ライフサイエンスコーパス: GSK-3

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

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

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

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

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

6 4%) whose levels decreased in the absence of GSK-3.

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

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

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

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

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

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

13 apid expansion of drug development targeting GSK-3.

14 predicted sites increased upon inhibition of GSK-3.

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

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

17 d noticeable inactivating phosphorylation of GSK-3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 t NF-kappaB regulation and further establish GSK-3 and IKK as potential therapeutic targets for pancr

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

55 erapeutic agents that appropriately regulate GSK-3 and mTOR signaling may provide a feasible and avai

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

57 ing, prevent phosphorylation/inactivation of GSK-3 and promote activation of caspase-3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 he regulation of glycogen synthase kinase-3 (GSK-3)/beta-catenin and mTOR signaling represent key com

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 GSK-3 deletion resulted in massive hyperproliferation of

97 90 genes that are alternatively spliced in a GSK-3-dependent manner, supporting a broad role for GSK-

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

99 These data provide new insight into GSK-3-dependent NF-kappaB regulation and further establi

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

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

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

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

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

105 Furthermore, in adult cardiac myocytes from GSK-3 double knockin mice, insulin exposure was still as

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

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

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

109 congenital cardiac defects, we asked whether GSK-3 family members are required for normal heart devel

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

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

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

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

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

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

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

117 reclinical data, glycogen synthase kinase-3 (GSK-3) has been proposed to be a viable drug target for

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 GSK-3 inactivation by PKB abrogates phosphorylation of C

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

139 GSK-3 inactivation with pharmacologic inhibitors enhance

140 died the role of glycogen synthase kinase-3 (GSK-3) inactivation on neurite and axon growth from adul

141 Tau phosphorylation by GSK-3 increased binding, and dephosphorylated tau exhibi

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

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

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

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

146 A combination of GSK-3 inhibition and nutrient activation of mTOR contrib

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

150 king degree of synergism in combination with GSK-3 inhibition to enhance bromodeoxyuridine (BrdU) inc

151 kinases (e.g., Akt) is a major mechanism of GSK-3 inhibition.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 Treatments with GSK-3 inhibitors including a clinical dose of lithium to

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

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

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

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

180 Application of GSK-3 inhibitors stimulates axon formation and elongatio

181 these new drugs, which will be more powerful GSK-3 inhibitors than lithium, may potentially be given

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

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

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

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

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

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

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

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

202 GSK-3 is inactivated by hypertrophic stimuli through pho

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 report, we analyze the contributions of both GSK-3 isoforms (GSK-3alpha and GSK-3beta) in regulating

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

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

222 N-terminal phosphorylation of the GSK-3 isoforms GSK-3alpha and GSK-3beta by upstream kina

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

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

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

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

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

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

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

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

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

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

233 ortantly, we provide the first evidence that GSK-3 maintains constitutive NF-kappaB signaling in panc

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

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

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

237 au mutants, with serine/threonine targets of GSK-3 mutated to glutamate to mimic a permanent state of

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

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

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

241 of GSK-3 removes the negative constraint of GSK-3 on hypertrophy, thereby stimulating cardiac hypert

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

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

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

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

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

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

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

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

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

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

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

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

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

255 ic inhibition of glycogen synthase kinase-3 (GSK-3) reduces tau phosphorylation and significantly dec

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

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

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

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

260 GSK-3 regulation of migration in neurons was independent

261 Inactivation of GSK-3 removes the negative constraint of GSK-3 on hypert

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

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

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

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

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

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

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

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

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

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

272 GSK-3 specific inhibitors might be promising effective d

273 -3 inhibition through destabilization of the GSK-3 structure.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

290 aim of this study was to verify the role of GSK-3 using a targeted mouse line lacking the critical N

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

292 65 in gene induction following inhibition of GSK-3 was demonstrated by RNA interference experiments.

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

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

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

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

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

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

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

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