ライフサイエンスコーパス: glycogen synthase

1 ugh a remarkable adaptation of the bacterial glycogen synthase.

2 t, confirming the inhibitory role of Fgk3 on glycogen synthase.

3 1 lacking the C-terminal that normally binds glycogen synthase.

4 predominant, nutritionally regulated form of glycogen synthase.

5 ciated glycogen and with stable knockdown of glycogen synthase 1, which inhibited (18)F-NFTG uptake,

6 ence of interleukin-7 (IL-7), IL-21, and the glycogen synthase-3beta inhibitor TWS119, and geneticall

7 Furthermore, glycogen synthase activity and glycogen accumulation wer

8 is was associated with a reduction (>70%) in glycogen synthase activity in P-HFF versus P and increas

9 ates insulin and catecholamine signaling and glycogen synthase activity in skeletal muscle.

10 sensitivity was not associated with enhanced glycogen synthase activity or proximal insulin signaling

11 cogen content was approximately 50% greater, glycogen synthase activity was approximately 50% greater

12 Insulin-stimulated glycogen synthase activity was completely ablated during

13 rylation of TBC1D4 Ser(318) and Ser(704) and glycogen synthase activity were greater in the exercised

14 Akt2 activation, which specifically inhibits glycogen synthase activity.

15 inhibition of glucose-6-phosphate-stimulated glycogen synthase activity.

16 or cell cycle transit as well as controlling glycogen synthase activity.

17 e and phosphorylation of inhibiting sites on glycogen synthase all increased.

18 ogen shunt implicates the high activities of glycogen synthase and fructose bisphosphatase in tumors

19 The similarities in the active sites of glycogen synthase and glycogen phosphorylase support the

20 Firstly, the periportal zonation of both glycogen synthase and the oxidative phosphorylation enzy

21 Isogenic DeltaglgA (glycogen synthase) and DeltaglgB (glycogen-branching enz

22 lasses of glucan biosynthetic enzyme (starch/glycogen synthases, branching enzymes, and debranching e

23 ing also increased the insulin activation of glycogen synthase by 60%, GLUT4 expression by 16%, and 5

24 levels of oxidants or genetic inhibition of glycogen synthase depletes glycogen stores and extends t

25 Moreover, glycogen synthase expression was greatly enhanced, consi

26 the Gys2 gene encoding the liver isoform of glycogen synthase generates a mouse strain (LGSKO) that

27 e widely conserved in plant SS and bacterial glycogen synthase (GS) isoforms.

28 Insulin regulates glycogen synthase (GS) through incompletely defined path

29 om glucose through the cooperative action of glycogen synthase (GS), glycogenin (GN), and glycogen br

30 granules and the glycogen conversion enzymes glycogen synthase I and glycogen phosphorylase BB, dispe

31 They activate glycogen synthase in insulin receptor-expressing CHO-IR

32 lecular signaling at the level of TBC1D4 and glycogen synthase in muscle.

33 the latter possibly due to a direct role of Glycogen Synthase in regulating autophagy through its in

34 PKB/Akt in turn inactivates glycogen synthase kinase (GSK) 3, a major regulator of m

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

37 Glycogen synthase kinase (GSK)-3 is a ubiquitously expre

38 CRMP-2 and ROCK II is partially regulated by glycogen synthase kinase (GSK)-3 phosphorylation of CRMP

39 The enzymes 5-lipoxygenase (5-LO) and glycogen synthase kinase (GSK)-3 represent promising dru

40 Blast TBI increased glycogen synthase kinase (GSK)-3beta activities in ApoE4

41 These same stimuli enhance glycogen synthase kinase (GSK)-3beta activity through in

42 n vitro and in vivo, working through the Akt/Glycogen Synthase Kinase (GSK)-3beta pathway.

43 Glycogen synthase kinase (GSK)-3beta phosphorylates the

44 eptor is modulated, here, we have found that glycogen synthase kinase (GSK)-3beta phosphorylation of

45 Here, we provide evidence that glycogen synthase kinase (GSK)-3beta promotes cell proli

46 show that the dual phosphodiesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15, a het

47 Mechanistically, Tanshinone IIA blunted glycogen synthase kinase (GSK)3beta overactivity and hyp

48 used to deliver low doses of small molecule glycogen synthase kinase (GSK-3) antagonists that promot

49 exerted its positive effect by inhibition of glycogen synthase kinase (GSK3) activity and enhancement

50 Here we show that glycogen synthase kinase 3 (GSK-3) interacts with and ph

51 a-catenin pathway through phosphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this

52 racellular signal-regulated kinase (ERK) and glycogen synthase kinase 3 (GSK-3).

53 Glycogen synthase kinase 3 (GSK-3, isoforms alpha and be

54 ugh alpha-catenin and the kinase activity of glycogen synthase kinase 3 (GSK-3beta).

55 ignalling pathway or dual inhibition (2i) of glycogen synthase kinase 3 (Gsk3) and mitogen-activated

56 We show that glycogen synthase kinase 3 (GSK3) and protein arginine m

57 cells due to its constant phosphorylation by glycogen synthase kinase 3 (GSK3) and subsequent proteas

58 Here we show how inhibiting glycogen synthase kinase 3 (GSK3) can improve the differ

59 ition of protein kinase C-beta (PKCbeta) and glycogen synthase kinase 3 (GSK3) causes synergistic apo

60 ng approaches, we show how the activation of glycogen synthase kinase 3 (GSK3) contributes to neurona

61 differentiation through negatively affecting glycogen synthase kinase 3 (GSK3) function.

62 Herein, we investigated the role of glycogen synthase kinase 3 (GSK3) in liver regeneration

63 Appropriate temporal application of a glycogen synthase kinase 3 (GSK3) inhibitor combined wit

64 Glycogen synthase kinase 3 (GSK3) inhibitors were identi

65 Here we report that glycogen synthase kinase 3 (GSK3) inhibits AMPK function

66 Glycogen synthase kinase 3 (GSK3) is a genetically valid

67 Here we show that glycogen synthase kinase 3 (Gsk3) is a metabolic sensor

68 Phosphorylation of glycogen synthase kinase 3 (GSK3) isoforms alpha/beta by

69 phosphodegron (CPD) signal, a target site of glycogen synthase kinase 3 (GSK3) kinase and Fbw7 ubiqui

70 Previous studies have indicated that glycogen synthase kinase 3 (GSK3) may play a role in APP

71 We also demonstrate that the kinase glycogen synthase kinase 3 (GSK3) mediates the FBW7-depe

72 Here, we show the expression of the Glycogen synthase kinase 3 (GSK3) MoGSK1 in M. oryzae is

73 we demonstrate a potent effect of inhibiting glycogen synthase kinase 3 (GSK3) on definitive endoderm

74 lt gastric epithelium via deletion of either glycogen synthase kinase 3 (GSK3) or APC or via expressi

75 Suppression of glycogen synthase kinase 3 (GSK3) or FBXW7 rescued Mcl-1

76 PX-866 treatment abolished AKT/glycogen synthase kinase 3 (GSK3) phosphorylation, and c

77 Glycogen synthase kinase 3 (GSK3) plays a central role i

78 We also found that glycogen synthase kinase 3 (GSK3) regulated amyloid-beta

79 itor pools and plays a key role in mediating glycogen synthase kinase 3 (GSK3) signaling during brain

80 Here, we report that Wnt/glycogen synthase kinase 3 (GSK3) signaling functions po

81 Glycogen synthase kinase 3 (GSK3), a prominent enzyme in

82 clock proteins by casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3), appear conserved amon

83 Moreover, we show that glycogen synthase kinase 3 (GSK3), rather than mammalian

84 stabilizing many proteins phosphorylated by glycogen synthase kinase 3 (GSK3).

85 diated degradation due to phosphorylation by glycogen synthase kinase 3 (Gsk3).

86 gers a rapid lack of VDAC phosphorylation by glycogen synthase kinase 3 (GSK3).

87 ed that RNPC1 is phosphorylated at Ser195 by glycogen synthase kinase 3 (GSK3).

88 mine analogues which are inhibitors of human glycogen synthase kinase 3 (GSK3).

89 mitochondrial respiratory quiescence through glycogen synthase kinase 3 (GSK3).

90 We show that this process is dependent on glycogen synthase kinase 3 (GSK3): GSK3 was associated w

91 : it increases Akt phosphorylation, inhibits glycogen synthase kinase 3 activity, reduces IkappaB pho

92 hatidylinositol-dependent kinase 1 regulates glycogen synthase kinase 3 activity: a novel mechanism o

93 Acute responses of ERK1/2, p38, Akt, and glycogen synthase kinase 3 after mechanical stress were

94 evealed increased phosphorylation of AKT and glycogen synthase kinase 3 beta (GSK-3beta) in both the

95 Glycogen synthase kinase 3 beta (GSK-3beta) is a central

96 The BCR attenuates glycogen synthase kinase 3 beta (GSK3beta) activity to s

97 Glycogen synthase kinase 3 beta (GSK3beta) is a critical

98 Glycogen synthase kinase 3 beta (GSK3beta) is highly ina

99 We identify an interaction of BMP and Wnt/glycogen synthase kinase 3 beta (GSK3beta) pathways via

100 activator of smoothened, and phosphorylated glycogen synthase kinase 3 beta (pGSK-3B), an inactive f

101 ibition of the pro-apoptotic molecules, JNK, glycogen synthase kinase 3 beta, or caspases, toxicity i

102 evealed a role for heat shock protein 90 and glycogen synthase kinase 3 but not casein kinase 1 nor L

103 nt which was suppressed by co-treatment with glycogen synthase kinase 3 inhibitor SB216763.

104 Our data reveal that glycogen synthase kinase 3 signaling also regulates eEF2

105 way seems to occur from Dishevelleds to axin/glycogen synthase kinase 3(GSK3)/beta-catenin complexes

106 an be phosphorylated and stabilized by GSK3 (GLYCOGEN SYNTHASE KINASE 3)-like kinase BIN2 (BRASSINOST

107 (+) NPCs with a pharmacological inhibitor of glycogen synthase kinase 3, a known regulator of WNT sig

108 in sensitivity likely through increased Akt, glycogen synthase kinase 3, and AMPK phosphorylation; an

109 inhibition of Janus kinase 1, inhibition of Glycogen synthase kinase 3, or addition of NRG1 signific

110 y treating SH-SY5Y cells with inhibitors for glycogen synthase kinase 3-beta (GSK3beta) and cyclin-de

111 Insulin/GSK-3beta (glycogen synthase kinase 3-beta) signalling induces cycl

112 TA accelerated beta-catenin degradation by a glycogen synthase kinase 3-beta-dependent mechanism.

113 ytosis enzyme dynamin I via an inhibition of glycogen synthase kinase 3.

114 s of the brassinosteroid (BR) signaling, the glycogen synthase kinase 3/Arabidopsis SHAGGY-like kinas

115 y phosphorylated at Thr(714) and Ser(727) by glycogen synthase kinase 3alpha and -beta (GSK-3alpha/be

116 eta-catenin signaling cascades, which switch glycogen synthase kinase 3beta (GSK-3beta) activation on

117 Phosphorylation of tau at Thr212 and glycogen synthase kinase 3beta (GSK-3beta) at Ser9 was r

118 Glycogen synthase kinase 3beta (GSK-3beta) has been sugg

119 Glycogen synthase kinase 3beta (GSK-3beta) is a primary

120 Glycogen synthase kinase 3beta (GSK-3beta) is an enzyme

121 ected T cells and reduces phosphorylation of glycogen synthase kinase 3beta (GSK-3beta), a downstream

122 of cyclin B1, cyclin D3, and phosphorylated glycogen synthase kinase 3beta (GSK-3beta), while infect

123 ion of specific Akt substrates, most notably glycogen synthase kinase 3beta (Gsk-3beta).

124 ound a residue that can be phosphorylated by glycogen synthase kinase 3beta (GSK-3beta).

125 Consequently, GRbeta-Ad mice had increased glycogen synthase kinase 3beta (GSK3beta) activity and r

126 , N-methyl-d-aspartate receptor function, or glycogen synthase kinase 3beta (GSK3beta) activity or ex

127 ver, hypoinsulinemia leads to an increase in glycogen synthase kinase 3beta (GSK3beta) activity that,

128 ssociated with insulin resistance, decreased glycogen synthase kinase 3beta (GSK3beta) activity, acti

129 (NF-kappaB) pathway and in the induction of glycogen synthase kinase 3beta (GSK3beta) activity, resu

130 of beta-catenin by enhancing binding between glycogen synthase kinase 3beta (GSK3beta) and beta-caten

131 tcome on different molecular targets such as glycogen synthase kinase 3beta (GSK3beta) and Forkhead b

132 Cellular targets of Li(+), such as glycogen synthase kinase 3beta (GSK3beta) and G proteins

133 Unexpectedly, RNAi-mediated silencing of glycogen synthase kinase 3beta (GSK3beta) and phosphoino

134 oteasomal degradation via phosphorylation by glycogen synthase kinase 3beta (GSK3beta) and recognitio

135 ted protein kinase kinase 4 (MKK4), JNK, and glycogen synthase kinase 3beta (GSK3beta) and thereby de

136 (APC), casein kinase 1alpha (CK1alpha), and glycogen synthase kinase 3beta (GSK3beta) and undergoes

137 In silico kinase prediction revealed glycogen synthase kinase 3beta (GSK3beta) as the most li

138 TGF-beta1 expression and hyperacetylation of glycogen synthase kinase 3beta (GSK3beta) at residue K15

139 ects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing s

140 Glycogen synthase kinase 3beta (GSK3beta) has been shown

141 quent signaling, causing overt activation of glycogen synthase kinase 3beta (GSK3beta) in nerves of m

142 synthesis is associated with inactivation of glycogen synthase kinase 3beta (GSK3beta) in renal cells

143 A member of this family is glycogen synthase kinase 3beta (GSK3beta) interaction pr

144 We show that glycogen synthase kinase 3beta (GSK3beta) interacts with

145 Glycogen synthase kinase 3beta (GSK3beta) is a constitut

146 Inhibition of glycogen synthase kinase 3beta (GSK3beta) is a shared ac

147 At low glucose levels, glycogen synthase kinase 3beta (GSK3beta) is known to ph

148 of TGF-beta receptors and p38 MAPK increased glycogen synthase kinase 3beta (GSK3beta) phosphorylatio

149 In this study, we demonstrate that glycogen synthase kinase 3beta (GSK3beta) regulates ST2L

150 d by the core clock oscillator BMAL1 and AKT/glycogen synthase kinase 3beta (GSK3beta) signaling path

151 [e.g., strong bias toward phosphorylation of glycogen synthase kinase 3beta (GSK3beta) via the full-l

152 kt, mammalian target of rapamycin complex 1, glycogen synthase kinase 3beta (GSK3beta), and CREB.

153 e IGF-I, IGF binding protein-1 (IGFBP-1) and glycogen synthase kinase 3beta (GSK3beta), as one major

154 Psychotropic medications target glycogen synthase kinase 3beta (GSK3beta), but the funct

155 ivation, which results in hyperactivation of glycogen synthase kinase 3beta (GSK3beta), followed by p

156 The phosphorylation is catalyzed by glycogen synthase kinase 3beta (GSK3beta), ultimately re

157 hic signaling intermediates, such as Akt and glycogen synthase kinase 3beta (GSK3beta), were dephosph

158 y sites in the N-terminus of beta-catenin as glycogen synthase kinase 3beta (GSK3beta), which are rec

159 dent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase 3beta (GSK3beta), which is medi

160 PI exposure abrogated glycogen synthase kinase 3beta (GSK3beta)-mediated degra

161 1 interacts with Nrf2 and stabilizes it from glycogen synthase kinase 3beta (GSK3beta)-mediated phosp

162 FN signaling pathways occurs at the point of glycogen synthase kinase 3beta (GSK3beta)-TANK-binding k

163 g protein binding protein kinase A (PKA) and glycogen synthase kinase 3beta (GSK3beta).

164 These include protein kinase A (PKA) and glycogen synthase kinase 3beta (GSK3beta).

165 ivation and this occurs in part by targeting glycogen synthase kinase 3beta (GSK3beta).

166 inhibition of the tumor suppressors PTEN and glycogen synthase kinase 3beta (GSK3beta).

167 n (mTOR) signaling pathway and inhibition of glycogen synthase kinase 3beta (GSK3beta).

168 t VRK2 activity was negatively controlled by glycogen synthase kinase 3beta (GSK3beta).

169 atty acids, and this suppression depended on glycogen synthase kinase 3beta activation and induction

170 au phosphorylation and solubility, increased glycogen synthase kinase 3beta activity, compromised lon

171 protein that plays a key role in attenuating glycogen synthase kinase 3beta activity, leading to aber

172 2A and recruits protein phosphatase 2A with glycogen synthase kinase 3beta and beta-catenin, inducin

173 Glycogen synthase kinase 3beta and Foxo1 are two PI-3K-r

174 isms involved demonstrate that ASPH binds to glycogen synthase kinase 3beta and inhibits its subseque

175 ibition of ASPH activity, phosphorylation of glycogen synthase kinase 3beta and p16 expression were i

176 reasing Ser9 phosphorylation-inactivation of glycogen synthase kinase 3beta by RBMY, thereby impeding

177 ted with release of the inhibitory effect of glycogen synthase kinase 3beta function by decreasing Se

178 in, and that beta-catenin activation through glycogen synthase kinase 3beta inhibition leads to FANCC

179 decreased DJ-1 and increased phosphorylated glycogen synthase kinase 3beta levels may account for im

180 Wnt/beta-catenin pathway by inactivation of glycogen synthase kinase 3beta of NKT cells.

181 ment, and reduced Akt (protein kinase B) and glycogen synthase kinase 3beta phosphorylation.

182 increase in phospho-beta-catenin and active glycogen synthase kinase 3beta, a kinase known to target

183 t3a (the canonical activator), inhibitors of glycogen synthase kinase 3beta, and small-interfering RN

184 Akt murine thymoma viral oncogene homolog-1, glycogen synthase kinase 3beta, cyclin-dependent kinase

185 Downstream of glycogen synthase kinase 3beta, cytoplasmic linker-assoc

186 ver, inhibition of protein phosphatase 1 and glycogen synthase kinase 3beta, downstream targets of Ca

187 ced tumor growth, induced phosphorylation of glycogen synthase kinase 3beta, enhanced p16 expression

188 n showed AQP1 interaction with beta-catenin, glycogen synthase kinase 3beta, LRP6, and Axin1.

189 of cyclin-dependent protein kinase 5 (Cdk5), glycogen synthase kinase 3beta, protein phosphatase 1, o

190 e kinase 3beta by RBMY, thereby impeding the glycogen synthase kinase 3beta-dependent degradation of

191 Molecularly, ROCK inhibition induced glycogen synthase kinase 3beta-dependent phosphorylation

192 ta-catenin expression and stabilization in a glycogen synthase kinase 3beta-independent manner.

193 ) transcriptional activity via inhibition of glycogen synthase kinase 3beta.

194 7, p38 mitogen-activated protein kinase, and glycogen synthase kinase 3beta.

195 Apc participates in a complex that includes glycogen synthase kinase beta (Gsk3beta) and betacatenin

196 Here we show that the glycogen synthase kinase beta (GSK3beta) expression is e

197 In a previous study, the FGK3 glycogen synthase kinase gene orthologous to mammalian G

198 A point mutation in a putative glycogen synthase kinase phosophorylation site within th

199 lates alcohol-induced BK internalization via glycogen synthase kinase phosphorylation.

200 f lithium, in which fine-tuned regulation of glycogen synthase kinase type 3, a prime target for lith

201 sly showed that the serine/threonine kinase, glycogen synthase kinase, GSK-3alpha/beta, is a central

202 The glycogen synthase kinase-3 (GSK-3) family of serine/thre

203 The role of glycogen synthase kinase-3 (GSK-3) in Alzheimer disease

204 The challenge for glycogen synthase kinase-3 (GSK-3) inhibitor design lies

205 Combining glycogen synthase kinase-3 (GSK-3) inhibitors with VPA o

206 Glycogen synthase kinase-3 (GSK-3) is a constitutively a

207 Glycogen synthase kinase-3 (Gsk-3) is a key regulator of

208 Glycogen synthase kinase-3 (GSK-3) is a key regulator of

209 Glycogen synthase kinase-3 (GSK-3) is one of the few sig

210 Glycogen synthase kinase-3 (GSK-3) regulates multiple ce

211 de et al. uses phosphoproteomics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse e

212 DydA is phosphorylated by glycogen synthase kinase-3 (GSK-3), which is required fo

213 together with inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3), which relieves its i

214 Predictably, inhibition of glycogen synthase kinase-3 (GSK-3), which results from a

215 ling events that result in the inhibition of glycogen synthase kinase-3 (GSK-3)beta represent an adap

216 ositol-3 kinase/Akt (IRS-PI3K-Akt) pathways, glycogen synthase kinase-3 (GSK3) and mammalian target o

217 T3 signaling, and simultaneous inhibition of glycogen synthase kinase-3 (GSK3) and MAP kinase/ERK kin

218 Glycogen synthase kinase-3 (GSK3) are ubiquitously expre

219 haracterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids p

220 The glycogen synthase kinase-3 (GSK3) family kinases are cen

221 Treatment with lithium or a glycogen synthase kinase-3 (GSK3) inhibitor corrects beh

222 ia containing fetal bovine serum (FBS) and a glycogen synthase kinase-3 (GSK3) inhibitor, and in seru

223 Here, we report that glycogen synthase kinase-3 (GSK3) is a critical determin

224 Hippocampal glycogen synthase kinase-3 (GSK3) is hyperactive in the

225 gated the effect of inhibitors targeting the glycogen synthase kinase-3 (GSK3) on the expression of N

226 Moreover, induction of glycogen synthase kinase-3 (GSK3) performed using a Wnt

227 Glycogen synthase kinase-3 (GSK3) regulates many physiol

228 rrent study, we tested whether inhibitors of glycogen synthase kinase-3 (GSK3), previously reported t

229 ogenesis, immunomodulation and regulation of glycogen synthase kinase-3 activity.

230 lian target of rapamycin signaling, glucose, glycogen synthase kinase-3 and liver kinase B1, protein

231 ardiomyocytes in early developmental stages, glycogen synthase kinase-3 and p38 mitogen-activated pro

232 Next, we apply this strategy to study glycogen synthase kinase-3 beta (GSK-3beta), a kinase ab

233 drogenase kinase-1, or its downstream target glycogen synthase kinase-3 did not prevent CCR9 expressi

234 Glycogen synthase kinase-3 is a Ser/Thr kinase, tonicall

235 enhanced risk for SZ and/or BD can activate glycogen synthase kinase-3 isozymes (GSK3alpha and beta)

236 The glycogen synthase kinase-3 of the parasite (PfGSK-3) was

237 Pharmacological inhibition of glycogen synthase kinase-3 was sufficient to reverse the

238 , while application of Bikinin (inhibitor of glycogen synthase kinase-3), which activated BR signalin

239 lations of AMPK, acetyl CoA carboxylase, and glycogen synthase kinase-3, decreased glycogen synthase

240 to ERK1/2 and Akt, including p70 S6-kinase, glycogen synthase kinase-3, ribosomal S6 kinase, c-Jun,

241 hium chloride, a reversible inhibitor of the glycogen synthase kinase-3, that rescued NMJ defects in

242 lation primes for Ser-159 phosphorylation by glycogen synthase kinase-3.

243 m of this study was to determine the role of glycogen synthase kinase-3alpha (GSK-3alpha) in post-MI

244 rexpression of TDP-43 leads to activation of glycogen synthase kinase-3beta (GSK-3beta) and that GSK-

245 dated AD targets beta-secretase (BACE-1) and glycogen synthase kinase-3beta (GSK-3beta) by attacking

246 In addition, application of glycogen synthase kinase-3beta (GSK-3beta) inhibitor com

247 etin, reactivation of beta-catenin using the glycogen synthase kinase-3beta (GSK-3beta) inhibitor LiC

248 Herein we report that glycogen synthase kinase-3beta (GSK-3beta) is phosphoryl

249 sis coli tumor suppressor protein (APC), and glycogen synthase kinase-3beta (GSK-3beta), which could

250 atocytes, which led to a delayed increase in glycogen synthase kinase-3beta (GSK-3beta)-mediated hepa

251 demonstrate that alcohol intake also blocks glycogen synthase kinase-3beta (GSK-3beta)-phosphorylati

252 ein function are via a pathway that involves glycogen synthase kinase-3beta (GSK-3beta).

253 teins, which were predicted to be targets of glycogen synthase kinase-3beta (GSK-3beta).

254 hase and the phosphorylation (inhibition) of glycogen synthase kinase-3beta (GSK-3beta).

255 hase and the phosphorylation (inhibition) of glycogen synthase kinase-3beta (GSK-3beta).

256 Glycogen synthase kinase-3beta (GSK3beta) activity is in

257 nted pre-synaptic protein deficit, decreased glycogen synthase kinase-3beta (GSK3beta) activity, and

258 finding is the pronounced downregulation of glycogen synthase kinase-3beta (Gsk3beta) and upregulati

259 Glycogen synthase kinase-3beta (GSK3beta) has diverse bi

260 Here we demonstrate that hyperactivity of glycogen synthase kinase-3beta (GSK3beta) in the atrium

261 While glycogen synthase kinase-3beta (GSK3beta) is known to pa

262 Glycogen synthase kinase-3beta (GSK3beta) plays a critic

263 uclear Nrf2 export/degradation machinery via glycogen synthase kinase-3beta (Gsk3beta) signaling was

264 lted in increased phosphorylation of Akt and glycogen synthase kinase-3beta (GSK3beta), leading to en

265 tion and insulin secretion via regulation of glycogen synthase kinase-3beta (GSK3beta).

266 s (ankyrin G, EB1) were knocked down or when glycogen synthase kinase-3beta (GSK3beta; an AD-associat

267 panied by hyperphosphorylation of substrates glycogen synthase kinase-3beta and mammalian target of r

268 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa

269 hase survival pathway, and the inhibition of glycogen synthase kinase-3beta and nuclear factor kappa

270 ion and completely blocked the inhibition of glycogen synthase kinase-3beta gene transcription.

271 Overexpression of Snail1 and inhibition of glycogen synthase kinase-3beta in colorectal tumor cells

272 Such glycogen synthase kinase-3beta inactivation causes chang

273 erentiated hPSCs into mesoderm cells using a glycogen synthase kinase-3beta inhibitor for 3 days, the

274 mbinant Wnt3a protein or CHIR-99021 (CHIR, a glycogen synthase kinase-3beta inhibitor) caused a dose-

275 L is stabilized in a complex with axin1 when glycogen synthase kinase-3beta is overexpressed.

276 ha/wrd pathway in the motoneuron antagonizes glycogen synthase kinase-3beta kinase activity to preven

277 on of GABAergic transmission via D2 receptor-glycogen synthase kinase-3beta signaling dramatically re

278 The phosphorylation and inactivation of glycogen synthase kinase-3beta was dependent on mammalia

279 l as by inhibition of the Akt-GSK-3beta (Akt-glycogen synthase kinase-3beta) pathway.

280 orylation of the inhibitory Ser-9 residue of glycogen synthase kinase-3beta, a primary Tau kinase inv

281 ollowed by phosphorylation (inactivation) of glycogen synthase kinase-3beta, at least in part via STA

282 cyclin D1, E-cadherin, beta-catenin, Dvl-1, glycogen synthase kinase-3beta, axin-1, and adenomatous

283 no changes in Ctnnb1 expression, activity of glycogen synthase kinase-3beta, known to phosphorylate a

284 activator of beta-catenin via inhibition of glycogen synthase kinase-3beta, reversed the inhibition

285 on, and increased phosphorylation of Akt and glycogen synthase kinase-3beta, ultimately resulting in

286 d to the phosphorylation and inactivation of glycogen synthase kinase-3beta, which resulted in inhibi

287 inding (CREB) protein levels to decreaseviaa glycogen synthase kinase-3beta-dependent mechanism.

288 pstream signaling pathways known to regulate glycogen synthase kinase-3beta.

289 ial-mesenchymal transition by repressing AKT/glycogen synthase kinase-3beta/beta-catenin signaling.

290 nalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3beta, in maternal liver (P < 0

291 ological or genetic inhibition of tau kinase glycogen-synthase-kinase-3beta (GSK-3beta).

292 ntify the Arabidopsis (Arabidopsis thaliana) GLYCOGEN SYNTHASE KINASE3 (GSK3)/Shaggy-like kinase ASKa

293 nt link between phosphoinositol-3-kinase and glycogen synthase kinase3 and demonstrates the potential

294 athway has many downstream targets including glycogen synthase kinase3 which is a major regulatory ki

295 lucan synthesis (via expression of bacterial glycogen synthase) or by increasing the volumes of indiv

296 e, and glycogen synthase kinase-3, decreased glycogen synthase phosphorylation, and increased the int

297 b The Ppp1r3b deletion significantly reduced glycogen synthase protein abundance, and the remaining p

298 of glycogenin-1 or impaired interaction with glycogen synthase underlies this new form of glycogen st

299 50% lower, and the amount of phosphorylated glycogen synthase was 34% lower, indicating activation o

300 NMR studies of UDP-Glc hydrolysis by yeast glycogen synthase were used to verify the stereochemistr