ライフサイエンスコーパス: GSK

1 GSK and MSD varicella-containing vaccines (VCVs) were co

2 GSK induced hyperpolarization of PDGFRalpha(+) cells and

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 siRNA downregulation, or inhibition by small molec

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 250-fold) by glycogen synthase kinase-3beta (GSK-3beta) inhibition using CHIR99021 and concurrent rem

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

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

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

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

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

34 0.030 nM) and selective (>10-fold GSK-3beta/GSK-3alpha) GSK-3beta inhibitor known to date.

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

36 90 genes that are alternatively spliced in a GSK-3-dependent manner, supporting a broad role for GSK-

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

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

39 Screening of a GSK-proprietary library against intracellular Mycobacter

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 tage BET inhibitors BMS-986158, OTX-015, and GSK-525762.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 sponse pathway was probed with salubrial and GSK-2606414.

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

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

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

75 After OAG as well as GSK-1702934A activation, FRET efficiency was simultaneou

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

77 confer high levels of resistance to AT9283, GSK-690693, and gedatolisib, whereas ispinesib, AT7519,

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

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

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

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

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

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

84 , but glycogen synthase kinase 3 alpha/beta (GSK-3alpha/beta) inhibition did not restore BRB properti

85 independently of, both the 4CMenB (Bexsero; GSK) and rLP2086 (Trumenba; Pfizer, Inc.) vaccine manufa

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

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

88 n) or a store-operated Ca(2+) entry blocker (GSK 7975 A) reversed the effects of TTX, L-NNA and ODQ.

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

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

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

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

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

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

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

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

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

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

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

100 enyl)amino]-8-methylquinoline-3-carboxamide (GSK 256066) after 1, 2, 6, or 18 hours of exposure.

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

104 In mature Th17 cells, GSK-J4 induces an altered transcriptional program with a

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

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

107 ardiologie et de pneumologie de Quebec, CIHR/GSK research Chair on COPD at Universite Laval, and the

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

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

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

111 ble effectiveness as MSD VCV at lower costs, GSK VCV may offer higher value for money.

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

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

114 Disrupting GSK activity diminishes Gpa2 phosphorylation levels in v

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

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

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

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

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

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

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

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

123 Furthermore, GSK 256066, roflumilast, and its biologically active met

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

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

126 re than 300 laboratories by GlaxoSmithKline (GSK) between 2011 and 2015 and by SGC-UNC from 2015 to 2

127 7213 study) is sponsored by GlaxoSmithKline (GSK) with associated exploratory studies supported by th

128 Diseases initiative (DNDi), GlaxoSmithKline (GSK), and the University of Dundee.

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

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

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

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

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

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

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

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

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

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

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

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

144 KDM6-specific chemical inhibition (GSK J4) in BMDC led to decreased production of chemokine

145 Histone lysine demethylase inhibition (GSK-J1, 2,4-PDCA) decreased colony formation and invasio

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

147 The prototypic KDM6 inhibitor GSK-J4 increases genome-wide levels of the repressive H3

148 ds in the presence of RIPK3 kinase inhibitor GSK'840 or MLKL inhibitor necrosulfonomide but requires

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

150 mercially available small-molecule inhibitor GSK 872 showed that RIPK3-mediated inflammation promoted

151 e/mammalian target of rampamycin inhibitor), GSK-690693 (AKT inhibitor), and KW-2478 (heat-shock prot

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

153 , in vivo treatment with the KDM6 inhibitor, GSK J4, during RSV infection reduced inflammatory DC in

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

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

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

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

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

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

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

161 of Gpa2 depends on glycogen synthase kinase (GSK).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 4%) whose levels decreased in the absence of GSK-3.

185 h differentially regulated the activities of GSK-3alpha/beta and beta-catenin and further contributed

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

192 These data are consistent with an effect of GSK-J4 on Th17 T cell differentiation pathways directly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 responses measured using an unenhanced PRNT (GSK; seropositivity cutoff and threshold, 2.5 and 4 time

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

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

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

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

242 orylation of AKT, ERK-1/2, PDK1, mTOR, PTEN, GSK-3alphabeta, and p70S6K.

243 phorylation levels in vivo, and the purified GSK isoforms Mck1 and Ygk3 are capable of phosphorylatin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 merase chain reaction analysis revealed that GSK 256066 was a weak stimulus, and the negative microar

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

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

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

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

271 -3 in SHH-driven proliferation suggests that GSK-3 may be targeted for SHH-driven medulloblastoma the

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

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

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

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

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

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

278 we performed a high-throughput screen of the GSK Full Diversity Collection using recombinant P. falci

279 Focused in vitro screening of the GSK Kinetobox library and structure-activity relationshi

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

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

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

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

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

285 British Lung Foundation through the GSK/British Lung Foundation Chair of Respiratory Researc

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

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

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

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

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

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

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

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

294 ngs of our study reveal a mechanism by which GSK- and nutrient-dependent phosphorylation regulates su

295 h salubrial had no significant effect, while GSK-2606414 mitigated the effects of aggregation leading

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

297 te through chemical inhibition of KDM6B with GSK-J4 inhibitor and through exogenous addition of IL-11

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

299 ost-effective in medium- and long-terms with GSK VCV, and only cost-effective at long-term with MSD V

300 RSV-infected BMDC treated with GSK J4 altered coactivation of T cell cytokine productio

301 t was inhibited when BMDCs were treated with GSK J4 prior to sensitization.