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1                            Here we show that glycogen synthase kinase 3 (GSK-3) interacts with and ph
2 a-catenin pathway through phosphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this
3 racellular signal-regulated kinase (ERK) and glycogen synthase kinase 3 (GSK-3).
4                                              Glycogen synthase kinase 3 (GSK-3, isoforms alpha and be
5 but REDD1-mediated Nrf2 degradation required glycogen synthase kinase 3 (GSK3) activity and Ser-351/S
6                                              Glycogen synthase kinase 3 (GSK3) alpha and beta are 2 h
7 maller receptor-mediated vesicles containing glycogen synthase kinase 3 (GSK3) and protein arginine e
8                                 We show that glycogen synthase kinase 3 (GSK3) and protein arginine m
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
11                  Here we show how inhibiting glycogen synthase kinase 3 (GSK3) can improve the differ
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
15 differentiation through negatively affecting glycogen synthase kinase 3 (GSK3) function.
16          Herein, we investigated the role of glycogen synthase kinase 3 (GSK3) in liver regeneration
17  in collagen I 3D cultures in the absence of glycogen synthase kinase 3 (GSK3) inhibition, hPSC-deriv
18        Appropriate temporal application of a glycogen synthase kinase 3 (GSK3) inhibitor combined wit
19                                              Glycogen synthase kinase 3 (GSK3) inhibitors were identi
20                          Here we report that glycogen synthase kinase 3 (GSK3) inhibits AMPK function
21                                              Glycogen synthase kinase 3 (GSK3) is a genetically valid
22                            Here we show that glycogen synthase kinase 3 (Gsk3) is a metabolic sensor
23                           Phosphorylation of glycogen synthase kinase 3 (GSK3) isoforms alpha/beta by
24 phosphodegron (CPD) signal, a target site of glycogen synthase kinase 3 (GSK3) kinase and Fbw7 ubiqui
25         Previous studies have indicated that glycogen synthase kinase 3 (GSK3) may play a role in APP
26          We also demonstrate that the kinase glycogen synthase kinase 3 (GSK3) mediates the FBW7-depe
27          Here, we show the expression of the Glycogen synthase kinase 3 (GSK3) MoGSK1 in M. oryzae is
28 we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm
29                               Suppression of glycogen synthase kinase 3 (GSK3) or FBXW7 rescued Mcl-1
30               PX-866 treatment abolished AKT/glycogen synthase kinase 3 (GSK3) phosphorylation, and c
31                                              Glycogen synthase kinase 3 (GSK3) plays a central role i
32                           We also found that glycogen synthase kinase 3 (GSK3) regulated amyloid-beta
33 itor pools and plays a key role in mediating glycogen synthase kinase 3 (GSK3) signaling during brain
34                     Here, we report that Wnt/glycogen synthase kinase 3 (GSK3) signaling functions po
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
38                                              Glycogen synthase kinase 3 (GSK3) was identified as an e
39                                              Glycogen synthase kinase 3 (GSK3), a prominent enzyme in
40  clock proteins by casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3), appear conserved amon
41                       Moreover, we show that glycogen synthase kinase 3 (GSK3), rather than mammalian
42 ation of proteins (Wnt/STOP), which inhibits glycogen synthase kinase 3 (GSK3)-dependent protein ubiq
43                                  Arabidopsis GLYCOGEN SYNTHASE KINASE 3 (GSK3)-like kinases play vari
44 mitochondrial respiratory quiescence through glycogen synthase kinase 3 (GSK3).
45  stabilizing many proteins phosphorylated by glycogen synthase kinase 3 (GSK3).
46 diated degradation due to phosphorylation by glycogen synthase kinase 3 (Gsk3).
47 gers a rapid lack of VDAC phosphorylation by glycogen synthase kinase 3 (GSK3).
48 al domain, priming it for phosphorylation by glycogen synthase kinase 3 (GSK3).
49 mine analogues which are inhibitors of human glycogen synthase kinase 3 (GSK3).
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
54     Acute responses of ERK1/2, p38, Akt, and glycogen synthase kinase 3 after mechanical stress were
55 atenin was required for BRB restoration, but glycogen synthase kinase 3 alpha/beta (GSK-3alpha/beta)
56            We demonstrate that inhibitors of glycogen synthase kinase 3 alpha/beta (GSK3alpha/beta) e
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
59                                              Glycogen synthase kinase 3 beta (GSK-3beta) is a central
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
62                           The BCR attenuates glycogen synthase kinase 3 beta (GSK3beta) activity to s
63                                              Glycogen synthase kinase 3 beta (GSK3beta) is a critical
64                                              Glycogen synthase kinase 3 beta (GSK3beta) is highly ina
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
70 nt which was suppressed by co-treatment with glycogen synthase kinase 3 inhibitor SB216763.
71                         Our data reveal that glycogen synthase kinase 3 signaling also regulates eEF2
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
82                           Insulin/GSK-3beta (glycogen synthase kinase 3-beta) signalling induces cycl
83 TA accelerated beta-catenin degradation by a glycogen synthase kinase 3-beta-dependent mechanism.
84 ytosis enzyme dynamin I via an inhibition of glycogen synthase kinase 3.
85 s of the brassinosteroid (BR) signaling, the glycogen synthase kinase 3/Arabidopsis SHAGGY-like kinas
86                                          The glycogen synthase kinase-3 (GSK-3) family of serine/thre
87                                  The role of glycogen synthase kinase-3 (GSK-3) in Alzheimer disease
88                            The challenge for glycogen synthase kinase-3 (GSK-3) inhibitor design lies
89 plex 1 (mTORC1) inhibitor rapamycin, and the glycogen synthase kinase-3 (GSK-3) inhibitor lithium act
90                                    Combining glycogen synthase kinase-3 (GSK-3) inhibitors with VPA o
91                                Activation of glycogen synthase kinase-3 (GSK-3) interferes with micro
92                                              Glycogen synthase kinase-3 (GSK-3) is a constitutively a
93                                              Glycogen synthase kinase-3 (Gsk-3) is a key regulator of
94                                              Glycogen synthase kinase-3 (GSK-3) is a key regulator of
95                                              Glycogen synthase kinase-3 (GSK-3) is one of the few sig
96 bition of the histone deacetylase (HDAC) and glycogen synthase kinase-3 (GSK-3) pathways, which cause
97                                              Glycogen synthase kinase-3 (GSK-3) regulates multiple ce
98 de et al. uses phosphoproteomics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse e
99                    DydA is phosphorylated by glycogen synthase kinase-3 (GSK-3), which is required fo
100  together with inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3), which relieves its i
101                   Predictably, inhibition of glycogen synthase kinase-3 (GSK-3), which results from a
102 nt oxazole-4-carboxamide-based inhibitors of glycogen synthase kinase-3 (GSK-3).
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
106                                              Glycogen synthase kinase-3 (GSK3) are ubiquitously expre
107 haracterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids p
108                                          The glycogen synthase kinase-3 (GSK3) family kinases are cen
109                  Treatment with lithium or a glycogen synthase kinase-3 (GSK3) inhibitor corrects beh
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
112                         Here, we report that glycogen synthase kinase-3 (GSK3) is a critical determin
113                                              Glycogen synthase kinase-3 (GSK3) is an important signal
114                                  Hippocampal glycogen synthase kinase-3 (GSK3) is hyperactive in the
115                                We found that glycogen synthase kinase-3 (GSK3) is overactivated in co
116 gated the effect of inhibitors targeting the glycogen synthase kinase-3 (GSK3) on the expression of N
117                       Moreover, induction of glycogen synthase kinase-3 (GSK3) performed using a Wnt
118                                              Glycogen synthase kinase-3 (GSK3) regulates many physiol
119                                              Glycogen synthase kinase-3 (GSK3) was found to be an ups
120 rrent study, we tested whether inhibitors of glycogen synthase kinase-3 (GSK3), previously reported t
121 ogenesis, immunomodulation and regulation of glycogen synthase kinase-3 activity.
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
124        Next, we apply this strategy to study glycogen synthase kinase-3 beta (GSK-3beta), a kinase ab
125                                              Glycogen synthase kinase-3 beta (GSK-3beta), a serine/th
126 drogenase kinase-1, or its downstream target glycogen synthase kinase-3 did not prevent CCR9 expressi
127                                              Glycogen synthase kinase-3 is a Ser/Thr kinase, tonicall
128  enhanced risk for SZ and/or BD can activate glycogen synthase kinase-3 isozymes (GSK3alpha and beta)
129                                          The glycogen synthase kinase-3 of the parasite (PfGSK-3) was
130                Pharmacological inhibition of glycogen synthase kinase-3 was sufficient to reverse the
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
134 lation primes for Ser-159 phosphorylation by glycogen synthase kinase-3.
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
138         Phosphorylation of tau at Thr212 and glycogen synthase kinase 3beta (GSK-3beta) at Ser9 was r
139 ave been some reports on MTDLs targeting the glycogen synthase kinase 3beta (GSK-3beta) enzyme, due t
140                                              Glycogen synthase kinase 3beta (GSK-3beta) has been sugg
141                                              Glycogen synthase kinase 3beta (GSK-3beta) is a primary
142                                              Glycogen synthase kinase 3beta (GSK-3beta) is an enzyme
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
145 ion of specific Akt substrates, most notably glycogen synthase kinase 3beta (Gsk-3beta).
146 ound a residue that can be phosphorylated by glycogen synthase kinase 3beta (GSK-3beta).
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
154           Cellular targets of Li(+), such as glycogen synthase kinase 3beta (GSK3beta) and G proteins
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
161                                              Glycogen synthase kinase 3beta (GSK3beta) deactivation a
162                                              Glycogen synthase kinase 3beta (GSK3beta) has been shown
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
166                   A member of this family is glycogen synthase kinase 3beta (GSK3beta) interaction pr
167                                 We show that glycogen synthase kinase 3beta (GSK3beta) interacts with
168                                              Glycogen synthase kinase 3beta (GSK3beta) is a constitut
169                                Inhibition of glycogen synthase kinase 3beta (GSK3beta) is a shared ac
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
172           In this study, we demonstrate that glycogen synthase kinase 3beta (GSK3beta) regulates ST2L
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
178              Psychotropic medications target glycogen synthase kinase 3beta (GSK3beta), but the funct
179 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p
180          The phosphorylation is catalyzed by glycogen synthase kinase 3beta (GSK3beta), ultimately re
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
183             CUGBP1 activity is controlled by glycogen synthase kinase 3beta (GSK3beta), which is elev
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
186                        PI exposure abrogated glycogen synthase kinase 3beta (GSK3beta)-mediated degra
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
189 t VRK2 activity was negatively controlled by glycogen synthase kinase 3beta (GSK3beta).
190 g protein binding protein kinase A (PKA) and glycogen synthase kinase 3beta (GSK3beta).
191     These include protein kinase A (PKA) and glycogen synthase kinase 3beta (GSK3beta).
192 ivation and this occurs in part by targeting glycogen synthase kinase 3beta (GSK3beta).
193 inhibition of the tumor suppressors PTEN and glycogen synthase kinase 3beta (GSK3beta).
194  at S199 (hTau-S199-P) by the protein kinase glycogen synthase kinase 3beta (GSK3beta).
195 n (mTOR) signaling pathway and inhibition of glycogen synthase kinase 3beta (GSK3beta).
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
200                                              Glycogen synthase kinase 3beta and Foxo1 are two PI-3K-r
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
207  Wnt/beta-catenin pathway by inactivation of glycogen synthase kinase 3beta of NKT cells.
208 ment, and reduced Akt (protein kinase B) and glycogen synthase kinase 3beta phosphorylation.
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
216 n showed AQP1 interaction with beta-catenin, glycogen synthase kinase 3beta, LRP6, and Axin1.
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
219         Molecularly, ROCK inhibition induced glycogen synthase kinase 3beta-dependent phosphorylation
220 ta-catenin expression and stabilization in a glycogen synthase kinase 3beta-independent manner.
221  signal-regulated protein kinase modules and glycogen synthase kinase 3beta.
222 ) transcriptional activity via inhibition of glycogen synthase kinase 3beta.
223 ead box protein O1 transcription factors and glycogen synthase kinase 3beta.
224 7, p38 mitogen-activated protein kinase, and glycogen synthase kinase 3beta.
225 nalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3beta, in maternal liver (P < 0
226                Recent evidence suggests that glycogen-synthase kinase 3beta (GSK3beta) plays a key ro
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
230                  In addition, application of glycogen synthase kinase-3beta (GSK-3beta) inhibitor com
231 etin, reactivation of beta-catenin using the glycogen synthase kinase-3beta (GSK-3beta) inhibitor LiC
232                        Herein we report that glycogen synthase kinase-3beta (GSK-3beta) is phosphoryl
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
236 ein function are via a pathway that involves glycogen synthase kinase-3beta (GSK-3beta).
237 teins, which were predicted to be targets of glycogen synthase kinase-3beta (GSK-3beta).
238 hase and the phosphorylation (inhibition) of glycogen synthase kinase-3beta (GSK-3beta).
239                                              Glycogen synthase kinase-3beta (GSK3beta) activity is in
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
242                                              Glycogen synthase kinase-3beta (GSK3beta) controls many
243                                              Glycogen synthase kinase-3beta (GSK3beta) has diverse bi
244    Here we demonstrate that hyperactivity of glycogen synthase kinase-3beta (GSK3beta) in the atrium
245                                              Glycogen synthase kinase-3beta (GSK3beta) plays a critic
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
248 tion and insulin secretion via regulation of glycogen synthase kinase-3beta (GSK3beta).
249 ith emerin and beta-actin, and activation of glycogen synthase kinase-3beta (GSK3beta).
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
253 ion and completely blocked the inhibition of glycogen synthase kinase-3beta gene transcription.
254   Overexpression of Snail1 and inhibition of glycogen synthase kinase-3beta in colorectal tumor cells
255                                         Such glycogen synthase kinase-3beta inactivation causes chang
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
261                                   GSK-3beta (glycogen synthase kinase-3beta) is highly associated wit
262 l as by inhibition of the Akt-GSK-3beta (Akt-glycogen synthase kinase-3beta) pathway.
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.
271 pstream signaling pathways known to regulate glycogen synthase kinase-3beta.
272 ial-mesenchymal transition by repressing AKT/glycogen synthase kinase-3beta/beta-catenin signaling.
273 ological or genetic inhibition of tau kinase glycogen-synthase-kinase-3beta (GSK-3beta).
274          Additionally, in the current study, glycogen synthase kinase appears to attenuate tau pathol
275           In both cell types, insulin blocks glycogen synthase kinase beta (GSK3beta) activity.
276  Apc participates in a complex that includes glycogen synthase kinase beta (Gsk3beta) and betacatenin
277                        Here we show that the glycogen synthase kinase beta (GSK3beta) expression is e
278                In a previous study, the FGK3 glycogen synthase kinase gene orthologous to mammalian G
279                  PKB/Akt in turn inactivates glycogen synthase kinase (GSK) 3, a major regulator of m
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
282                                              Glycogen synthase kinase (GSK)-3 is a ubiquitously expre
283 CRMP-2 and ROCK II is partially regulated by glycogen synthase kinase (GSK)-3 phosphorylation of CRMP
284        The enzymes 5-lipoxygenase (5-LO) and glycogen synthase kinase (GSK)-3 represent promising dru
285                          Blast TBI increased glycogen synthase kinase (GSK)-3beta activities in ApoE4
286                   These same stimuli enhance glycogen synthase kinase (GSK)-3beta activity through in
287 n vitro and in vivo, working through the Akt/Glycogen Synthase Kinase (GSK)-3beta pathway.
288                                              Glycogen synthase kinase (GSK)-3beta phosphorylates the
289 eptor is modulated, here, we have found that glycogen synthase kinase (GSK)-3beta phosphorylation of
290               Here, we provide evidence that glycogen synthase kinase (GSK)-3beta promotes cell proli
291 rved that phosphorylation of Gpa2 depends on glycogen synthase kinase (GSK).
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-
298               A point mutation in a putative glycogen synthase kinase phosophorylation site within th
299 lates alcohol-induced BK internalization via glycogen synthase kinase phosphorylation.
300 f lithium, in which fine-tuned regulation of glycogen synthase kinase type 3, a prime target for lith

 
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