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1 ugh a remarkable adaptation of the bacterial glycogen synthase.
2 t, confirming the inhibitory role of Fgk3 on glycogen synthase.
3 ciated glycogen and with stable knockdown of glycogen synthase 1, which inhibited (18)F-NFTG uptake,
5 ulation of glucose transporter 2 (GLUT2) and glycogen synthase 2 (GYS2); while expression of gluconeo
6 ence of interleukin-7 (IL-7), IL-21, and the glycogen synthase-3beta inhibitor TWS119, and geneticall
9 sensitivity was not associated with enhanced glycogen synthase activity or proximal insulin signaling
10 cogen content was approximately 50% greater, glycogen synthase activity was approximately 50% greater
12 rylation of TBC1D4 Ser(318) and Ser(704) and glycogen synthase activity were greater in the exercised
13 wer starting glycogen content, and increased glycogen synthase activity, together with increased musc
18 ogen shunt implicates the high activities of glycogen synthase and fructose bisphosphatase in tumors
19 Firstly, the periportal zonation of both glycogen synthase and the oxidative phosphorylation enzy
20 ing also increased the insulin activation of glycogen synthase by 60%, GLUT4 expression by 16%, and 5
21 levels of oxidants or genetic inhibition of glycogen synthase depletes glycogen stores and extends t
23 the Gys2 gene encoding the liver isoform of glycogen synthase generates a mouse strain (LGSKO) that
27 om glucose through the cooperative action of glycogen synthase (GS), glycogenin (GN), and glycogen br
28 bitors of the key glycogen synthetic enzyme, glycogen synthase (GS), we identified a substituted imid
29 phosphorylated glycogen phosphorylase (GPa), glycogen synthase (GSa) - respectively activated and ina
30 c process, in Neurospora crassa We find that glycogen synthase (gsn) mRNA, glycogen phosphorylase (gp
31 granules and the glycogen conversion enzymes glycogen synthase I and glycogen phosphorylase BB, dispe
35 Studies have implicated signaling through glycogen synthase kinase (GSK) 3alpha/beta in the activa
36 work, we demonstrate that overexpression of glycogen synthase kinase (GSK) 3beta in neural precursor
44 show that the dual phosphodiesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15, a het
46 used to deliver low doses of small molecule glycogen synthase kinase (GSK-3) antagonists that promot
47 exerted its positive effect by inhibition of glycogen synthase kinase (GSK3) activity and enhancement
48 contrast, phosphomimetic substitution of the glycogen synthase kinase (GSK3beta) site in the Pro/Ala-
50 a-catenin pathway through phosphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this
53 but REDD1-mediated Nrf2 degradation required glycogen synthase kinase 3 (GSK3) activity and Ser-351/S
55 maller receptor-mediated vesicles containing glycogen synthase kinase 3 (GSK3) and protein arginine e
57 ion in p-AKT (S473), which in turn activated glycogen synthase kinase 3 (GSK3) and reduced beta-caten
58 cells due to its constant phosphorylation by glycogen synthase kinase 3 (GSK3) and subsequent proteas
60 ition of protein kinase C-beta (PKCbeta) and glycogen synthase kinase 3 (GSK3) causes synergistic apo
61 ng approaches, we show how the activation of glycogen synthase kinase 3 (GSK3) contributes to neurona
62 rt the evolutionary importance of the enzyme Glycogen Synthase Kinase 3 (GSK3) for maintaining podocy
65 in collagen I 3D cultures in the absence of glycogen synthase kinase 3 (GSK3) inhibition, hPSC-deriv
70 phosphodegron (CPD) signal, a target site of glycogen synthase kinase 3 (GSK3) kinase and Fbw7 ubiqui
73 we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm
77 itor pools and plays a key role in mediating glycogen synthase kinase 3 (GSK3) signaling during brain
79 ptor (D2R) and protein kinase B (PKB or Akt)/glycogen synthase kinase 3 (GSK3) signaling in the ventr
80 sites and secondary casein kinase 1 (CK1) or glycogen synthase kinase 3 (GSK3) sites was carefully ev
81 here show a novel mode of eIF6 regulation by glycogen synthase kinase 3 (GSK3) that is predominantly
84 clock proteins by casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3), appear conserved amon
85 ation of proteins (Wnt/STOP), which inhibits glycogen synthase kinase 3 (GSK3)-dependent protein ubiq
92 We show that this process is dependent on glycogen synthase kinase 3 (GSK3): GSK3 was associated w
93 pathways including phosphoinositide 3-kinase/glycogen synthase kinase 3 (PI3K/GSK3) signaling, with s
94 : it increases Akt phosphorylation, inhibits glycogen synthase kinase 3 activity, reduces IkappaB pho
95 hatidylinositol-dependent kinase 1 regulates glycogen synthase kinase 3 activity: a novel mechanism o
96 atenin was required for BRB restoration, but glycogen synthase kinase 3 alpha/beta (GSK-3alpha/beta)
98 ing protein, p53, which is phosphorylated by glycogen synthase kinase 3 at serine 33 and then ubiquit
99 evealed increased phosphorylation of AKT and glycogen synthase kinase 3 beta (GSK-3beta) in both the
101 through a kinome-wide screen, we found that glycogen synthase kinase 3 beta (GSK-3beta) was robustly
102 he virulence of P. gingivalis (Pg) affecting glycogen synthase kinase 3 beta (GSK-3beta)/nuclear fact
106 We identify an interaction of BMP and Wnt/glycogen synthase kinase 3 beta (GSK3beta) pathways via
107 activator of smoothened, and phosphorylated glycogen synthase kinase 3 beta (pGSK-3B), an inactive f
108 we found that CAMK4 phosphorylates GSK3beta (glycogen synthase kinase 3 beta), activates the Wnt path
109 ibition of the pro-apoptotic molecules, JNK, glycogen synthase kinase 3 beta, or caspases, toxicity i
110 evealed a role for heat shock protein 90 and glycogen synthase kinase 3 but not casein kinase 1 nor L
113 way seems to occur from Dishevelleds to axin/glycogen synthase kinase 3(GSK3)/beta-catenin complexes
114 d THC-induced downregulation of local GSK-3 (glycogen synthase kinase 3) and Akt signaling pathways d
115 cked cortical downregulation of local GSK-3 (glycogen synthase kinase 3) and Akt signaling pathways,
116 (+) NPCs with a pharmacological inhibitor of glycogen synthase kinase 3, a known regulator of WNT sig
117 in sensitivity likely through increased Akt, glycogen synthase kinase 3, and AMPK phosphorylation; an
118 an inhibitor of cyclin-dependent kinases and glycogen synthase kinase 3, as a modulator of parkin rec
119 inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3, or addition of NRG1 signific
120 screen for anti-fibrotic compounds targeting glycogen synthase kinase 3, which has a consistent role
121 y treating SH-SY5Y cells with inhibitors for glycogen synthase kinase 3-beta (GSK3beta) and cyclin-de
123 TA accelerated beta-catenin degradation by a glycogen synthase kinase 3-beta-dependent mechanism.
124 s of the brassinosteroid (BR) signaling, the glycogen synthase kinase 3/Arabidopsis SHAGGY-like kinas
125 y phosphorylated at Thr(714) and Ser(727) by glycogen synthase kinase 3alpha and -beta (GSK-3alpha/be
127 ave been some reports on MTDLs targeting the glycogen synthase kinase 3beta (GSK-3beta) enzyme, due t
130 ected T cells and reduces phosphorylation of glycogen synthase kinase 3beta (GSK-3beta), a downstream
133 Consequently, GRbeta-Ad mice had increased glycogen synthase kinase 3beta (GSK3beta) activity and r
134 , N-methyl-d-aspartate receptor function, or glycogen synthase kinase 3beta (GSK3beta) activity or ex
135 ver, hypoinsulinemia leads to an increase in glycogen synthase kinase 3beta (GSK3beta) activity that,
136 ssociated with insulin resistance, decreased glycogen synthase kinase 3beta (GSK3beta) activity, acti
137 (NF-kappaB) pathway and in the induction of glycogen synthase kinase 3beta (GSK3beta) activity, resu
138 of beta-catenin by enhancing binding between glycogen synthase kinase 3beta (GSK3beta) and beta-caten
139 osphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and DNA-depend
141 oteasomal degradation via phosphorylation by glycogen synthase kinase 3beta (GSK3beta) and recognitio
142 ted protein kinase kinase 4 (MKK4), JNK, and glycogen synthase kinase 3beta (GSK3beta) and thereby de
143 (APC), casein kinase 1alpha (CK1alpha), and glycogen synthase kinase 3beta (GSK3beta) and undergoes
144 TGF-beta1 expression and hyperacetylation of glycogen synthase kinase 3beta (GSK3beta) at residue K15
145 tes diminished inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser-9 in th
146 ects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing s
149 ppress many signaling pathways that activate glycogen synthase kinase 3beta (GSK3beta) implicated in
150 quent signaling, causing overt activation of glycogen synthase kinase 3beta (GSK3beta) in nerves of m
151 synthesis is associated with inactivation of glycogen synthase kinase 3beta (GSK3beta) in renal cells
156 g pathway involving AKT Ser/Thr kinase (AKT)/glycogen synthase kinase 3beta (GSK3beta) or paxillin.
157 of TGF-beta receptors and p38 MAPK increased glycogen synthase kinase 3beta (GSK3beta) phosphorylatio
159 d by the core clock oscillator BMAL1 and AKT/glycogen synthase kinase 3beta (GSK3beta) signaling path
160 ide 3-kinase (PI3K)-AKT Ser/Thr kinase (AKT)-glycogen synthase kinase 3beta (GSK3beta) signaling path
161 [e.g., strong bias toward phosphorylation of glycogen synthase kinase 3beta (GSK3beta) via the full-l
162 peractivation and subsequent inactivation of glycogen synthase kinase 3beta (GSK3beta), a negative re
163 e IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta), as one major
165 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p
167 hic signaling intermediates, such as Akt and glycogen synthase kinase 3beta (GSK3beta), were dephosph
169 dent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase 3beta (GSK3beta), which is medi
170 the canonical regulation of beta-catenin via glycogen synthase kinase 3beta (GSK3beta)-dependent degr
172 1 interacts with Nrf2 and stabilizes it from glycogen synthase kinase 3beta (GSK3beta)-mediated phosp
173 FN signaling pathways occurs at the point of glycogen synthase kinase 3beta (GSK3beta)-TANK-binding k
181 atty acids, and this suppression depended on glycogen synthase kinase 3beta activation and induction
182 au phosphorylation and solubility, increased glycogen synthase kinase 3beta activity, compromised lon
183 protein that plays a key role in attenuating glycogen synthase kinase 3beta activity, leading to aber
184 2A and recruits protein phosphatase 2A with glycogen synthase kinase 3beta and beta-catenin, inducin
186 isms involved demonstrate that ASPH binds to glycogen synthase kinase 3beta and inhibits its subseque
187 ibition of ASPH activity, phosphorylation of glycogen synthase kinase 3beta and p16 expression were i
188 reasing Ser9 phosphorylation-inactivation of glycogen synthase kinase 3beta by RBMY, thereby impeding
189 ted with release of the inhibitory effect of glycogen synthase kinase 3beta function by decreasing Se
190 in, and that beta-catenin activation through glycogen synthase kinase 3beta inhibition leads to FANCC
192 al nuclear factor kappaB pathway and the Akt-glycogen synthase kinase 3beta signaling axis, respectiv
193 bound IRF1 turnover is promoted by GSK3beta (Glycogen Synthase Kinase 3beta) via phosphorylation of t
194 t3a (the canonical activator), inhibitors of glycogen synthase kinase 3beta, and small-interfering RN
195 cocorticoid kinase 1 (SGK1), an inhibitor of glycogen synthase kinase 3beta, as part of this pathway.
196 ced tumor growth, induced phosphorylation of glycogen synthase kinase 3beta, enhanced p16 expression
198 of cyclin-dependent protein kinase 5 (Cdk5), glycogen synthase kinase 3beta, protein phosphatase 1, o
199 e kinase 3beta by RBMY, thereby impeding the glycogen synthase kinase 3beta-dependent degradation of
211 f lithium, in which fine-tuned regulation of glycogen synthase kinase type 3, a prime target for lith
212 sly showed that the serine/threonine kinase, glycogen synthase kinase, GSK-3alpha/beta, is a central
214 plex 1 (mTORC1) inhibitor rapamycin, and the glycogen synthase kinase-3 (GSK-3) inhibitor lithium act
221 bition of the histone deacetylase (HDAC) and glycogen synthase kinase-3 (GSK-3) pathways, which cause
223 de et al. uses phosphoproteomics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse e
226 ling events that result in the inhibition of glycogen synthase kinase-3 (GSK-3)beta represent an adap
227 ositol-3 kinase/Akt (IRS-PI3K-Akt) pathways, glycogen synthase kinase-3 (GSK3) and mammalian target o
228 T3 signaling, and simultaneous inhibition of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kin
230 haracterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids p
233 ia containing fetal bovine serum (FBS) and a glycogen synthase kinase-3 (GSK3) inhibitor, and in seru
234 e describe a cell-engineering strategy using glycogen synthase kinase-3 (GSK3) inhibitor-loaded nanop
242 lian target of rapamycin signaling, glucose, glycogen synthase kinase-3 and liver kinase B1, protein
245 drogenase kinase-1, or its downstream target glycogen synthase kinase-3 did not prevent CCR9 expressi
246 enhanced risk for SZ and/or BD can activate glycogen synthase kinase-3 isozymes (GSK3alpha and beta)
248 , while application of Bikinin (inhibitor of glycogen synthase kinase-3), which activated BR signalin
249 to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun,
250 hium chloride, a reversible inhibitor of the glycogen synthase kinase-3, that rescued NMJ defects in
252 m of this study was to determine the role of glycogen synthase kinase-3alpha (GSK-3alpha) in post-MI
253 rexpression of TDP-43 leads to activation of glycogen synthase kinase-3beta (GSK-3beta) and that GSK-
254 dated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3beta (GSK-3beta) by attacking
255 PSC-CMs in vitro (i.e., 100- to 250-fold) by glycogen synthase kinase-3beta (GSK-3beta) inhibition us
257 sis coli tumor suppressor protein (APC), and glycogen synthase kinase-3beta (GSK-3beta), which could
258 atocytes, which led to a delayed increase in glycogen synthase kinase-3beta (GSK-3beta)-mediated hepa
259 demonstrate that alcohol intake also blocks glycogen synthase kinase-3beta (GSK-3beta)-phosphorylati
263 nted pre-synaptic protein deficit, decreased glycogen synthase kinase-3beta (GSK3beta) activity, and
264 finding is the pronounced downregulation of glycogen synthase kinase-3beta (Gsk3beta) and upregulati
267 Here we demonstrate that hyperactivity of glycogen synthase kinase-3beta (GSK3beta) in the atrium
269 uclear Nrf2 export/degradation machinery via glycogen synthase kinase-3beta (Gsk3beta) signaling was
270 lted in increased phosphorylation of Akt and glycogen synthase kinase-3beta (GSK3beta), leading to en
273 s (ankyrin G, EB1) were knocked down or when glycogen synthase kinase-3beta (GSK3beta; an AD-associat
274 panied by hyperphosphorylation of substrates glycogen synthase kinase-3beta and mammalian target of r
275 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa
277 erentiated hPSCs into mesoderm cells using a glycogen synthase kinase-3beta inhibitor for 3 days, the
278 mbinant Wnt3a protein or CHIR-99021 (CHIR, a glycogen synthase kinase-3beta inhibitor) caused a dose-
279 ha/wrd pathway in the motoneuron antagonizes glycogen synthase kinase-3beta kinase activity to preven
280 on of GABAergic transmission via D2 receptor-glycogen synthase kinase-3beta signaling dramatically re
281 The phosphorylation and inactivation of glycogen synthase kinase-3beta was dependent on mammalia
284 orylation of the inhibitory Ser-9 residue of glycogen synthase kinase-3beta, a primary Tau kinase inv
285 ollowed by phosphorylation (inactivation) of glycogen synthase kinase-3beta, at least in part via STA
286 cyclin D1, E-cadherin, beta-catenin, Dvl-1, glycogen synthase kinase-3beta, axin-1, and adenomatous
287 no changes in Ctnnb1 expression, activity of glycogen synthase kinase-3beta, known to phosphorylate a
288 activator of beta-catenin via inhibition of glycogen synthase kinase-3beta, reversed the inhibition
289 d to the phosphorylation and inactivation of glycogen synthase kinase-3beta, which resulted in inhibi
290 inding (CREB) protein levels to decreaseviaa glycogen synthase kinase-3beta-dependent mechanism.
291 ial-mesenchymal transition by repressing AKT/glycogen synthase kinase-3beta/beta-catenin signaling.
293 nalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3beta, in maternal liver (P < 0
295 ntify the Arabidopsis (Arabidopsis thaliana) GLYCOGEN SYNTHASE KINASE3 (GSK3)/Shaggy-like kinase ASKa
296 nt link between phosphoinositol-3-kinase and glycogen synthase kinase3 and demonstrates the potential
297 athway has many downstream targets including glycogen synthase kinase3 which is a major regulatory ki
298 b The Ppp1r3b deletion significantly reduced glycogen synthase protein abundance, and the remaining p
299 of glycogenin-1 or impaired interaction with glycogen synthase underlies this new form of glycogen st
300 50% lower, and the amount of phosphorylated glycogen synthase was 34% lower, indicating activation o