinase-3 did not prevent CCR9 expressi
128 enhanced risk for SZ and/or BD can activate glycogen synthase kinase-3 isozymes (GSK3alpha and beta)
131 , while application of Bikinin (inhibitor of glycogen synthase kinase-3), which activated BR signalin
132 to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun,
133 hium chloride, a reversible inhibitor of the glycogen synthase kinase-3, that rescued NMJ defects in
135 y phosphorylated at Thr(714) and Ser(727) by glycogen synthase kinase 3alpha and -beta (GSK-3alpha/be
136 m of this study was to determine the role of glycogen synthase kinase-3alpha (GSK-3alpha) in post-MI
137 eta-catenin signaling cascades, which switch glycogen synthase kinase 3beta (GSK-3beta) activation on
139 ave been some reports on MTDLs targeting the glycogen synthase kinase 3beta (GSK-3beta) enzyme, due t
143 ected T cells and reduces phosphorylation of glycogen synthase kinase 3beta (GSK-3beta), a downstream
144 of cyclin B1, cyclin D3, and phosphorylated glycogen synthase kinase 3beta (GSK-3beta), while infect
147 Consequently, GRbeta-Ad mice had increased glycogen synthase kinase 3beta (GSK3beta) activity and r
148 , N-methyl-d-aspartate receptor function, or glycogen synthase kinase 3beta (GSK3beta) activity or ex
149 ver, hypoinsulinemia leads to an increase in glycogen synthase kinase 3beta (GSK3beta) activity that,
150 ssociated with insulin resistance, decreased glycogen synthase kinase 3beta (GSK3beta) activity, acti
151 (NF-kappaB) pathway and in the induction of glycogen synthase kinase 3beta (GSK3beta) activity, resu
152 of beta-catenin by enhancing binding between glycogen synthase kinase 3beta (GSK3beta) and beta-caten
153 osphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and DNA-depend
155 oteasomal degradation via phosphorylation by glycogen synthase kinase 3beta (GSK3beta) and recognitio
156 ted protein kinase kinase 4 (MKK4), JNK, and glycogen synthase kinase 3beta (GSK3beta) and thereby de
157 (APC), casein kinase 1alpha (CK1alpha), and glycogen synthase kinase 3beta (GSK3beta) and undergoes
158 TGF-beta1 expression and hyperacetylation of glycogen synthase kinase 3beta (GSK3beta) at residue K15
159 tes diminished inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser-9 in th
160 ects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing s
163 ppress many signaling pathways that activate glycogen synthase kinase 3beta (GSK3beta) implicated in
164 quent signaling, causing overt activation of glycogen synthase kinase 3beta (GSK3beta) in nerves of m
165 synthesis is associated with inactivation of glycogen synthase kinase 3beta (GSK3beta) in renal cells
170 g pathway involving AKT Ser/Thr kinase (AKT)/glycogen synthase kinase 3beta (GSK3beta) or paxillin.
171 of TGF-beta receptors and p38 MAPK increased glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
173 d by the core clock oscillator BMAL1 and AKT/glycogen synthase kinase 3beta (GSK3beta) signaling path
174 ide 3-kinase (PI3K)-AKT Ser/Thr kinase (AKT)-glycogen synthase kinase 3beta (GSK3beta) signaling path
175 [e.g., strong bias toward phosphorylation of glycogen synthase kinase 3beta (GSK3beta) via the full-l
176 peractivation and subsequent inactivation of glycogen synthase kinase 3beta (GSK3beta), a negative re
177 e IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta), as one major
179 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p
181 hic signaling intermediates, such as Akt and glycogen synthase kinase 3beta (GSK3beta), were dephosph
182 y sites in the N-terminus of beta-catenin as glycogen synthase kinase 3beta (GSK3beta), which are rec
184 dent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase 3beta (GSK3beta), which is medi
185 the canonical regulation of beta-catenin via glycogen synthase kinase 3beta (GSK3beta)-dependent degr
187 1 interacts with Nrf2 and stabilizes it from glycogen synthase kinase 3beta (GSK3beta)-mediated phosp
188 FN signaling pathways occurs at the point of glycogen synthase kinase 3beta (GSK3beta)-TANK-binding k
196 atty acids, and this suppression depended on glycogen synthase kinase 3beta activation and induction
197 au phosphorylation and solubility, increased glycogen synthase kinase 3beta activity, compromised lon
198 protein that plays a key role in attenuating glycogen synthase kinase 3beta activity, leading to aber
199 2A and recruits protein phosphatase 2A with glycogen synthase kinase 3beta and beta-catenin, inducin
201 isms involved demonstrate that ASPH binds to glycogen synthase kinase 3beta and inhibits its subseque
202 ibition of ASPH activity, phosphorylation of glycogen synthase kinase 3beta and p16 expression were i
203 reasing Ser9 phosphorylation-inactivation of glycogen synthase kinase 3beta by RBMY, thereby impeding
204 ted with release of the inhibitory effect of glycogen synthase kinase 3beta function by decreasing Se
205 in, and that beta-catenin activation through glycogen synthase kinase 3beta inhibition leads to FANCC
206 decreased DJ-1 and increased phosphorylated glycogen synthase kinase 3beta levels may account for im
209 al nuclear factor kappaB pathway and the Akt-glycogen synthase kinase 3beta signaling axis, respectiv
210 bound IRF1 turnover is promoted by GSK3beta (Glycogen Synthase Kinase 3beta) via phosphorylation of t
211 increase in phospho-beta-catenin and active glycogen synthase kinase 3beta, a kinase known to target
212 t3a (the canonical activator), inhibitors of glycogen synthase kinase 3beta, and small-interfering RN
213 cocorticoid kinase 1 (SGK1), an inhibitor of glycogen synthase kinase 3beta, as part of this pathway.
214 ver, inhibition of protein phosphatase 1 and glycogen synthase kinase 3beta, downstream targets of Ca
215 ced tumor growth, induced phosphorylation of glycogen synthase kinase 3beta, enhanced p16 expression
217 of cyclin-dependent protein kinase 5 (Cdk5), glycogen synthase kinase 3beta, protein phosphatase 1, o
218 e kinase 3beta by RBMY, thereby impeding the glycogen synthase kinase 3beta-dependent degradation of
225 nalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3beta, in maternal liver (P < 0
227 rexpression of TDP-43 leads to activation of glycogen synthase kinase-3beta (GSK-3beta) and that GSK-
228 dated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3beta (GSK-3beta) by attacking
229 PSC-CMs in vitro (i.e., 100- to 250-fold) by glycogen synthase kinase-3beta (GSK-3beta) inhibition us
231 etin, reactivation of beta-catenin using the glycogen synthase kinase-3beta (GSK-3beta) inhibitor LiC
233 sis coli tumor suppressor protein (APC), and glycogen synthase kinase-3beta (GSK-3beta), which could
234 atocytes, which led to a delayed increase in glycogen synthase kinase-3beta (GSK-3beta)-mediated hepa
235 demonstrate that alcohol intake also blocks glycogen synthase kinase-3beta (GSK-3beta)-phosphorylati
240 nted pre-synaptic protein deficit, decreased glycogen synthase kinase-3beta (GSK3beta) activity, and
241 finding is the pronounced downregulation of glycogen synthase kinase-3beta (Gsk3beta) and upregulati
244 Here we demonstrate that hyperactivity of glycogen synthase kinase-3beta (GSK3beta) in the atrium
246 uclear Nrf2 export/degradation machinery via glycogen synthase kinase-3beta (Gsk3beta) signaling was
247 lted in increased phosphorylation of Akt and glycogen synthase kinase-3beta (GSK3beta), leading to en
250 s (ankyrin G, EB1) were knocked down or when glycogen synthase kinase-3beta (GSK3beta; an AD-associat
251 panied by hyperphosphorylation of substrates glycogen synthase kinase-3beta and mammalian target of r
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 erentiated hPSCs into mesoderm cells using a glycogen synthase kinase-3beta inhibitor for 3 days, the
257 mbinant Wnt3a protein or CHIR-99021 (CHIR, a glycogen synthase kinase-3beta inhibitor) caused a dose-
258 ha/wrd pathway in the motoneuron antagonizes glycogen synthase kinase-3beta kinase activity to preven
259 on of GABAergic transmission via D2 receptor-glycogen synthase kinase-3beta signaling dramatically re
260 The phosphorylation and inactivation of glycogen synthase kinase-3beta was dependent on mammalia
263 orylation of the inhibitory Ser-9 residue of glycogen synthase kinase-3beta, a primary Tau kinase inv
264 ollowed by phosphorylation (inactivation) of glycogen synthase kinase-3beta, at least in part via STA
265 cyclin D1, E-cadherin, beta-catenin, Dvl-1, glycogen synthase kinase-3beta, axin-1, and adenomatous
266 no changes in Ctnnb1 expression, activity of glycogen synthase kinase-3beta, known to phosphorylate a
267 activator of beta-catenin via inhibition of glycogen synthase kinase-3beta, reversed the inhibition
268 on, and increased phosphorylation of Akt and glycogen synthase kinase-3beta, ultimately resulting in
269 d to the phosphorylation and inactivation of glycogen synthase kinase-3beta, which resulted in inhibi
270 inding (CREB) protein levels to decreaseviaa glycogen synthase kinase-3beta-dependent mechanism.
272 ial-mesenchymal transition by repressing AKT/glycogen synthase kinase-3beta/beta-catenin signaling.
276 Apc participates in a complex that includes glycogen synthase kinase beta (Gsk3beta) and betacatenin
280 Studies have implicated signaling through glycogen synthase kinase (GSK) 3alpha/beta in the activa
281 work, we demonstrate that overexpression of glycogen synthase kinase (GSK) 3beta in neural precursor
283 CRMP-2 and ROCK II is partially regulated by glycogen synthase kinase (GSK)-3 phosphorylation of CRMP
289 eptor is modulated, here, we have found that glycogen synthase kinase (GSK)-3beta phosphorylation of
292 show that the dual phosphodiesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15, a het
293 Mechanistically, Tanshinone IIA blunted glycogen synthase kinase (GSK)3beta overactivity and hyp
294 used to deliver low doses of small molecule glycogen synthase kinase (GSK-3) antagonists that promot
295 sly showed that the serine/threonine kinase, glycogen synthase kinase, GSK-3alpha/beta, is a central
296 exerted its positive effect by inhibition of glycogen synthase kinase (GSK3) activity and enhancement
297 contrast, phosphomimetic substitution of the glycogen synthase kinase (GSK3beta) site in the Pro/Ala-
300 f lithium, in which fine-tuned regulation of glycogen synthase kinase type 3, a prime target for lith