ライフサイエンスコーパス: GSK

1 GSK induced hyperpolarization of PDGFRalpha(+) cells and

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

3 GSK-3 inactivation by PKB abrogates phosphorylation of C

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

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

6 GSK-3 regulation of migration in neurons was independent

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

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

9 GSK-3beta inhibition and siRNA gene knockdown decreased

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

11 one template, as exemplified by compound 14 (GSK'481), makes it an excellent starting point for furth

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

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

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

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

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

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

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

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

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

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

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

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

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

25 the role of glycogen synthase kinase-3alpha (GSK-3alpha) in post-MI remodeling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 90 genes that are alternatively spliced in a GSK-3-dependent manner, supporting a broad role for GSK-

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

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

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

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

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

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

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

49 ds, compound 27 showed high activity against GSK-3alpha/beta with the highest GSK-3alpha selectivity

50 We screened RIP1 against GSK's DNA-encoded small-molecule libraries and identifie

51 In addition, TRPV4 agonist GSK 1016790A treatment reduced intraocular pressure in m

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

53 TOR inhibition through modulation of the AKT-GSK signaling axis.

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

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

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

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

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

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

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

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

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

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

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

65 ion, two other ROCK inhibitors, RKI 1447 and GSK 429286, selectively targeted VHL-deficient CC-RCC.

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

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

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

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

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

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

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

73 mineralocorticoid receptor (MR) blocker, and GSK-650394, an inhibitor of the serum- and glucocorticoi

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

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

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

77 Candidate kinases CKII and GSK-3b phosphorylate CREB-H in vitro with specificities

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

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

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

81 ng ascorbic acid (AA) and 2i (MAP kinase and GSK inhibitors) increases the efficiency of reprogrammin

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

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

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

85 they carry out the design and synthesis, and GSK tests the compounds.

86 stgraduate training of medicinal chemists at GSK is also briefly described.

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

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

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

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

91 mall-molecule inhibitors of GSK-3alpha/beta (GSK-3i) to reduce pcdc1 (PD-1) transcription and express

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

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

94 SK channels inhibited currents activated by GSK and increased detrusor contractions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 ted proteins can be confirmed by using CyaA, GSK, or microinjection assays.

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

111 of doubly phosphorylated STAT3 by depleting GSK-3alpha/beta is sufficient to disrupt signal integrat

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

113 opyranyl-4-carboxylic acid derived dipeptide GSK-2793660, which is currently in clinical trials as ca

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

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

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

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

118 fforts to develop acyclic scaffold-hops from GSK-690 (1).

119 ng CREB, ss-catenin, AKT, p42/44 MAPK, GAB2, GSK-3ss, FOXO1, and YAP.

120 ity of Nottingham (UoN) and GlaxoSmithKline (GSK).

121 7213 study) is sponsored by GlaxoSmithKline (GSK) with associated exploratory studies supported by th

122 ned in a post-hoc analysis (GlaxoSmithKline [GSK] e-track number 202142) to investigate the efficacy

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

124 GSK1016790A (GSK), a TRPV4 channel agonist, activated a non-selective

125 High-GSK had no effect on startle potentiation during unpredi

126 The increased fear by high-GSK replicates animal findings and suggests a lift of th

127 GSK561679 (low-GSK), 400 mg GSK561679 (high-GSK), and 1 mg alprazolam in a crossover design.

128 developed by our group achieved the highest GSK-3alpha selectivity reported so far but suffered from

129 ity against GSK-3alpha/beta with the highest GSK-3alpha selectivity reported to date.

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

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

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

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

134 combinatorial signaling context and identify GSK-3alpha/beta-STAT3 signaling as a potential therapeut

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

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

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

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

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

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

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

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

143 nostat and the histone demethylase inhibitor GSK-J4 revealed that the two had synergistic effects.

144 r and chloroquine or the LDHA/LDHB inhibitor GSK 2837808A.

145 Akt inhibitor, GSK-2141795, which is in clinical trials for treatment o

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

147 approved the first second generation INSTI, GSK's Dolutegravir (DTG) (August 2013).

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

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

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

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

152 n turn inactivates glycogen synthase kinase (GSK) 3, a major regulator of metabolism.

153 signaling through glycogen synthase kinase (GSK) 3alpha/beta in the activation of pro-atherogenic pa

154 overexpression of glycogen synthase kinase (GSK) 3beta in neural precursor cells (NPCs) using the gl

155 Glycogen synthase kinase (GSK)-3 is a ubiquitously expressed kinase inhibited by i

156 last TBI increased glycogen synthase kinase (GSK)-3beta activities in ApoE4 mice, and synj1 knockdown

157 me stimuli enhance glycogen synthase kinase (GSK)-3beta activity through increased phosphorylation of

158 Glycogen synthase kinase (GSK)-3beta phosphorylates the IL-22R within a consensus

159 vide evidence that glycogen synthase kinase (GSK)-3beta promotes cell proliferation through positive

160 diesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15, a heterocyclic small molecule w

161 hinone IIA blunted glycogen synthase kinase (GSK)3beta overactivity and hyperactivation of its downst

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

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

164 /threonine kinase, glycogen synthase kinase, GSK-3alpha/beta, is a central regulator of PD-1 transcri

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

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

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

168 l trial of mepolizumab (substudy of a larger GSK sponsored global phase III trial, MEA115575) where s

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

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

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

172 Low-GSK did not affect startle potentiation across condition

173 ur treatments: placebo, 50 mg GSK561679 (low-GSK), 400 mg GSK561679 (high-GSK), and 1 mg alprazolam i

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

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

176 In each model, GSK-3i inhibited PD-1 expression on tumor-infiltrating l

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

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

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

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

181 a patient population with a high unmet need (GSK Study 204664).

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

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

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

185 4%) whose levels decreased in the absence of GSK-3.

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

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

188 discuss our recent findings that deletion of GSK-3alpha specifically in cardiomyocytes attenuates ven

189 hermore, the conditional genetic deletion of GSK-3alpha/beta reduced PD-1 expression on CD8(+) T cell

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

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

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

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

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

195 further highlighted by the recent failure of GSK HSV-2 vaccine Simplirix (gD/AS04) to protect humans

196 kinase 3 beta (pGSK-3B), an inactive form of GSK-3B degrading glioblastoma 2 (GLI2), followed by the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 that the use of small-molecule inhibitors of GSK-3alpha/beta (GSK-3i) to reduce pcdc1 (PD-1) transcri

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

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

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

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

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

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

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

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

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

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

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

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

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

225 tion impairment, confirming the potential of GSK-3alpha inhibition in AML therapy.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 ease-specific target Identification Program [GSK-HiTDiP] study (113 patients and 57 healthy control s

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

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

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

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

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

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

251 together, these findings show that reducing GSK-3alpha expression in cardiomyocytes limits ventricul

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

253 Selective GSK-3alpha targeting in AML cell lines was achieved with

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

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

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

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

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

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

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

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

262 Specifically targeting GSK-3alpha could be a novel strategy to limit adverse re

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

264 Here we demonstrate that GSK-J4, a specific inhibitor of the H3K27me3 histone dem

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

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

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

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

269 Further, we found that GSK-J1 inhibited the demethylase activity of KDM5C with

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

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

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

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

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

275 PubMed and the GSK Clinical Study Register were searched for suitable s

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

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

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

279 From the GSK antimalarial set, we identified an aminoxadiazole wi

280 icinal chemistry program and others from the GSK collection were used to build a pharmacophore model

281 Screening of the GSK corporate collection, some 1.9 million compounds, ag

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

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

284 adjacent normal tissue, suggesting that the GSK-3alpha/beta-STAT3 pathway is active in the disease.

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

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

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

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

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

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

291 from three different manufacturers (VariVax, GSK, and Biken) that 137 single-nucleotide polymorphism

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

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

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

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

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

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

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

299 Docking studies with GSK-J1, a selective inhibitor of the KDM6/KDM5 subfamili

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