ライフサイエンスコーパス: GSK-3beta

1 GSK-3beta down-regulation blocked induction of MesoMT.

2 GSK-3beta inhibition and siRNA gene knockdown decreased

3 GSK-3beta is perhaps best known for glycogen regulation,

4 GSK-3beta knock-out cells exhibit reduced IGF-1R cell su

5 GSK-3beta messenger RNA was identified as a direct targe

6 GSK-3beta not only increases survival of MSCs but also i

7 GSK-3beta overexpression results in accumulation of IL-2

8 GSK-3beta positively affected p53 expression in pancreat

9 GSK-3beta restored calcium sensitivity in HF(dys), but d

10 GSK-3beta-mediated phosphorylation of serine 390 in PR-A

11 GSK-3beta-MSCs also increased capillary density and upre

12 on of GSK-3beta functional variation with 1) GSK-3beta mRNA expression from postmortem prefrontal cor

13 ession from postmortem prefrontal cortex, 2) GSK-3beta and beta-catenin protein expression from perip

14 /-) hypertrophy by the Erk-1/2/Egr-1/miR-26a/GSK-3beta pathway is consistent in human recombinant ASM

15 nase activity of glycogen synthase kinase 3 (GSK-3beta).

16 MSCs overexpressing either GSK-3beta (GSK-3beta-MSCs), LacZ (LacZ-MSCs), or saline was injecte

17 which switch glycogen synthase kinase 3beta (GSK-3beta) activation on and off, were causally related

18 ion site for glycogen synthase kinase 3beta (GSK-3beta) and its priming kinase site Ser219, are essen

19 t Thr212 and glycogen synthase kinase 3beta (GSK-3beta) at Ser9 was reduced by 50% in the brain with

20 orylation of glycogen synthase kinase 3beta (GSK-3beta) at Ser9, which is known to inhibit GSK-3beta

21 Glycogen synthase kinase 3beta (GSK-3beta) has been suggested to be a key player in the

22 Glycogen synthase kinase 3beta (GSK-3beta) is a primary tau kinase that is most implicat

23 Glycogen synthase kinase 3beta (GSK-3beta) is an enzyme implicated in neurodevelopmental

24 orylation of glycogen synthase kinase 3beta (GSK-3beta), a downstream target in the signaling pathway

25 tory site of glycogen synthase kinase 3beta (GSK-3beta), and this effect can be blocked by inhibition

26 osphorylated glycogen synthase kinase 3beta (GSK-3beta), while infection with the ORF12 deletion muta

27 horylated by glycogen synthase kinase 3beta (GSK-3beta).

28 regulated by glycogen synthase kinase 3beta (GSK-3beta).

29 n (mTOR) and glycogen synthase kinase 3beta (GSK-3beta)/adenomatous polyposis coli (APC) pathways.

30 riggering of glycogen synthase kinase-3beta (GSK-3beta) activation, degradation of beta-catenin, and

31 converged on glycogen synthase kinase-3beta (GSK-3beta) and beta-catenin.

32 ctivation of glycogen synthase kinase-3beta (GSK-3beta) and c-Jun N-terminal kinase (JNK/SAPK) in bet

33 ctivation of glycogen synthase kinase-3beta (GSK-3beta) and that GSK-3beta regulates the VAPB-PTPIP51

34 We show glycogen synthase kinase-3beta (GSK-3beta) as a target gene of miR-26a.

35 ctivation of glycogen synthase kinase-3beta (GSK-3beta) at serine 9, as the latter was abrogated by i

36 (BACE-1) and glycogen synthase kinase-3beta (GSK-3beta) by attacking both beta-amyloid and tau protei

37 ured retina, glycogen synthase kinase-3beta (GSK-3beta) inhibition was sufficient to stimulate MG ded

38 plication of glycogen synthase kinase-3beta (GSK-3beta) inhibitor completely blocked LY37's effect on

39 in using the glycogen synthase kinase-3beta (GSK-3beta) inhibitor LiCl restores calcium accumulation,

40 report that glycogen synthase kinase-3beta (GSK-3beta) is phosphorylated (inhibited) in fibrotic tis

41 Activity of glycogen synthase kinase-3beta (GSK-3beta) is required for long-term depression (LTD) vi

42 ctivation of glycogen synthase kinase-3beta (GSK-3beta) was required for ceramide-induced NF-kappaB a

43 n (APC), and glycogen synthase kinase-3beta (GSK-3beta), which could shed light on this issue.

44 increase in glycogen synthase kinase-3beta (GSK-3beta)-mediated hepatocyte apoptosis.

45 also blocks glycogen synthase kinase-3beta (GSK-3beta)-phosphorylation of CRMP-2, which results in e

46 hat involves glycogen synthase kinase-3beta (GSK-3beta).

47 e targets of glycogen synthase kinase-3beta (GSK-3beta).

48 ates such as glycogen synthase kinase-3beta (GSK-3beta).

49 hibition) of glycogen synthase kinase-3beta (GSK-3beta).

50 hibition) of glycogen synthase kinase-3beta (GSK-3beta).

51 f tau kinase glycogen-synthase-kinase-3beta (GSK-3beta).

52 nin pathway (glycogen synthase kinase 3beta [GSK-3beta] inhibitors), and antagonists of the Wnt/beta-

53 manipulation of the PI-3K/Akt/mTOR and PI-3K/GSK-3beta/APC pathways.

54 We recently demonstrated that dynein is a GSK-3beta substrate and that inhibition of GSK-3beta pro

55 ed HCEKs with either a myristolated Akt or a GSK-3beta inhibitor restored glycogen stores, confirming

56 in HCEKs decreased AKT signaling, activated GSK-3beta, and inactivated glycogen synthase.

57 evels of sarkosyl-insoluble tau in an active GSK-3beta-induced tau aggregation model.

58 Both pHLXB9 and active GSK-3beta are elevated in beta cells with menin knockdow

59 vation of GSK-3beta in constitutively active GSK-3beta knock-in mice (betaKI) significantly decreased

60 Overexpression of active GSK-3beta (S9A) or knock-down of GSK-3beta delayed PI-in

61 Excess of active GSK-3beta perturbed axonal transport by causing axonal b

62 with IL-22, but this effect is reduced after GSK-3beta knockdown.

63 cle arrest through dephosphorylation of AKT, GSK-3beta, c-Raf, and Foxo proteins.

64 ceptors, as well as by inhibition of the Akt-GSK-3beta (Akt-glycogen synthase kinase-3beta) pathway.

65 cycle progression via activation of the Akt-GSK-3beta-cyclinD1 pathway.

66 nd MMP2 expression and inhibition of the Akt-GSK-3beta-cyclinD1 pathway.

67 ctivation of the cellular COX-2/PGE2 and Akt/GSK-3beta signaling pathways.

68 ting beta-Klotho, and activating ERK and Akt/GSK-3beta signaling pathways.

69 l for COX-2/prostaglandin E2 (PGE2)- and Akt/GSK-3beta-dependent tumor invasion/metastasis.

70 nuation of MIG-7 blocked COX-2/PGE2- and Akt/GSK-3beta-mediated migration/invasion effects.

71 ch is partially attributed to inhibiting Akt/GSK-3beta signaling pathway.

72 es, confirming the direct involvement of Akt/GSK-3beta signaling.

73 RK) and phosphoinositide 3-kinase (PI3K)/AKT/GSK-3beta kinase cascades, resulting in phosphorylation

74 n tumor suppressor PTEN, modulating PI3K/Akt/GSK-3beta signaling and eventually leading to the high e

75 ibited protein phosphatase 2A to sustain Akt/GSK-3beta phosphorylation and cancer-cell migration/inva

76 own to affect glucose metabolism via the Akt/GSK-3beta pathway.

77 These results suggest that altered GSK-3beta/beta-catenin signaling in MSCs of infants expo

78 ght into the key requirements for BACE-1 and GSK-3beta inhibition.

79 gest that ETH interacts with Akt, Dkk-1, and GSK-3beta.

80 /2 signaling in GluA1 and/or both ERK1/2 and GSK-3beta signaling pathways in the GluA2 subunit.

81 nd downstream substrates ACC-1, PFKFB-2, and GSK-3beta.

82 inhibition of PKs, such as VEGFR, FLT-3, and GSK-3beta which are related to carcinogenesis.

83 f the Wnt/beta-catenin pathway by Wnt-3a and GSK-3beta inhibitors led to inhibition of SZP accumulati

84 SH-SY5Y cells confirmed that GSK-3alpha and GSK-3beta impair lysosomal acidification and that treatm

85 al mouse mutants lacking both GSK-3alpha and GSK-3beta in newly born cortical excitatory neurons.

86 Moreover, both GSK-3alpha and GSK-3beta KD reduced tau phosphorylation and tau misfold

87 e respective contributions of GSK-3alpha and GSK-3beta to AD pathology and AML is ongoing.

88 to elucidate the role of each GSK-3alpha and GSK-3beta using novel viral and genetic approaches.

89 ng reduced phosphorylation of GSK-3alpha and GSK-3beta.

90 Cleaved caspase 3, 8 and 9, and GSK-3beta, pGSK-3beta(tyr216) and pGSK-3beta(ser9) expre

91 of phosphorylation of serine 390 of PR-A and GSK-3beta activity is observed in the Brca1-deficient ma

92 OPN in increased phosphorylation of Akt and GSK-3beta followed by the activation of beta-catenin, wh

93 COX-2/PGE2 activated EP4 to enhance Akt and GSK-3beta phosphorylation and beta-catenin/T-cell factor

94 from alterations in the activity of AKT and GSK-3beta.

95 differentiation through ERalpha-, Akt-, and GSK-3beta-dependent activation of beta-catenin signaling

96 Of interest, both APC and GSK-3beta interact with microtubules and cellular membra

97 ssion of mNLS-I2 (PP2A) activated CAMKII and GSK-3beta, which are Tau kinases regulated by PP2A.

98 tures have been reported to inhibit CDKs and GSK-3beta in recent years.

99 of Tyr-216 in pleural mesothelial cells and GSK-3beta mobilization from the cytoplasm to the nucleus

100 ence of a covalent bond between the drug and GSK-3beta.

101 ralization, caspase and GSK-3 inhibitors and GSK-3beta siRNA were applied to further explore underlyi

102 puts from two signaling pathways, mTORC1 and GSK-3beta, that in turn drives excessive alcohol-drinkin

103 C and acts as an adaptor protein for p38 and GSK-3beta kinases to facilitate local TGFbeta/p38-depend

104 tallized with DYRK1A, DYRK2, CLK3, PIM1, and GSK-3beta.

105 irect interaction of I2 (PP2A) with PP2A and GSK-3beta but not with CAMKII.

106 llectively, our findings suggest that PS and GSK-3beta are required for normal motor protein function

107 mechanistic link between IL-1 signaling and GSK-3beta activation.

108 Our data suggest that Wnt signaling and GSK-3beta inhibition, in particular, are crucial for suc

109 Wnt signalling independently of the AXIN-APC-GSK-3beta complex partly by limiting the activity of dis

110 of AKT and glycogen synthase kinase 3 beta (GSK-3beta) in both the Pten(LKO) and Pten(LKO);Tgfbr2(LK

111 Glycogen synthase kinase 3 beta (GSK-3beta) is a central target in several unmet diseases

112 Glycogen synthase kinase-3 beta (GSK-3beta) is overexpressed in a number of human maligna

113 gy to study glycogen synthase kinase-3 beta (GSK-3beta), a kinase able to compete with O-GlcNAc trans

114 at disrupt the regulation of beta-catenin by GSK-3beta cause colorectal cancer in humans.

115 the zebrafish "eyeless" phenotype induced by GSK-3beta antagonist 6-bromoindirubin-30-oxime (BIO) for

116 , but it is not required for that induced by GSK-3beta inhibition.

117 Ser-1248 phosphorylation is mediated by GSK-3beta in a mechanism that involves a priming phospho

118 adation when C/EBPdelta is phosphorylated by GSK-3beta.

119 Its phosphorylation by GSK-3beta restrains kinase activity and regulates recept

120 tion factors that is negatively regulated by GSK-3beta is CREB, which itself positively regulates IL-

121 data indicate that phosphorylation on T19 by GSK-3beta destabilizes PSD-95 within the PSD and is a cr

122 , is phosphorylated on threonine-19 (T19) by GSK-3beta.

123 ealed significant activation of beta-catenin/GSK-3beta signaling, whereas MAPK and MKL1/serum-respons

124 Notably, anti-DENV NS1 Abs caused GSK-3beta-mediated NF-kappaB activation and iNOS express

125 otoxicity induced by kainic acid (KA) caused GSK-3beta truncation at C-terminus and hyperphosphorylat

126 Specifically, IL-17 causes GSK-3beta-dependent phosphorylation of C/EBPbeta, which

127 ia a mechanism involving the aSMase/ceramide/GSK-3beta/NF-kappaB/iNOS/NO signaling pathway.

128 rder to elucidate the use of ATP-competitive GSK-3beta inhibitors as new tools in the development of

129 ne-nitrogen to obtain potent ATP-competitive GSK-3beta inhibitors with good cell activity.

130 ) animals incubated with GSK-3beta confirmed GSK-3beta-dependent phosphorylation at many of the same

131 tes Wnt/beta-catenin signalling by degrading GSK-3beta in vitro and in cells, increasing levels of Cy

132 In our ongoing efforts to develop GSK-3beta inhibitors for the treatment of mood disorders

133 importantly, we also have found a different GSK-3beta complex present only in HIV-1-infected cells.

134 gous for a null allele of shaggy (Drosophila GSK-3beta) both fail to complete meiosis and lack phosph

135 MSCs overexpressing either GSK-3beta (GSK-3beta-MSCs), LacZ (LacZ-MSCs), or saline

136 using gel electrophoresis to grossly enrich GSK-3beta from whole cell lysate, we discover by MRM-MS

137 d in mouse embryonic fibroblasts deleted for GSK-3beta.

138 ased phosphorylation of Akt substrates FoxO, GSK-3beta, PRAS40, AS160, and Tsc2.

139 Excess of non-functional GSK-3beta did not affect axonal transport.

140 we discover by MRM-MS a novel O-GlcNAcylated GSK-3beta peptide, bearing 3 potential O-GlcNAcylation s

141 nic mice (Tg-DnGSK-3beta) or in heterozygous GSK-3beta knock-out mice (GSK-3beta+/-) significantly in

142 We identified GSK-3beta and PP2B as effectors of abnormal tau phosphor

143 Collectively, these studies identify GSK-3beta as a newly identified target for amelioration

144 Wnt-signaling hyperactivation, albeit in GSK-3beta independent manner, differentiated colon cance

145 eolytic processing, but not amyloid-beta, in GSK-3beta activation and tau phosphorylation in human ne

146 otype of a single-nucleotide polymorphism in GSK-3beta (rs12630592) was associated with reduced GSK-3

147 ar (LV) function was observed at 12 weeks in GSK-3beta-MSC-injected mice compared with in LacZ-MSC- o

148 vastatin activated Akt and mTOR, inactivated GSK-3beta and dephosphorylated APC in the injured PCNs.

149 Inactive GSK-3beta accelerated PI-induced IkappaBalpha degradatio

150 lly high levels of phosphorylated (inactive) GSK-3beta and high levels of active beta-catenin in the

151 onstitutively active Ras signaling increases GSK-3beta gene expression via the canonical mitogen-acti

152 SK-3beta) at Ser9, which is known to inhibit GSK-3beta function.

153 Compound 18 inhibited GSK-3beta with an IC50 of 0.24 muM and inhibited tau pho

154 by potentiating Akt signaling and inhibiting GSK-3beta-mediated apoptosis in hepatocytes.

155 Thus, Akt3 is important in inhibiting GSK-3beta.

156 and represses its degradation via inhibiting GSK-3beta-dependent phosphorylation and ubiquitination o

157 and represses its degradation via inhibiting GSK-3beta-dependent phosphorylation and ubiquitination o

158 iptional function, NOTCH profoundly inhibits GSK-3beta activity.

159 We report here that tideglusib inhibits GSK-3beta irreversibly, as demonstrated by the lack of r

160 Insulin/GSK-3beta (glycogen synthase kinase 3-beta) signalling i

161 n, and one that is PS-independent, involving GSK-3beta activation and operative at all concentrations

162 mediated beta-catenin is destabilized and is GSK-3beta or beta-TrCP independent.

163 erestingly, stathmin 3 phosphorylated at its GSK-3beta target site displays a specific subcellular lo

164 cells to apoptosis by inhibiting the kinases GSK-3beta and cyclin-dependent kinase (CDK) 1.

165 led to augment the half-life of GLI2 lacking GSK-3beta phosphorylation sites, indicating that MEK-RSK

166 Likewise, GSK-3beta inhibitor 9ING41 blocked induction of MesoMT a

167 Mechanistically, GSK-3beta inhibits profibrotic transforming growth facto

168 nin signaling with RNA interference-mediated GSK-3beta knockdown or GSK-3beta antagonism reversed MPT

169 or in heterozygous GSK-3beta knock-out mice (GSK-3beta+/-) significantly increased, whereas activatio

170 The PI3K-AKT pathway modulates GSK-3beta activity, and cells from individuals with PIK3

171 fic inhibition of GSK-3 by dominant negative GSK-3beta in transgenic mice (Tg-DnGSK-3beta) or in hete

172 tarting point for the rational design of new GSK-3beta inhibitors.

173 identification of a structural class of new GSK-3beta inhibitors.

174 d that knockdown (KD) of GSK-3alpha, but not GSK-3beta, reduced SP formation in PDAPP(+)/(-) and PS19

175 ponse a signaling module encompassing NOTCH, GSK-3beta, SNAI1 and beta-catenin.

176 A series of novel GSK-3beta inhibitors having the common N-[(1-alkylpiperi

177 lations at serine 473 of Akt and serine 9 of GSK-3beta.

178 These findings reveal the ability of GSK-3beta to modulate IL-22R protein stability that migh

179 - significantly reduced, while activation of GSK-3beta in betaKI significantly enhanced, myocardial I

180 gnificantly increased, whereas activation of GSK-3beta in constitutively active GSK-3beta knock-in mi

181 rs investigated in humans the association of GSK-3beta functional variation with 1) GSK-3beta mRNA ex

182 , these data suggest that the combination of GSK-3beta and pHLXB9 forms a therapeutically targetable

183 ur recent findings that specific deletion of GSK-3beta in cardiac fibroblasts leads to fibrogenesis,

184 ckout mouse models, we show that deletion of GSK-3beta in cardiac fibroblasts leads to fibrogenesis,

185 Deletion of GSK-3beta induces a profibrotic myofibroblast phenotype

186 Moreover, deletion of GSK-3beta resulted in the significant increase of SMAD-3

187 n of active GSK-3beta (S9A) or knock-down of GSK-3beta delayed PI-induced IkappaBalpha degradation.

188 e influence of rapamycin over the effects of GSK-3beta inhibition on myocardial injury was reversed b

189 The recent emergence of GSK-3beta as a regulator of myocardial fibrosis will als

190 eneral mechanism for increased expression of GSK-3beta in pancreatic cancer and perhaps other cancers

191 Phosphorylation/inactivation of GSK-3beta and phosphorylation/activation of mTOR, critic

192 consistent with the phosphor-inactivation of GSK-3beta by CCCP and by the induction of PRC by the GSK

193 also inhibited the phosphor-inactivation of GSK-3beta by CCCP, a result consistent with the ability

194 local TGFbeta/p38-dependent inactivation of GSK-3beta, accumulation of beta-catenin, and recruitment

195 n and 2) phosphorylation and inactivation of GSK-3beta, which leads to the activation of CRMP2, promo

196 n, PIs induced Akt-dependent inactivation of GSK-3beta.

197 Inhibition of GSK-3beta activity reversed the effects induced by mAb16

198 less-like phenotype induced by inhibition of GSK-3beta activity, suggesting that OTG acts upstream of

199 ition of Akt worsened, whereas inhibition of GSK-3beta and caspases protected mice from AILI.

200 ngs suggest that combinatorial inhibition of GSK-3beta and CDK1 augment the apoptotic sensitivity of

201 s cholangiocarcinoma growth by inhibition of GSK-3beta and subsequent activation of beta-catenin.

202 Pharmacologic inhibition of GSK-3beta blocked cell proliferation in three different

203 Inhibition of GSK-3beta by pharmacological inhibitors or siRNA-mediate

204 Inhibition of GSK-3beta has been well documented to account for the be

205 In contrast, inhibition of GSK-3beta in Tg-DnGSK-3beta or GSK-3beta+/- significantl

206 Lithium chloride inhibition of GSK-3beta increased nuclear beta-catenin content and nor

207 Finally, pharmacological inhibition of GSK-3beta induces a redistribution of stathmin 3, but no

208 s reports in which deletion or inhibition of GSK-3beta is protective.

209 tive site, suggesting that its inhibition of GSK-3beta obeys to a specific mechanism and is not a con

210 a GSK-3beta substrate and that inhibition of GSK-3beta promotes dynein-dependent transport.

211 Moreover, pharmacological inhibition of GSK-3beta reduced hepatic endothelial cell apoptosis in

212 hat genetic or pharmacological inhibition of GSK-3beta resulted in anxiolytic-like and pro-social beh

213 Inhibition of GSK-3beta stimulated mTOR signaling and inhibited autoph

214 is sensitive to small-molecule inhibition of GSK-3beta.

215 pathway using a pharmacological inhibitor of GSK-3beta ameliorates the Pb inhibition of Wnt signaling

216 on in TZM-bl cells and a potent inhibitor of GSK-3beta kinase in vitro.

217 e, we report that an allosteric inhibitor of GSK-3beta, 4-benzyl-2-(naphthalene-1-yl)-1,2,4-thiadiazo

218 Injection of GSK-3beta-MSCs in which Vegfa had been knocked down abol

219 trong rationale for further investigation of GSK-3beta signaling in the control of MesoMT and pleural

220 mall molecules allowing subtle modulation of GSK-3beta activity.

221 zide derivatives as allosteric modulators of GSK-3beta are presented here.

222 gs suggest that the allosteric modulators of GSK-3beta may be used for future development of drugs fo

223 However, the exact molecular nature of GSK-3beta involved in AD is unclear.

224 by inhibition of Akt or by overexpression of GSK-3beta markedly attenuated IL-10 production in respon

225 through inhibitory serine phosphorylation of GSK-3beta and inhibition of FBXW7 recruitment, prevents

226 with 25% lower inhibitory phosphorylation of GSK-3beta in Ob-MSCs (P < 0.05), these data suggest grea

227 Bupivacaine increased the phosphorylation of GSK-3beta(Tyr216) in SKOV-3 but without measurable effec

228 Similar to phosphorylation of GSK-3beta, both phosphorylation of CREB at serine 133 an

229 way, increased inhibitory phosphorylation of GSK-3beta, increased synaptic spine density/diameter, in

230 tion and increased Tyr216 phosphorylation of GSK-3beta, leptin increased Ser9 phosphorylation and att

231 tration of NP12 increased phosphorylation of GSK-3beta, reduced fibrosis, and restored diastolic func

232 miR-26a-mediated reduction of GSK-3beta resulted in activation of beta-catenin and ind

233 probably is responsible for up-regulation of GSK-3beta and consequent abnormal hyperphosphorylation o

234 ex 2, which further results in repression of GSK-3beta activity.

235 Although the role of GSK-3beta has been well studied in cancer development, t

236 SOJ-6 cells, supporting the pivotal role of GSK-3beta signaling in the mechanisms of action induced

237 oth Ser9 and Tyr216 phosphorylation sites of GSK-3beta.

238 To increase the specificity of GSK-3beta inhibitors in chronic treatments, we developed

239 tion of beta-catenin, a primary substrate of GSK-3beta and a key regulator in controlling hippocampal

240 d by pharmacologic or genetic suppression of GSK-3beta.

241 These findings suggest that truncation of GSK-3beta by Ca(2+)/calpain I markedly increases its act

242 Truncation of GSK-3beta was positively correlated with tau hyperphosph

243 tivity, suggesting that OTG acts upstream of GSK-3beta.

244 triggered beta-catenin activation by way of GSK-3beta phosphorylation.

245 Switching off GSK-3beta promotes disease pathogenesis.

246 mmalian cells exhibits no kinase activity on GSK-3beta in the presence of either Mn(2+) or the conven

247 ced expression and activity of GSK-3alpha or GSK-3beta.

248 inhibition of GSK-3beta in Tg-DnGSK-3beta or GSK-3beta+/- significantly reduced, while activation of

249 ls in response to acute insulin exposure (or GSK-3beta inhibition) is blocked by tumor-promoting isof

250 interference-mediated GSK-3beta knockdown or GSK-3beta antagonism reversed MPTP-induced neurogenic im

251 abilizing beta-catenin through Wnt ligand or GSK-3beta inhibition achieved partial restoration of blu

252 ed the levels of phospho-Akt/Akt and phospho-GSK-3beta/GSK-3beta compared with untreated I/R mice.

253 , resulting in high levels of phosphorylated GSK-3beta and active beta-catenin and in enhanced prolif

254 selective GSK-3 inhibitor) or a preferential GSK-3beta inhibitor; these effects included rapid activa

255 ity of the antihypertrophic and proapoptotic GSK-3beta molecule.

256 Calpain I proteolyzed GSK-3beta in vitro at C-terminus, leading to an increase

257 olar proteins NPM1 and PHF6, and recombinant GSK-3beta phosphorylated these proteins in vitro RNA-Seq

258 eta (rs12630592) was associated with reduced GSK-3beta mRNA from postmortem prefrontal cortex.

259 n which PS likely plays a role in regulating GSK-3beta activity during transport.

260 that the phosphorylation of Sarah by Shaggy/GSK-3beta is required to complete meiosis.

261 genes screened, including the kinases shaggy/GSK-3beta, par-1/MARK, CamKI and Mekk1.

262 findings suggest a mechanism in which Shaggy/GSK-3beta activates calcineurin through Sarah phosphoryl

263 Using 2 fibroblast-specific GSK-3beta knockout mouse models, we show that deletion o

264 Strikingly, GSK-3beta-activity-dependent axonal transport defects we

265 -catenin side effects associated with strong GSK-3beta inhibition.

266 AKAP220 suppresses GSK-3beta and positions this kinase to allow recruitment

267 RSK stabilizes GLI2 by controlling targeting GSK-3beta-mediated phosphorylation and ubiquitination of

268 These studies support targeting GSK-3beta in myocardial fibrotic disorders and establish

269 n synthase kinase-3beta (GSK-3beta) and that GSK-3beta regulates the VAPB-PTPIP51 interaction.

270 We demonstrate that GSK-3beta is itself modified by O-GlcNAc in human embryo

271 We found that GSK-3beta phosphorylates and inactivates 4E-BP1, thereby

272 We found that GSK-3beta was deactivated in HF(dys) and reactivated by

273 In the present study, we found that GSK-3beta was truncated at C-terminus and correlated wit

274 r, these results support the hypothesis that GSK-3beta inhibition could influence neuroactive steroid

275 Our results reveal that GSK-3beta and pHLXB9 can serve as novel targets for insu

276 3beta and Fbw7-deficient cells revealed that GSK-3beta and Fbw7-dependent HIF-1alpha degradation can

277 Here we show that GSK-3beta inactivates the proapoptotic activity of HLXB9

278 These results suggest that GSK-3beta variation is implicated in multiple phenotypes

279 This suggests that GSK-3beta differentially mediates GluA1 and GluA2 traffi

280 hippocampal neurogenesis via activating the GSK-3beta/beta-catenin signaling pathway.

281 itory action of IL-17 can be reversed at the GSK-3beta level by PI3K/Akt signalling induced by D-reso

282 stigated the association of variation in the GSK-3beta gene with a series of progressively more compl

283 These GSK-3beta-mediated axonal defects do not appear to be ca

284 herein for the first time that some of these GSK-3beta inhibitors, in particular analogues 1 and 9, w

285 ss of myofilaments following HF(dys) through GSK-3beta reactivation, identifying a therapeutic approa

286 Thus, GSK-3beta negatively regulates myeloid cell IL-10 produc

287 GF1 receptor (IGF1R) to PI3 kinase to AKT to GSK-3beta pathway required for activation of the canonic

288 al sites, reversing the response of CEBPB to GSK-3beta-mediated phosphorylation from repression to ac

289 (414), and IL-22 treatment of cells triggers GSK-3beta inactivation.

290 r DM1, SMA, and other chronic diseases where GSK-3beta inhibition exhibits therapeutic effects.

291 effect on GluA2 surface expression, whereas GSK-3beta inhibitor itself induced decreases in the surf

292 s in accumulation of IL-22R protein, whereas GSK-3beta depletion in cells reduces levels of the recep

293 t myocardial fibrosis in the models in which GSK-3beta is specifically deleted in cardiac fibroblasts

294 ibutes to both SP and NFT pathogenesis while GSK-3beta only modulates NFT formation, suggesting commo

295 X-ray cocrystal structure of compound 5 with GSK-3beta.

296 rthermore, this genotype was associated with GSK-3beta protein expression and kinase activity, as wel

297 Further, experiments with GSK-3beta and Fbw7-deficient cells revealed that GSK-3be

298 proteins from HF(dys) animals incubated with GSK-3beta confirmed GSK-3beta-dependent phosphorylation

299 were still observed in MI mice injected with GSK-3beta-MSCs without Vegfa.

300 PS genetically interacts with GSK-3beta in an activity-dependent manner.