ライフサイエンスコーパス: GSK-3beta

1 GSK-3beta (glycogen synthase kinase-3beta) is highly ass

2 GSK-3beta (Serine 9)/JNK phosphorylation is mainly invol

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

4 GSK-3beta inhibition and siRNA gene knockdown decreased

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

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

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

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

9 GSK-3beta positively affected p53 expression in pancreat

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

11 GSK-3beta-isozyme selectivity was assessed to reveal OCM

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

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

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

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

16 nd selective (>10-fold GSK-3beta/GSK-3alpha) GSK-3beta inhibitor known to date.

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 argeting the glycogen synthase kinase 3beta (GSK-3beta) enzyme, due to its appealing properties.

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

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

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

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

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

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

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

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

33 250-fold) by glycogen synthase kinase-3beta (GSK-3beta) inhibition using CHIR99021 and concurrent rem

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

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

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

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

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

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

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

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

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

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

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

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

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

47 IP-induced depotentiation was prevented by a GSK-3beta inhibitor, 6-bromoindirubin-3-acetoxime (BIO-a

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

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

50 Kindlin-2 loss activates GSK-3beta and downregulates beta-catenin, leading to red

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 e that the phosphatidylinositol 3-kinase/AKT/GSK-3beta pathway interferes with NF-kappaB-driven gene

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

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

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

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

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

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

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

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

74 /2 signaling in GluA1 and/or both ERK1/2 and GSK-3beta signaling pathways in the GluA2 subunit.

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

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

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

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

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

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

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

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

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

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

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

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

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

88 protein stability, signaling through AKT and GSK-3beta to increase MYC half-life.

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

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

91 ling kinases that in turn inhibits (AMPK and GSK-3beta) or stimulates (AKT, ERK and RSK-1) mTORC1 act

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

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

94 ed to an increase in active beta-catenin and GSK-3beta phosphorylation.

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

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

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

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

99 tions with anesthetic sevoflurane, miRNA and GSK-3beta.

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

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

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

103 , and induced beta-catenin translocation and GSK-3beta phosphorylation in the absence of AnxA8.

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

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

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

107 found that glycogen synthase kinase 3 beta (GSK-3beta) was robustly activated by ZIP in vitro.

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

109 Glycogen synthase kinase-3 beta (GSK-3beta), a serine/threonine kinase, has been identifi

110 ) affecting glycogen synthase kinase 3 beta (GSK-3beta)/nuclear factor (erythroid-derived 2)-like 2 (

111 bled 10 to 25 times greater expansion beyond GSK-3beta inhibition alone.

112 CAY10594 administration strongly blocked GSK-3beta (Serine 9)/JNK phosphorylation in the APAP-ind

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

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

115 acetoxime infusion or GSK-3beta knockdown by GSK-3beta shRNA in the LA attenuated ZIP-induced disrupt

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

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

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

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

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

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

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

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

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

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

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

127 ently, PDO325901 (MEK inhibitor), CHIR99021 (GSK-3beta inhibitor) and Dasatinib (Abl, Src and c-Kit i

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 Consistently, GSK-3beta inhibition by BIO-acetoxime infusion or GSK-3b

132 and miR-101a-3p overexpression all decreased GSK-3beta levels.

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

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

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

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

137 cause significant changes in the endothelial GSK-3beta/BH(4) /eNOS/Nrf2 pathways, which may lead to i

138 These same mediators enhanced GSK-3beta activation via phosphorylation of tyrosine-216

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

140 (IC(50) = 0.030 nM) and selective (>10-fold GSK-3beta/GSK-3alpha) GSK-3beta inhibitor known to date.

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

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

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

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

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

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

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

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

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

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

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

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

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 Notably, either inhibiting GSK-3beta or disrupting the D(2)R-DISC1 complex was able

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 or analogous compounds against human kinases GSK-3beta, CDK-2, and CDK-4 were leveraged to try to imp

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

170 ted the antitumor effect of a small molecule GSK-3beta inhibitor, 9-ING-41, currently in clinical stu

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

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

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

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

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

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

177 w conditional cell-type-specific ablation of GSK-3beta in D(2)R+ neurons (D(2)R-GSK-3beta(-/-)) in th

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

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

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

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

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

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

184 iscuss the reasons behind the development of GSK-3beta-directed MTDLs and highlight some of the recen

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

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

187 d by expression of a non-inhibitable form of GSK-3beta in the LA.

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

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

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

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

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

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

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

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

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

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

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

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

200 riven gene expression and that inhibition of GSK-3beta mimics tolerance in vivo.

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

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

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

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

205 Inhibition of GSK-3beta signaling with the novel inhibitor 9-ING-41 bl

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

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

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

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

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

211 MeCP2 T158A mice show decreased level of GSK-3beta phosphorylation and increased level of beta-ca

212 ant (P <0.05) decrease, while mRNA levels of GSK-3beta were elevated.

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

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

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

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

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

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

219 toma cells also increased phosphorylation of GSK-3beta at Ser(9).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 Switching off GSK-3beta promotes disease pathogenesis.

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

241 nhibition of Erk1/2, tyrosine kinase, and/or GSK-3beta was implied to be involved in the enhancement

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

243 beta inhibition by BIO-acetoxime infusion or GSK-3beta knockdown by GSK-3beta shRNA in the LA attenua

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

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

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

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

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

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

250 Indeed, D(2)R-GSK-3beta(-/-) mice also exhibited a resistance of worki

251 n layer V pyramidal neurons in mPFC of D(2)R-GSK-3beta(-/-) mice, along with increased dopamine modul

252 V pyramidal neurons, were detected in D(2)R-GSK-3beta(-/-) mice.

253 rotein levels were elevated in mPFC of D(2)R-GSK-3beta(-/-) mice.

254 lation of GSK-3beta in D(2)R+ neurons (D(2)R-GSK-3beta(-/-)) in the brain affects synaptic function i

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

256 y inhibiting miR-101a-3p's ability to reduce GSK-3beta levels and that LncRNAs would serve as the mec

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

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

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

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

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

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

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

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

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

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

267 This study demonstrates that GSK-3beta modulates cognition via D(2)R-DISC1 interactio

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

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

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

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

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

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

274 We show that GSK-3beta inhibition suppresses CM maturation, while con

275 Our findings suggest that GSK-3beta activation is a critical step for ZIP-induced

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

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

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

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

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

281 upporting the continued investigation of the GSK-3beta signaling pathway in the control of fibroblast

282 studies clearly show that activation of the GSK-3beta signaling pathway is critical for the inductio

283 However, the mechanisms underlying the GSK-3beta modulation of cognitive function via D(2)Rs re

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

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

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

287 Cs and inhibits osteoblast formation through GSK-3beta-mediated degradation of beta-catenin.

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

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

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

291 mulation of the Wnt/beta-catenin pathway via GSK-3beta inhibitor small molecules polarises macrophage

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

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

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

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

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

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

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

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

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