ライフサイエンスコーパス: GSK-3

1 kinase (ERK) and glycogen synthase kinase 3 (GSK-3).

2 /threonine kinase Shaggy (Sgg; also known as GSK-3).

3 ed inhibitors of glycogen synthase kinase-3 (GSK-3).

4 PP, showed reduced levels in the presence of GSK-3.

5 RK and limit the activity of another kinase, GSK-3.

6 targeted for degradation in the presence of GSK-3.

7 phosphorylated by the combination of ERK and GSK-3.

8 omparable cellular effectiveness on 5-LO and GSK-3.

9 of Thr-72 by the exogenous activating kinase GSK-3.

10 al protein, 4E-BP1, IRS-1, Akt, ERK-1/2, and GSK-3.

11 ective for a subset of pathways regulated by GSK-3.

12 activation of PP-1I phosphatase activity by GSK-3.

13 nduced phosphorylation of Rho-GDP at S192 by GSK-3.

14 with small interfering RNA (siRNA) targeting GSK-3.

15 pts the complex through direct inhibition of GSK-3.

16 in-2/Akt/PP2A complex by directly inhibiting GSK-3.

17 apid expansion of drug development targeting GSK-3.

18 predicted sites increased upon inhibition of GSK-3.

19 eam regions of 75% of the genes regulated by GSK-3.

20 h sustained MKP-1 phosphorylation induced by GSK-3.

21 4%) whose levels decreased in the absence of GSK-3.

22 zheimer's disease-relevant major tau kinase, GSK-3.

23 d to the ability of this agent to inactivate GSK-3.

24 cyclase, activating PKA/CREB, and inhibiting GSK-3.

25 arA function is JAK-independent but requires GSK-3, a key regulator of metabolism and development.

26 pacity to block BCR-mediated inactivation of GSK-3, a major negative regulator of Mcl-1.

27 induce APC dissociation from Axin to reduce GSK-3 activity and activate downstream signaling.

28 cells (mESCs), providing a broad profile of GSK-3 activity and defining a new role for this central

29 Because CREB and GSK-3 activity appeared to be important for ET-induced A

30 ion of target serines and drug inhibition of GSK-3 activity coordinately induce both forward transpor

31 oring their biological significance, altered Gsk-3 activity has been implicated in diabetes, Alzheime

32 Thus, GSK-3 activity in DC is regulated via signaling linked t

33 ese results indicate that the high levels of GSK-3 activity in quiescent cells repress gene expressio

34 Our data demonstrate the importance of Gsk-3 activity in the maintenance of DNA methylation at

35 Significantly, inhibition of GSK-3 activity or exogenous expression of the GSK-3 subs

36 We examined the effect of these mutations on GSK-3 activity toward Tau, activity in Wnt signaling, in

37 n of ANTXR in macrophages was decreased when GSK-3 activity was disrupted with chemical inhibitors or

38 tes multiple signaling pathways by enhancing GSK-3 activity, and that Wnts induce APC dissociation fr

39 o-receptors LRP5/6, and these motifs inhibit GSK-3 activity.

40 We find that APC directly enhances GSK-3 activity.

41 f the CRE reporter was decreased by reducing GSK-3 activity.

42 f Akt to phosphorylate, and thereby suppress GSK-3 activity.

43 wn-regulation of glycogen synthase kinase-3 (GSK-3) activity and could not be ascribed to enhanced Ak

44 manipulation of glycogen synthase kinase-3 (GSK-3) activity.

45 n suggested that glycogen synthase kinase 3 (GSK-3) acts as an integrating molecule for multiple prol

46 It proved to be a selective inhibitor of GSK-3 against a panel of 17 kinases and showed >10-fold

47 ut the specific contributions of each of the GSK-3 alpha and beta isoforms to mechanisms of AD have n

48 GSK-3 alpha/beta inactivation in the tumors in vivo and

49 tion, glycogen synthase kinase-3 alpha/beta (GSK-3 alpha/beta) inactivation, and cytoplasmic localiza

50 XIN1, or treating cells with an inhibitor of GSK-3 also enhanced melanoma cell sensitivity to TRAIL.

51 APC regulation of GSK-3 also provides a novel mechanism for Wnt regulation

52 served protein kinase-encoding genes yielded gsk-3 (an ortholog of human GSK3B) and cdk-2 (a CDK2-rel

53 a of APC helping direct interactions between GSK-3 and C/EBP beta.

54 tion but does not bypass the requirement for gsk-3 and cdk-2 This analysis supports a model whereby M

55 but also shed light on interactions between GSK-3 and CREB pathways in host immune cells.

56 effects of lithium and VPA are mediated via GSK-3 and HDAC inhibition, respectively.

57 can be attributed to its dual inhibition of GSK-3 and HGK kinases.

58 both PI3K/Akt and PKA signaling inactivated GSK-3 and increased beta-catenin translocation.

59 currently available medications that target GSK-3 and mTOR, and provide a compelling explanation for

60 d downstream molecular targets converging on GSK-3 and suggest a new mechanism to disrupt cocaine neu

61 how what we believe to be a new link between GSK-3 and the beta-arrestin-2 complex in mice and propos

62 Further study of Akt/GSK-3 and Wnt signaling may ultimately lead to alternati

63 The authors review evidence that Akt/GSK-3 and Wnt-related pathways are involved in the patho

64 E(2) inactivated glycogen synthase kinase 3 (GSK-3) and promoted nuclear localization and accumulatio

65 g focused on Akt/glycogen synthase kinase-3 (GSK-3) and wingless (Wnt) signaling pathways, which have

66 onophosphatases, glycogen synthase kinase-3 (GSK-3), and a beta-arrestin-2/AKT/protein phosphatase 2A

67 action of at least 3 different kinases: CK1, GSK-3, and DYRK.

68 dy in clinical trial target both isoforms of GSK-3, and none are isoform specific.

69 gh modulation of levels and activity of Akt, GSK-3, and Wnt-related intracellular signaling.

70 e pathway can be activated by small-molecule GSK-3 antagonists, resulting in enhanced reparative dent

71 of small molecule glycogen synthase kinase (GSK-3) antagonists that promote the natural processes of

72 gesting that epigenetic changes regulated by Gsk-3 are likely an unrecognized facet of Gsk-3 signalin

73 Here, we identified GSK-3 as a key upstream kinase that regulated PD-1 expre

74 Our findings identify GSK-3 as a regulator of PD-1 expression and demonstrate

75 epidermal melanocytes and identifies ILK and GSK-3 as important modulators of melanin transfer to ker

76 by elevated phosphorylation of both Akt and GSK-3 as well as by the attenuating effect of a specific

77 H-driven medulloblastomas similarly required GSK-3, as co-deleting Gsk3a/b blocked tumor growth in me

78 Prior phosphorylation with GSK-3 at one or more of the adjacent serines substantial

79 progression (CDK1, CDK2, CDK8, CHEK1, CHEK2, GSK-3 beta, NPM, PAK1, PP2C-alpha).

80 he inhibition of glycogen synthase kinase-3 (GSK-3)beta represent an adaptive response that might lim

81 phila homolog of glycogen synthase kinase-3 (GSK-3)beta, Shaggy, is required for ethanol-induced apop

82 atocellular carcinoma cells mediated through GSK-3-beta activation, and enhancement of protein degrad

83 e found that rhubarb suppressed the p-ser(9) GSK-3-beta protein level to inactivate Wnt signalling an

84 ist function more generally, is regulated by GSK-3-beta-mediated phosphorylation of conserved sites i

85 GSK-3 binds to and directly phosphorylates SRF on a high

86 We present crystal structures of GSK-3 bound to its phosphorylated N-terminus and to two

87 K-3 phosphoproteome and strong evidence that GSK-3 broadly regulates alternative splicing.

88 evidence that mTOR is a target activated by GSK-3 but inhibited by impaired lysosomal acidification

89 herefore hypothesized that Wnts may regulate GSK-3 by disrupting the interaction between APC and the

90 Beta isoform-specific inhibition of GSK-3 by dominant negative GSK-3beta in transgenic mice

91 We show that inhibition of Gsk-3 by phosphatidylinositol 3-kinase (PI3K)-mediated a

92 rmore, knockdown of APC mimics inhibition of GSK-3 by reducing phosphorylation of glycogen synthase a

93 Effector mimicry of gp130 suggests GSK-3 can regulate normal cytokine signaling, potentiall

94 ing the interaction between APC and the Axin-GSK-3 complex.

95 e been predicted on the basis of a recurrent GSK-3 consensus motif ((pS/pT)XXX(S/T)), but this predic

96 evidence that Mck1 directly phosphorylates a GSK-3 consensus site in the C-terminus of Cdc6.

97 show that mammalian target of rapamycin and GSK-3 cooperate to control the activity of S6K1, an impo

98 We demonstrate that inhibition of GSK-3 dampens ET-induced maturation and migration proces

99 printed loci have reduced DNA methylation in Gsk-3-deficient ESCs.

100 GSK-3 deletion resulted in massive hyperproliferation of

101 90 genes that are alternatively spliced in a GSK-3-dependent manner, supporting a broad role for GSK-

102 pS/pT)XXX(S/T) sites are phosphorylated in a GSK-3-dependent manner.

103 d MS techniques to analyze the repertoire of GSK-3-dependent phosphorylation in mouse embryonic stem

104 knock-out (Gsk3 DKO) ESCs revealed prominent GSK-3-dependent phosphorylation of multiple splicing fac

105 Finally, we find that N-Myc is a potent Gsk-3-dependent regulator of Dnmt3a2 expression.

106 stigated a role for APC in the regulation of GSK-3-dependent signaling.

107 Furthermore, many of the Gsk-3-dependent, differentially methylated regions (DMRs

108 est that beta isoform-specific inhibition of GSK-3 exacerbates ischemic injury but protects against I

109 conserved kinases of the LAMMER/Cdc-like and GSK-3 families function downstream of TOR complex 1 to r

110 A polymerase III subunit Rpc53 by a specific GSK-3 family member, Mck1.

111 The glycogen synthase kinase-3 (GSK-3) family of serine/threonine kinases consists of 2

112 The glycogen synthase kinase-3 (GSK-3) family of serine/threonine kinases regulates seve

113 thway that could be targeted at the level of GSK-3, Fbw7, or USP28 to influence HIF-1alpha-dependent

114 Our results demonstrate that GSK-3 function is essential for chemotaxis, regulating m

115 onserved sequence near the amino terminus of GSK-3 generates an auto-inhibitory peptide.

116 ns, blocked cortical downregulation of local GSK-3 (glycogen synthase kinase 3) and Akt signaling pat

117 blocked THC-induced downregulation of local GSK-3 (glycogen synthase kinase 3) and Akt signaling pat

118 analysis supports a model whereby MPK-1/ERK, GSK-3/GSK3 and CDK-2/CDK2, along with SEL-10/FBXW7, cons

119 As GSK-3 has the ability to phosphorylate primed substrates

120 The glycogen synthase kinase-3 (GSK-3) has been linked to the pathogenesis of colorectal

121 genetic and pharmacological manipulations of GSK-3 have identified more than 100 putative GSK-3 subst

122 We previously showed that a yeast GSK-3 homologue, Mck1 kinase, promotes Cdc6 degradation

123 Being less active on GSK-3 homologues of other species, the title compounds s

124 of a related molecule in complex with human GSK-3 (HsGSK-3), a model was computed for the comparison

125 We also report that inhibition of GSK-3 impedes the ability of LPS-stimulated DCs to induc

126 as the first small molecules able to inhibit GSK-3 in a substrate competitive manner.

127 To study the role of GSK-3 in Abeta pathology, we used 5XFAD mice co-expressi

128 Mechanistically, loss of GSK-3 in adult cardiac myocytes resulted in induction of

129 s several of these pathways, but the role of GSK-3 in aging is unknown.

130 Activation of GSK-3 in Keap1-null mouse embryonic fibroblasts (MEFs),

131 e findings identify unexpected functions for GSK-3 in mouse HSC homeostasis, suggest a therapeutic ap

132 hat deleted both the alpha and beta forms of GSK-3 in mouse neural progenitors.

133 Furthermore, inhibition of GSK-3 in quiescent cells resulted in activation of Ikapp

134 ependent manner, supporting a broad role for GSK-3 in regulating alternative splicing.

135 The requirement for GSK-3 in SHH-driven proliferation suggests that GSK-3 ma

136 quiescent T98G cells solely by inhibition of GSK-3 in the absence of growth factor stimulation.

137 al for discovery of radiopharmaceuticals for GSK-3 in the central nervous system.

138 of NF-kappaB is consistent with the role of GSK-3 in the induction of apoptosis or cell cycle arrest

139 Recently we described a novel role for Gsk-3 in the regulation of DNA methylation at imprinted

140 The role of glycogen synthase kinase-3 (GSK-3) in Alzheimer disease pathogenesis has been debate

141 GSK-3 inactivation by PKB abrogates phosphorylation of C

142 Mechanistically, GSK-3 inactivation increased Tbx21 transcription, promot

143 s degraded after glycogen synthase kinase-3 (GSK-3)-induced phosphorylation and recruitment of the ub

144 GSK-3-induced MKP-1 phosphorylation mediates negative fe

145 axonal growth deficits of SRF-deficient and GSK-3-inhibited neurons.

146 LY294002 (50 microM) eliminated EGF-induced GSK-3 inhibition and Erk1/2 phosphorylation as well as i

147 l strategy for 5-LO targeting, and dual 5-LO/GSK-3 inhibition as an unconventional and promising conc

148 Axonal growth deficits caused by GSK-3 inhibition could be rescued by expression of a con

149 so required for normal melanin transfer, and GSK-3 inhibition in melanocytes partially restored melan

150 gent C terminus may lead to isoform-specific GSK-3 inhibition through destabilization of the GSK-3 st

151 ssociated with enhanced Akt-1 activation and GSK-3 inhibition.

152 thium-induced Akt-1 activation and augmented GSK-3 inhibition.

153 on; conversely pretreatment with a selective GSK-3 inhibitor and shRNA GSK-3beta knockdown restored M

154 Here we show that the GSK-3 inhibitor AR-A014418 regulated alpha-amino-3-hydro

155 etamine combined with lithium or a selective GSK-3 inhibitor are equivalent to higher doses of ketami

156 a by CCCP and by the induction of PRC by the GSK-3 inhibitor AZD2858.

157 The GSK-3 inhibitor CHIR-98014 similarly downregulated SHH-d

158 uated by simultaneous pre-treatment with the GSK-3 inhibitor CT99021.

159 Tideglusib is a GSK-3 inhibitor currently in phase II clinical trials fo

160 e transfer of T cells treated ex vivo with a GSK-3 inhibitor delayed the onset of EL4 lymphoma growth

161 catenin signaling activity by small-molecule GSK-3 inhibitor drugs following pulp exposure in mouse m

162 fects observed in individuals prescribed the GSK-3 inhibitor lithium.

163 A GSK-3 inhibitor reduced basal NHE3 activity as well as e

164 GSK-3 inhibitor trials suggest that Wnt/beta-catenin or

165 gle dose of lithium chloride (a nonselective GSK-3 inhibitor) or a preferential GSK-3beta inhibitor;

166 the adenosine triphosphate (ATP)-competitive GSK-3 inhibitor, CHIR99021 (CHIR), and the ATP noncompet

167 t of WT cardiomyocytes with a small molecule GSK-3 inhibitor, confirming that the response was not du

168 XFAD mice with a novel substrate competitive GSK-3 inhibitor, L803-mts, reduced Abeta deposits and am

169 ic stem cells and neural stem cells with the Gsk-3 inhibitor, lithium, phenocopies the DNA hypomethyl

170 he challenge for glycogen synthase kinase-3 (GSK-3) inhibitor design lies in achieving high selectivi

171 pamycin, and the glycogen synthase kinase-3 (GSK-3) inhibitor lithium act additively to increase long

172 Lithium, a glycogen synthase kinase-3 (GSK-3) inhibitor, and VPA, a histone deacetylase (HDAC)

173 FAS ligand neutralization, caspase and GSK-3 inhibitors and GSK-3beta siRNA were applied to fur

174 The scorpion shaped GSK-3 inhibitors developed by our group achieved the hig

175 Injection of GSK-3 inhibitors in mice increased in vivo CD8(+) OT-I C

176 ression and demonstrate the applicability of GSK-3 inhibitors in the modulation of PD-1 in immunother

177 sting that anti-invasive glioma therapy with GSK-3 inhibitors in vivo not only inhibits invasion of t

178 The possible mitigation by GSK-3 inhibitors of the eventual fading of ketamine's an

179 Here we show that GSK-3 inhibitors of the indirubin family reduce invasion

180 GSK-3 inhibitors or loss of one copy of the Gsk3b gene r

181 the molecular mechanisms of both lithium and GSK-3 inhibitors remain unclear.

182 Overall, our findings show how GSK-3 inhibitors that downregulate PD-1 expression can e

183 bodies.Significance: These findings show how GSK-3 inhibitors that downregulate PD-1 expression can e

184 The GSK-3 inhibitors were further profiled for efficacy and

185 GSK-3 inhibitors, including LiCl, SB 216743, and BIO, ab

186 des that are potent, highly kinase-selective GSK-3 inhibitors, the members of which demonstrated oral

187 the bisindole core of indirubin, present in GSK-3 inhibitors, to innovatively target 5-LO at the ATP

188 ATP-binding site for the design of dual 5-LO/GSK-3 inhibitors.

189 the identification of novel scorpion shaped GSK-3 inhibitors.

190 Like lithium, glycogen synthase kinase 3 (GSK-3) inhibitors display both antimanic-like and antide

191 Combining glycogen synthase kinase-3 (GSK-3) inhibitors with VPA or histone deacetylase (HDAC)

192 a was blocked by glycogen synthase kinase 3 (GSK-3) inhibitors, suggesting that GSK-3 is involved in

193 ere we show that glycogen synthase kinase 3 (GSK-3) interacts with and phosphorylates UNG2 at Thr(60)

194 Activation of glycogen synthase kinase-3 (GSK-3) interferes with microtubule assembly.

195 e beta-arrestin complex and demonstrate that GSK-3 is a critical target of lithium in mammalian behav

196 Taken together, our data indicate that GSK-3 is a player in Abeta pathology.

197 GSK-3 is a serine-threonine kinase involved in diverse c

198 GSK-3 is a serine/threonine kinase that has numerous sub

199 GSK-3 is active in the absence of growth factor stimulat

200 GSK-3 is an essential mediator of several signaling path

201 Unlike most kinases, GSK-3 is controlled by inhibition rather than by specifi

202 We unexpectedly found that cardiac myocyte GSK-3 is essential for cardiac homeostasis and overall s

203 kinase 3 (GSK-3) inhibitors, suggesting that GSK-3 is involved in the activation of C/EBP beta and su

204 lation of CM-specific genes, suggesting that GSK-3 is necessary and sufficient for CM differentiation

205 r, our findings suggest that cardiac myocyte GSK-3 is required to maintain normal cardiac homeostasis

206 The inactivation of GSK-3 is thought to decrease the probability of opening

207 Glycogen synthase kinase-3 (GSK-3) is a constitutively active, ubiquitously expresse

208 Glycogen synthase kinase-3 (GSK-3) is a key regulator of many cellular signaling pat

209 Glycogen synthase kinase-3 (Gsk-3) is a key regulator of multiple signal transductio

210 ly supports that glycogen synthase kinase-3 (GSK-3) is a pathogenic molecule when it is up-dysregulat

211 Glycogen synthase kinase-3 (GSK-3) is essential for many signaling pathways and cell

212 to determine if glycogen synthase kinase 3 (GSK-3) is important for ET-induced modulation of macroph

213 Glycogen synthase kinase-3 (GSK-3) is increasingly recognized as a major contributor

214 Glycogen synthase kinase-3 (GSK-3) is linked to the pathogenesis of Alzheimer's dise

215 Glycogen synthase kinase-3 (GSK-3) is one of the few signaling molecules that regula

216 remains unknown about the function of either GSK-3 isoform in the postnatal heart.

217 e understanding of the mechanistic basis for GSK-3 isoform-specific functions could lead to the devel

218 e cardiac myocyte-specific mice lacking both GSK-3 isoforms (double knockout).

219 ted the noncatalytic N and C termini in both GSK-3 isoforms and generated point mutations of key regu

220 GSK-3 isoforms function redundantly in some settings, wh

221 We will highlight the role of the GSK-3 isoforms in various pathological conditions includ

222 We found that the N termini of both GSK-3 isoforms were dispensable, whereas progressive C-t

223 nvestigation into the physiological roles of GSK-3 isoforms, the basis for their differential activit

224 Glycogen synthase kinase-3 (Gsk-3) isoforms, Gsk-3alpha and Gsk-3beta, are constitut

225 Glycogen synthase kinase-3 (GSK-3) isoforms, GSK-3alpha and GSK-3beta, are serine/th

226 Glycogen synthase kinase 3 (GSK-3, isoforms alpha and beta) is a serine-threonine ki

227 Both GSK-3 isozymes (alpha/beta) were hyperactive in this mod

228 to involve the Cdc-like kinase Kns1 and the GSK-3 kinase Mck1.

229 NHE3-Ser(526) is predicted to be a GSK-3 kinase phosphorylation site.

230 , which converge through the inactivation of GSK-3, leading to the increase in nuclear accumulation o

231 es and kinase families, including ATM, CDKs, GSK-3, MAPKs, PKA, PKB, PKC, and SRC.

232 -3 in SHH-driven proliferation suggests that GSK-3 may be targeted for SHH-driven medulloblastoma the

233 Inhibition of GSK-3 may be useful in treating a number of diseases inc

234 onstrating physiological control of CGNPs by GSK-3, mediated through WNT.

235 loci in ESCs and emphasize the importance of Gsk-3-mediated signal transduction in the epigenome.

236 overcome the two major obstacles for imaging GSK-3, namely, reasonable brain permeability and displac

237 indings suggest that indirubin inhibition of GSK-3 offers a novel treatment paradigm to target 2 of t

238 r ET-induced ANTXR expression, the impact of GSK-3 on ET-induced CREB activity was examined in RAW 26

239 Our data show that the protein kinase GSK-3, one of the first targets identified for PKB, cata

240 n stimulation of the phosphorylation of Akt, GSK-3 or S6 in skeletal muscle, liver and heart.

241 ketamine, indicating the pivotal role of the GSK-3 pathway in modulating the synaptogenic and antidep

242 ether, these data indicate that the PI3K-PKB-GSK-3 pathway is a novel regulatory axis that is importa

243 ylase (HDAC) and glycogen synthase kinase-3 (GSK-3) pathways, which caused transcriptional downregula

244 provides the first unbiased analysis of the GSK-3 phosphoproteome and strong evidence that GSK-3 bro

245 diction has not been tested by analyzing the GSK-3 phosphoproteome.

246 hypersensitive to floxuridine, we show that GSK-3 phosphorylation facilitates UNG2-dependent repair

247 This suggests that GSK-3 phosphorylation of KLC2 led to the dissociation of

248 , two other highly conserved motifs plus the GSK-3 phosphorylation site in RCANs, along with the E3 u

249 DSGIS, but not DSAPGS, contains a functional GSK-3 phosphorylation site.

250 This motif is subject to GSK-3 phosphorylation, promoting ER retention, while mut

251 tics of GflB translocation are fine-tuned by GSK-3 phosphorylation.

252 The conserved glycogen synthase kinase 3 (GSK-3) phosphorylation site was not required for inhibit

253 sis and identified [(11)C]OCM-44 as our lead GSK-3 radiotracer, with optimized brain uptake by PET im

254 Thus, GSK-3 regulated both Wnt and mTOR signaling in mouse HSC

255 Thus, GSK-3 regulates the stability of the beta-arrestin-2/Akt

256 These data suggest that GSK-3 regulates UNG2 and promotes DNA damage repair.

257 Glycogen synthase kinase-3 (GSK-3) regulates multiple cellular processes in diabetes

258 GSK-3 regulation of migration in neurons was independent

259 Inhibition of GSK-3 restores lysosomal acidification that in turn enab

260 was markedly increased upon mutation of two GSK-3 serine phosphorylation sites within the carboxyl-t

261 ow that Oskar is phosphorylated by Par-1 and GSK-3/Shaggy to create a phosphodegron that recruits the

262 Our results indicate that GSK-3 signaling is an essential mediator of homeostatic

263 eins in the mTOR, insulin/IGF-I, ERK1/2, and GSK-3 signaling pathways in placental homogenates and ex

264 PRC and c-MYC can act in concert through Akt-GSK-3 signaling to reprogram gene expression in response

265 by Gsk-3 are likely an unrecognized facet of Gsk-3 signaling.

266 ar calcium levels and activation of PP2B and GSK-3 signaling.

267 GSK-3 siRNA downregulation, or inhibition by small molec

268 Thus, the Par-1/GSK-3/Slimb pathway plays important roles in limiting th

269 GSK-3 specific inhibitors might be promising effective d

270 We discovered substantial ubiquitous GSK-3-specific radioligand binding in Tg2576 Alzheimer's

271 -3 inhibition through destabilization of the GSK-3 structure.

272 The analysis of all available crystallized GSK-3 structures provided a simplified scheme of the rel

273 SK-3 activity or exogenous expression of the GSK-3 substrate collapsin response mediator protein 2 (C

274 ncrease endogenous neurogenesis blocking the GSK-3 substrate site.

275 GSK-3 have identified more than 100 putative GSK-3 substrates in diverse cell types.

276 he assays identified 58 potential ERK-primed GSK-3 substrates, of which 23 had evidence for in vivo p

277 er analysis and were confirmed as ERK-primed GSK-3 substrates.

278 ed a human protein microarray for ERK-primed GSK-3 substrates.

279 mics to identify glycogen synthase kinase-3 (GSK-3) substrates in mouse embryonic stem cells (mESCs),

280 osphorylation of glycogen synthase kinase 3 (GSK-3), suggesting that this pathway is responsible for

281 t consideration because of the fact that all GSK-3-targeted drugs, including the drugs already in cli

282 vel phosphorylation and activation of SRF by GSK-3 that is critical for SRF-dependent axon growth in

283 Wnt signaling inhibits GSK-3 through an unknown mechanism, and this results in

284 sphorylation level of its downstream protein GSK-3 through the canonical WNT4 pathway which involved

285 h is among the most selective antagonists of GSK-3 to date.

286 that SRF is phosphorylated and activated by GSK-3 to promote axon outgrowth in mouse hippocampal neu

287 r the development and use of drugs targeting GSK-3 to treat diseases such as diabetes, cancer, and ag

288 A conserved loop unique to GSK-3 undergoes a dramatic conformational change that cl

289 The negative control of PRC expression by GSK-3 was consistent with the phosphor-inactivation of G

290 65 in gene induction following inhibition of GSK-3 was demonstrated by RNA interference experiments.

291 nd the levels of the phosphorylating enzyme, GSK-3, was raised in drug user brains.

292 hosphorylated by glycogen synthase kinase-3 (GSK-3), which is required for some, but not all, of DydA

293 osphorylation of glycogen synthase kinase-3 (GSK-3), which relieves its inhibitory in influence on mT

294 y, inhibition of glycogen synthase kinase-3 (GSK-3), which results from activation of D2/TAAR1 hetero

295 y sequential effects of two kinases, Akt and GSK-3, which act on a Ser cluster in the same NHE3 C-ter

296 We investigated CGNP regulation by GSK-3, which downregulates proliferation in the forebrai

297 l has validated the feasibility of targeting GSK-3 with small molecule inhibitors for human diseases.

298 riptional regulation of protein abundance by GSK-3, with approximately 47 proteins (1.4%) whose level

299 believe these findings reveal a new role for GSK-3 within the beta-arrestin complex and demonstrate t

300 These data show that a GSK-3/WNT axis modulates the developmental proliferation