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1 a manner that depends on phosphorylation by glycogen synthase kinase 3.
2 by an Ebp2 degron that is phosphorylated by glycogen synthase kinase 3.
3 vated protein kinase (Erk1/2) cascade and of glycogen synthase kinase 3.
4 ase and cyclin-dependent kinase families and glycogen synthase kinase 3.
5 blast growth factor (FGF)/Erk pathway and of glycogen synthase kinase 3.
6 these motifs in the endogenous LRP6 through glycogen synthase kinase 3.
7 se A and subsequently by casein kinase 1 and glycogen synthase kinase 3.
8 sphorylation of adjacent casein kinase 1 and glycogen synthase kinase 3.
9 ytosis enzyme dynamin I via an inhibition of glycogen synthase kinase 3.
10 termined by phosphorylation of its substrate glycogen synthase kinase-3.
11 lation primes for Ser-159 phosphorylation by glycogen synthase kinase-3.
12 (+) NPCs with a pharmacological inhibitor of glycogen synthase kinase 3, a known regulator of WNT sig
13 activated calcitonin receptor phosphorylated glycogen synthase kinase-3, a key regulator of cytosolic
14 racellular signal regulated kinase (ERK) and glycogen synthase kinase-3 activation, indicating their
15 l requirement of canonical Wnt signaling and glycogen synthase kinase 3 activity for MLL fusion oncog
16 : it increases Akt phosphorylation, inhibits glycogen synthase kinase 3 activity, reduces IkappaB pho
17 hatidylinositol-dependent kinase 1 regulates glycogen synthase kinase 3 activity: a novel mechanism o
19 E-cadherin, and CD44-mediated signaling and glycogen synthase kinase-3/adenomatous polyposis coli-me
22 rylation of AKT and expression of the kinase glycogen synthase kinase-3 alpha (GSK3-alpha) was also m
23 way activation, enhanced CGNP proliferation, glycogen synthase kinase-3 alpha/beta (GSK-3 alpha/beta)
24 s of the beta-catenin "destruction complex," glycogen synthase kinase 3 and beta-transducin repeat co
28 esenchymal progenitors through inhibition of glycogen synthase kinase 3 and stabilization of beta-cat
29 axons in vitro, including two inhibitors of glycogen synthase kinase 3 and two inhibitors of IkappaB
30 ent reports that suggest a possible role for glycogen synthase kinase 3 and upstream wingless (Wnt)-f
31 lian target of rapamycin signaling, glucose, glycogen synthase kinase-3 and liver kinase B1, protein
32 ardiomyocytes in early developmental stages, glycogen synthase kinase-3 and p38 mitogen-activated pro
33 kt activation, a pathway known to inactivate glycogen synthase kinase-3 and reduce tau phosphorylatio
34 (G6P) and reversible phosphorylation through glycogen synthase kinase-3 and the glycogen-associated f
35 in sensitivity likely through increased Akt, glycogen synthase kinase 3, and AMPK phosphorylation; an
36 ting in the "destruction complex" with Axin, glycogen synthase kinase 3, and casein kinase, APC targe
37 P); and three NFAT kinases, casein kinase 1, glycogen synthase kinase 3, and dual specificity tyrosin
38 ing pathways (protein kinase A/DARPP-32, Akt/glycogen synthase kinase 3, and ERK) are involved in the
39 l, the effects of insulin on Akt activation, glycogen synthase kinase 3, and FoxO1a phosphorylation,
40 m from p38 mitogen-activated protein kinase, glycogen synthase kinase 3, and insulin-like receptor pa
41 ctivation of the proapoptotic proteins FKHR, glycogen synthase kinase-3, and Bad, which are events in
42 s of the brassinosteroid (BR) signaling, the glycogen synthase kinase 3/Arabidopsis SHAGGY-like kinas
43 evealed increased phosphorylation of AKT and glycogen synthase kinase 3 beta (GSK-3beta) in both the
45 mmalian kinases, we found that inhibitors of glycogen synthase kinase 3 beta (GSK-3beta) protected ce
47 , axin2, were significantly reduced, whereas glycogen synthase kinase 3 beta (GSK3beta) and phospho-b
51 We identify an interaction of BMP and Wnt/glycogen synthase kinase 3 beta (GSK3beta) pathways via
52 ral studies in rodent models have shown that glycogen synthase kinase 3 beta (GSK3beta) plays an impo
53 dulate the activity of Tankyrase enzymes and glycogen synthase kinase 3 beta (GSK3beta), additional t
54 way involving protein phosphatase 2A (PP2A), glycogen synthase kinase 3 beta (GSK3beta), and their do
55 activator of smoothened, and phosphorylated glycogen synthase kinase 3 beta (pGSK-3B), an inactive f
57 aggregates was investigated by coexpressing glycogen synthase kinase 3 beta or microtubule-associate
58 on on Ser(552), a site that differs from the glycogen synthase kinase 3 beta phosphorylation site.
59 cells led to an increase of pS(9)-GSK3beta (glycogen synthase kinase 3 beta) compared with kinase-de
60 ibition of the pro-apoptotic molecules, JNK, glycogen synthase kinase 3 beta, or caspases, toxicity i
61 hosphorylation of direct downstream targets (glycogen synthase kinase 3 beta, proline-rich Akt substr
64 The present experiments examine changes in glycogen synthase kinase-3 beta (Gsk-3beta), and transcr
65 sphorylation (p-) of STAT5, ERK1/2, AKT, and glycogen synthase kinase-3 beta, and increased AKT enzym
68 ent (CTF), insulin receptor, IGF-1 receptor, glycogen synthase kinase 3-beta (GSK-3beta), protein kin
71 y treating SH-SY5Y cells with inhibitors for glycogen synthase kinase 3-beta (GSK3beta) and cyclin-de
73 TA accelerated beta-catenin degradation by a glycogen synthase kinase 3-beta-dependent mechanism.
75 evealed a role for heat shock protein 90 and glycogen synthase kinase 3 but not casein kinase 1 nor L
76 n or inhibition of the Akt downstream target glycogen synthase kinase 3 by its pharmacologic inhibito
78 in kinase and the Akt-mediated inhibition of glycogen synthase kinase 3, critical inhibitors of Smad
79 lations of AMPK, acetyl CoA carboxylase, and glycogen synthase kinase-3, decreased glycogen synthase
81 drogenase kinase-1, or its downstream target glycogen synthase kinase-3 did not prevent CCR9 expressi
82 ars has helped define the role of the GSK-3 (glycogen synthase kinase-3) family in a variety of physi
85 uclear antigen (LANA) protein interacts with glycogen synthase kinase 3 (GSK-3) and relocalizes GSK-3
86 interaction with the serine-threonine kinase glycogen synthase kinase 3 (GSK-3) and stabilization of
87 , we found that small molecule inhibitors of glycogen synthase kinase 3 (GSK-3) consistently caused a
89 phosphorylation of C/EBP beta was blocked by glycogen synthase kinase 3 (GSK-3) inhibitors, suggestin
94 ing evidence suggests that the regulation of glycogen synthase kinase 3 (GSK-3) might be important in
97 a-catenin pathway through phosphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this
102 ne/threonine protein kinase PIM1 (PIM-1) and glycogen synthase kinase 3 (GSK-3beta) are inhibited wit
106 ) DC resulted from failed down-regulation of glycogen synthase kinase-3 (GSK-3) activity and could no
108 Increasing attention is being focused on Akt/glycogen synthase kinase-3 (GSK-3) and wingless (Wnt) si
109 inositol biosynthetic pathway and the enzyme glycogen synthase kinase-3 (GSK-3) are targets of the mo
125 Cumulative evidence strongly supports that glycogen synthase kinase-3 (GSK-3) is a pathogenic molec
135 in the absence of stress, phosphorylation by glycogen synthase kinase-3 (GSK-3) prevents SKN-1 from a
136 We report here that specific inhibition of glycogen synthase kinase-3 (GSK-3) reduces tau phosphory
138 de et al. uses phosphoproteomics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse e
139 atment of cells with a specific inhibitor of glycogen synthase kinase-3 (GSK-3), a downstream effecto
140 andidates include inositol monophosphatases, glycogen synthase kinase-3 (GSK-3), and a beta-arrestin-
143 together with inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3), which relieves its i
146 hanism by which HIF-1alpha is degraded after glycogen synthase kinase-3 (GSK-3)-induced phosphorylati
148 gents to determine whether the regulation of glycogen synthase kinase-3 (GSK-3)/beta-catenin and mTOR
149 ling events that result in the inhibition of glycogen synthase kinase-3 (GSK-3)beta represent an adap
151 ce containing a mutant constitutively active glycogen synthase kinase-3 (GSK-3beta) transgene, driven
153 nonical Wnt signaling requires inhibition of Glycogen Synthase Kinase 3 (GSK3) activity, but the mole
154 ignalling pathway or dual inhibition (2i) of glycogen synthase kinase 3 (Gsk3) and mitogen-activated
156 cells due to its constant phosphorylation by glycogen synthase kinase 3 (GSK3) and subsequent proteas
157 hosphorylation at Thr41, Ser37, and Ser33 by glycogen synthase kinase 3 (GSK3) and that phosphorylate
159 kinases cyclin-dependent kinase 5 (Cdk5) and glycogen synthase kinase 3 (GSK3) at sites that are hype
160 by casein kinase 1 at the Ser-45 site and by glycogen synthase kinase 3 (GSK3) at the Thr-41, Ser-37,
162 ition of protein kinase C-beta (PKCbeta) and glycogen synthase kinase 3 (GSK3) causes synergistic apo
163 ation of a serine (S373A) in CIITA, within a glycogen synthase kinase 3 (GSK3) consensus site, decrea
164 ng approaches, we show how the activation of glycogen synthase kinase 3 (GSK3) contributes to neurona
170 nd this phosphorylation was inhibited by the glycogen synthase kinase 3 (GSK3) inhibitor indirubin-3'
173 ly that Wnt-induced Lrp6 phosphorylation via glycogen synthase kinase 3 (Gsk3) initiates Wnt/beta-cat
181 has been associated with altered activity of glycogen synthase kinase 3 (GSK3) isozymes, which are pr
182 phosphodegron (CPD) signal, a target site of glycogen synthase kinase 3 (GSK3) kinase and Fbw7 ubiqui
186 we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm
187 lt gastric epithelium via deletion of either glycogen synthase kinase 3 (GSK3) or APC or via expressi
189 cyclin-dependent kinase 1 (cdk1 [cdc2]) and glycogen synthase kinase 3 (GSK3) pathways as two probab
190 ation mediated by a phosphodegron created by glycogen synthase kinase 3 (GSK3) phosphorylation of Mcl
192 n target of rapamycin complex 1 (mTORC1) and glycogen synthase kinase 3 (GSK3) play pivotal roles in
197 schizophrenia, and depression, regulates Akt/glycogen synthase kinase 3 (GSK3) signaling and related
198 itor pools and plays a key role in mediating glycogen synthase kinase 3 (GSK3) signaling during brain
201 ted AMP-activated protein kinase (AMPK), and glycogen synthase kinase 3 (GSK3) underwent Western blot
202 molecule inhibition of MAP kinase (MEK) and glycogen synthase kinase 3 (GSK3) with LIF (2i/LIF) prov
205 n in DRG neurons leads to phosphorylation of glycogen synthase kinase 3 (GSK3), a protein that normal
207 clock proteins by casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3), appear conserved amon
208 n kinase A (PKA), casein kinase 1 (CK1), and glycogen synthase kinase 3 (GSK3), as well as the activi
210 such as cyclin-dependent kinase 5 (Cdk5) and glycogen synthase kinase 3 (GSK3), has been implicated i
211 kt inhibition was abrogated by inhibitors of glycogen synthase kinase 3 (GSK3), implying that the cen
212 ating axonal protein phosphatase 1 (PP1) and glycogen synthase kinase 3 (GSK3), independent of microt
214 Here, we report synergistic inhibition of glycogen synthase kinase 3 (GSK3), transforming growth f
219 ng inhibits stomatal development through the glycogen synthase kinase 3 (GSK3)-like kinase BIN2, and
235 We show that this process is dependent on glycogen synthase kinase 3 (GSK3): GSK3 was associated w
237 ositol-3 kinase/Akt (IRS-PI3K-Akt) pathways, glycogen synthase kinase-3 (GSK3) and mammalian target o
238 T3 signaling, and simultaneous inhibition of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kin
240 plementary signaling pathways and identified glycogen synthase kinase-3 (GSK3) as important in surviv
241 s to Th17 cells, we found that inhibition of glycogen synthase kinase-3 (GSK3) blocked IL-6 productio
242 haracterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids p
247 he phosphorylation and activities of Akt and glycogen synthase kinase-3 (GSK3) in peripheral tissues,
250 ia containing fetal bovine serum (FBS) and a glycogen synthase kinase-3 (GSK3) inhibitor, and in seru
255 gated the effect of inhibitors targeting the glycogen synthase kinase-3 (GSK3) on the expression of N
257 f-function approaches in mice, we found that glycogen synthase kinase-3 (Gsk3) plays a pivotal role i
260 ependent phosphorylation and inactivation of glycogen synthase kinase-3 (GSK3), an enzyme that regula
261 nvestigated whether lithium, an inhibitor of glycogen synthase kinase-3 (GSK3), can ameliorate EAE in
262 nation through Akt-independent inhibition of glycogen synthase kinase-3 (GSK3), itself a candidate th
263 rrent study, we tested whether inhibitors of glycogen synthase kinase-3 (GSK3), previously reported t
264 ivation of the constitutively active enzyme, glycogen synthase kinase-3 (GSK3), which has been implic
265 ivity in an adenomatous polyposis coli (APC)/glycogen synthase kinase-3 (GSK3)-independent manner, re
269 way seems to occur from Dishevelleds to axin/glycogen synthase kinase 3(GSK3)/beta-catenin complexes
270 level of protein stability and controlled by glycogen synthase kinase 3 in a cyclic AMP-protein kinas
271 he neighboring Ser-208, the priming site for glycogen synthase kinase 3 in vivo activity, strengthene
272 blocked cardiomyocyte specification, whereas glycogen synthase kinase 3 inhibition at this point enha
274 thermore, sequential treatment of hPSCs with glycogen synthase kinase 3 inhibitors followed by induci
275 g research results involving ethyl pyruvate, glycogen synthase kinase-3 inhibitors and 3-hydroxy-3-me
276 phosphorylated by recombinant GSK3beta; and glycogen synthase kinase-3 inhibitors effectively reduce
277 novel bi-directionality in the AKT and GSK3 (Glycogen synthase kinase 3) interaction, whereby genetic
278 addition to the two C-terminal residues, and glycogen synthase kinase 3 is responsible for phosphoryl
280 enhanced risk for SZ and/or BD can activate glycogen synthase kinase-3 isozymes (GSK3alpha and beta)
281 phorylation markedly enhances the binding of glycogen synthase kinase 3, leading to a more active bet
282 re is restoration of phospho-Akt and phospho-glycogen synthase kinase 3 levels in the treated mice, c
283 an be phosphorylated and stabilized by GSK3 (GLYCOGEN SYNTHASE KINASE 3)-like kinase BIN2 (BRASSINOST
284 through a signalling pathway that involves a glycogen synthase kinase-3-like kinase (BIN2) and a seri
285 lthough JNK activity is not required for the glycogen synthase kinase-3-mediated degradation of beta-
286 ellular signal-regulated kinase pathway, the glycogen synthase kinase-3-mediated pathway and Bcl-2 ar
287 ell; PI3K, phosphoinositide 3-kinases; GSK3, glycogen synthase kinase-3; mTOR, mammalian target of ra
289 inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3, or addition of NRG1 signific
290 ed 4 chemical compound groups: inhibitors of glycogen synthase kinase-3, p38 mitogen-activated protei
292 I cells with chemical inhibitors of MEKs and glycogen synthase kinase 3 resulted in their further rep
293 to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun,
295 hium chloride, a reversible inhibitor of the glycogen synthase kinase-3, that rescued NMJ defects in
298 , while application of Bikinin (inhibitor of glycogen synthase kinase-3), which activated BR signalin
299 to their ability to serve as substrates for glycogen synthase kinase 3, which acts at neighboring N-
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