PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 32812529-8 2021 Western blotting revealed that 7,3",4"-THIF diminished LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), glycogen synthase kinase-3beta (GSK-3beta), and nuclear factor kappa B (NF-kappaB). 7,3",4"-thif 31-43 glycogen synthase kinase 3 beta Mus musculus 162-192 33609145-6 2021 To address this, we generated tamoxifen-inducible, cartilage-specific Gsk3a/Gsk3b KO (described as "cDKO") in juvenile mice and investigated their skeletal phenotypes. Tamoxifen 30-39 glycogen synthase kinase 3 beta Mus musculus 76-81 34024109-0 2021 Discovery of Novel Tacrine-Pyrimidone Hybrids as Potent Dual AChE/GSK-3 Inhibitors for the Treatment of Alzheimer"s Disease. Tacrine 19-26 glycogen synthase kinase 3 beta Mus musculus 66-71 34024109-0 2021 Discovery of Novel Tacrine-Pyrimidone Hybrids as Potent Dual AChE/GSK-3 Inhibitors for the Treatment of Alzheimer"s Disease. Pyrimidinones 27-37 glycogen synthase kinase 3 beta Mus musculus 66-71 34024109-3 2021 The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3beta: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells. Scopolamine 227-238 glycogen synthase kinase 3 beta Mus musculus 55-60 34024109-3 2021 The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3beta: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells. Serine 326-329 glycogen synthase kinase 3 beta Mus musculus 55-60 34024109-3 2021 The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3beta: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells. Serine 338-341 glycogen synthase kinase 3 beta Mus musculus 55-60 34024109-3 2021 The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3beta: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells. Glyceraldehyde 355-369 glycogen synthase kinase 3 beta Mus musculus 55-60 34024109-3 2021 The optimal compound 27g possessed excellent dual AChE/GSK-3 inhibition both in terms of potency and equilibrium (AChE: IC50 = 51.1 nM; GSK-3beta: IC50 = 89.3 nM) and displayed significant amelioration on cognitive deficits in scopolamine-induced amnesia mice and efficient reduction against phosphorylation of tau protein on Ser-199 and Ser-396 sites in glyceraldehyde (GA)-stimulated differentiated SH-SY5Y cells. Glyceraldehyde 371-373 glycogen synthase kinase 3 beta Mus musculus 55-60 33964281-9 2021 Further study found that the phosphorylation rate of glycogen synthase kinase-3beta (GSK3beta) and beta-catenin nuclear translocation increased, as the levels of the beta-catenin target genes cyclinD1, c-myc, NeuroD1, and Ngn2 upregulated after baicalin treatment. baicalin 245-253 glycogen synthase kinase 3 beta Mus musculus 53-83 32814818-11 2021 We identified glycogen synthase kinase-3 beta (GSK-3beta) as a direct target of miR-99b-3p. mir-99b 80-87 glycogen synthase kinase 3 beta Mus musculus 14-45 33691258-0 2021 6-(methylsulfinyl)hexyl isothiocyanate (6-MITC) from Wasabia japonica alleviates inflammatory bowel disease (IBD) by potential inhibition of glycogen synthase kinase 3 beta (GSK-3beta). 6-(Methylsulfinyl)hexyl isothiocyanate 0-38 glycogen synthase kinase 3 beta Mus musculus 141-172 33691258-0 2021 6-(methylsulfinyl)hexyl isothiocyanate (6-MITC) from Wasabia japonica alleviates inflammatory bowel disease (IBD) by potential inhibition of glycogen synthase kinase 3 beta (GSK-3beta). 6-(Methylsulfinyl)hexyl isothiocyanate 40-46 glycogen synthase kinase 3 beta Mus musculus 141-172 33789427-0 2021 LY3023414 inhibits both osteogenesis and osteoclastogenesis through the PI3K/Akt/GSK3 signalling pathway. LY3023414 0-9 glycogen synthase kinase 3 beta Mus musculus 81-85 33789427-10 2021 RESULTS: LY3023414 attenuated PI3K/protein kinase B (Akt)/GSK3-dependent activation of beta-catenin and nuclear factor-activated T cell 1 (NFATc1) during osteogenesis and osteoclastogenesis, respectively. LY3023414 9-18 glycogen synthase kinase 3 beta Mus musculus 58-62 33789427-14 2021 CONCLUSION: LY3023414 can suppress osteogenesis and osteoclastogenesis through inhibition of the PI3K/Akt/GSK3 signalling pathway, which highlights the potential benefits and side effects of LY3023414 for future clinical applications. LY3023414 12-21 glycogen synthase kinase 3 beta Mus musculus 106-110 33389472-11 2021 Western blot analysis demonstrated that salidroside attenuated the CM-OGD-induced upregulation of phosphorylated Akt and glycogen synthase kinase 3beta (GSK-3beta). rhodioloside 40-51 glycogen synthase kinase 3 beta Mus musculus 121-151 33727611-5 2021 Investigation of oncogenic kinase signaling showed decreased phosphorylation levels of mTOR, CREB, GSK3 and GYS1 leading to altered glycogen metabolism and formation of intracellular reactive oxygen species. Glycogen 132-140 glycogen synthase kinase 3 beta Mus musculus 99-103 33727611-5 2021 Investigation of oncogenic kinase signaling showed decreased phosphorylation levels of mTOR, CREB, GSK3 and GYS1 leading to altered glycogen metabolism and formation of intracellular reactive oxygen species. Reactive Oxygen Species 183-206 glycogen synthase kinase 3 beta Mus musculus 99-103 33894211-12 2021 In a co-culture system, PexRAP knockdown in brain endothelial cells decreased GSK3 phosphorylation in co-cultured astrocytes that was rescued by incubation with the ether lipid alkylglycerol. alkylglycerol 177-190 glycogen synthase kinase 3 beta Mus musculus 78-82 33495840-8 2021 Notably, beta-Lapachone-cotreatment with L-DOPA increased phosphorylation at the Ser9 site of glycogen synthase kinase 3beta (GSK-3beta), indicating suppression of GSK-3beta activity in both the unlesioned and 6-OHDA-lesioned striata. beta-lapachone 9-23 glycogen synthase kinase 3 beta Mus musculus 94-124 33495840-8 2021 Notably, beta-Lapachone-cotreatment with L-DOPA increased phosphorylation at the Ser9 site of glycogen synthase kinase 3beta (GSK-3beta), indicating suppression of GSK-3beta activity in both the unlesioned and 6-OHDA-lesioned striata. Levodopa 41-47 glycogen synthase kinase 3 beta Mus musculus 94-124 33495840-8 2021 Notably, beta-Lapachone-cotreatment with L-DOPA increased phosphorylation at the Ser9 site of glycogen synthase kinase 3beta (GSK-3beta), indicating suppression of GSK-3beta activity in both the unlesioned and 6-OHDA-lesioned striata. Oxidopamine 210-216 glycogen synthase kinase 3 beta Mus musculus 94-124 33494672-1 2021 BACKGROUND: Glycogen synthase kinase 3 (GSK-3) is a serine/threonine kinase enzyme which controlled the neuronal functions such as neurite outgrowth, synapse formation, neurotransmission, and neurogenesis. Serine 52-58 glycogen synthase kinase 3 beta Mus musculus 40-45 33485878-9 2021 CONCLUSIONS: Our results indicated that the DSS rats had hypofunction of the basal dopamine release and AKT/GSK-3 signaling even at 7 days after the antipsychotic was discontinued. dss 44-47 glycogen synthase kinase 3 beta Mus musculus 108-113 33422940-4 2021 In this communication, we demonstrate the remote loading of GSK3 inhibitor AZD1080 into the porous interior of mesoporous silica nanoparticles coated with a lipid bilayer (a.k.a. 2-hydroxy-3-(5-((morpholin-4-yl)methyl)pyridin-2-yl)-1H-indole-5-carbonitrile 75-82 glycogen synthase kinase 3 beta Mus musculus 60-64 33422940-4 2021 In this communication, we demonstrate the remote loading of GSK3 inhibitor AZD1080 into the porous interior of mesoporous silica nanoparticles coated with a lipid bilayer (a.k.a. mesoporous silica 111-128 glycogen synthase kinase 3 beta Mus musculus 60-64 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. quinoline 93-106 glycogen synthase kinase 3 beta Mus musculus 63-68 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. benzothiazole 108-120 glycogen synthase kinase 3 beta Mus musculus 63-68 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. pyrazole 122-130 glycogen synthase kinase 3 beta Mus musculus 63-68 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. Pyrazines 132-140 glycogen synthase kinase 3 beta Mus musculus 63-68 33478120-4 2021 Mechanistically, lithium in islets cells induced inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta), the major molecular target of lithium that has been recently implicated in non-canonical regulation of Nrf2 activity. Lithium 17-24 glycogen synthase kinase 3 beta Mus musculus 79-109 33478120-4 2021 Mechanistically, lithium in islets cells induced inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta), the major molecular target of lithium that has been recently implicated in non-canonical regulation of Nrf2 activity. Lithium 152-159 glycogen synthase kinase 3 beta Mus musculus 79-109 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. dioxolo-benzoxazin 142-160 glycogen synthase kinase 3 beta Mus musculus 63-68 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. Oxadiazoles 162-172 glycogen synthase kinase 3 beta Mus musculus 63-68 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. benzimidazole 174-187 glycogen synthase kinase 3 beta Mus musculus 63-68 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. cyclopropylamide 209-225 glycogen synthase kinase 3 beta Mus musculus 63-68 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. phenyl carbamothioate 227-248 glycogen synthase kinase 3 beta Mus musculus 63-68 33494672-6 2021 Results and Conclusion: It was observed that structures of the GSK-3 inhibitors comprised of benzopyridine, benzthiazole, pyrazole, pyrazine, dioxolo-benzoxazin, oxadiazole, benzimidazole in the skeletal with cyclopropylamide, phenyl carbamothioate, 3-[(propan-2-yl)oxy]propan-1-amine in side chain. 3-[(propan-2-yl)oxy]propan-1-amine 250-284 glycogen synthase kinase 3 beta Mus musculus 63-68 33430188-7 2021 Quinpirole administration regulated D2R expression and significantly reduced glial cell-induced neuroinflammation via the D2R/Akt/glycogen synthase kinase 3 beta (GSK3-beta) signaling pathway after TBI. Quinpirole 0-10 glycogen synthase kinase 3 beta Mus musculus 130-161 33519426-9 2020 Moreover, FLX had no effect on the serotonin (5-HT) 1A receptor (5-HT1AR) content or number of 5-HT1AR+ oligodendrocytes, but it reduced the content and activity of glycogen synthase kinase 3beta (GSK3beta) in the hippocampus of APP/PS1 transgenic mice. Fluoxetine 10-13 glycogen synthase kinase 3 beta Mus musculus 165-195 33371815-9 2021 CRS-exposed mice treated with VBL had dramatically decreased total Tau and Tau phosphorylation in the synapse of the HC and PFC which might be mediated by the regulation of CaMKII and GSK3[Formula: see text] phosphorylation. 3-cresol 0-3 glycogen synthase kinase 3 beta Mus musculus 184-188 31926033-3 2021 Here we show that the mGluR5 PAM, VU0360172 (VuPAM), regulates microglial inflammatory responses through activation of Akt, resulting in the inhibition of GSK-3beta. N-cyclobutyl-6-((3-fluorophenyl)ethynyl)nicotinamide 34-43 glycogen synthase kinase 3 beta Mus musculus 155-164 33190828-3 2021 Glycogen synthase kinase-3beta (GSK-3beta) is a widely expressed serine/threonine kinase and associated with both DM and bone metabolism, which arouse our concern. Serine 65-71 glycogen synthase kinase 3 beta Mus musculus 0-30 31926033-8 2021 Taken together, our data show that VuPAM decreases pro-inflammatory microglial activation by modulating Akt/GSK-3beta/CREB signaling. prolyl-proline 51-54 glycogen synthase kinase 3 beta Mus musculus 108-117 32393087-7 2020 Moreover, berberine enhanced the phosphorylation levels of protein kinase B (PKB/AKT; 2.27-fold) and glycogen synthase kinase-3beta (GSK3beta; 2.56-fold), and increased hepatic glycogen content (from 0.19 to 1.65). Berberine 10-19 glycogen synthase kinase 3 beta Mus musculus 101-131 33000422-3 2021 We report that the treatment of epSPCs and human pluripotent stem cell-derived neural progenitors (hPSC-NPs) with the GSK-3 inhibitor Ro3303544 activates beta-catenin signaling and increases the expression of the bIII-tubulin neuronal marker; furthermore, the differentiation of Ro3303544-treated cells prompted an increase in the number of terminally differentiated neurons. ro3303544 134-143 glycogen synthase kinase 3 beta Mus musculus 118-123 33000422-3 2021 We report that the treatment of epSPCs and human pluripotent stem cell-derived neural progenitors (hPSC-NPs) with the GSK-3 inhibitor Ro3303544 activates beta-catenin signaling and increases the expression of the bIII-tubulin neuronal marker; furthermore, the differentiation of Ro3303544-treated cells prompted an increase in the number of terminally differentiated neurons. ro3303544 279-288 glycogen synthase kinase 3 beta Mus musculus 118-123 33000422-4 2021 Administration of a water-soluble, bioavailable form of this GSK-3 inhibitor (Ro3303544-Cl) in a severe SCI mouse model revealed the increased expression of bIII-tubulin in the injury epicenter. Water 20-25 glycogen synthase kinase 3 beta Mus musculus 61-66 33000422-4 2021 Administration of a water-soluble, bioavailable form of this GSK-3 inhibitor (Ro3303544-Cl) in a severe SCI mouse model revealed the increased expression of bIII-tubulin in the injury epicenter. ro3303544-cl 78-90 glycogen synthase kinase 3 beta Mus musculus 61-66 33288642-8 2020 Using PKCdelta splicing minigene and RNA-immunoprecipitation assays, our results demonstrate that upon LiCl treatment, NEAT1 levels are reduced, GSK3ss activity is inhibited and SFRS10 phosphorylation is decreased which leads to decreased expression of PKCdeltaI. Lithium Chloride 103-107 glycogen synthase kinase 3 beta Mus musculus 145-149 33080056-10 2020 Importantly, selective GSK3 inhibition using 4-Benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione increased levels of synapsin-1, BDNF and phosphorylated-GluA1 proteins, restored hippocampal basal synaptic transmission and LTP, and improved contextual fear memory in male Tg26 mice. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 45-94 glycogen synthase kinase 3 beta Mus musculus 23-27 33331415-7 2020 As expected, the immunoreactivities for brain GSK-3 and HDAC decreased compared to control groups in all areas (striatum, DG, CA1, CA3, and mainly pre-frontal cortex, PFC) after KET injection. Ketamine 178-181 glycogen synthase kinase 3 beta Mus musculus 46-51 32946868-9 2020 Besides, ECT improved the glycogen content by inhibiting the expression of glycogen synthase kinase3beta (GSK3beta) and promoting that of glycogen synthase (GS). Glycogen 26-34 glycogen synthase kinase 3 beta Mus musculus 75-104 33612762-5 2020 Glycogen synthase kinase-3beta (GSK3beta), a serine/threonine kinase plays a pivotal role in the regulation of inflammatory response during pathogenic infections. Serine 45-51 glycogen synthase kinase 3 beta Mus musculus 0-30 33328854-3 2020 Glycogen synthase kinase-3beta (GSK3beta), as a major Tau kinase and a downstream target of the serine protein kinase B (AKT) signaling pathway, can regulate Tau phosphorylation in AD. Serine 96-102 glycogen synthase kinase 3 beta Mus musculus 0-30 32960565-5 2020 Overall, the simultaneous modulation of 6h on multiple dysfunctions of disease network highlights this structural distinctively bisindole-substituted aminopyrazole could be useful prototype for the discovery of innovative therapeutic agents to tackle AD and other GSK-3 associated complex neurological syndromes. bisindole 128-137 glycogen synthase kinase 3 beta Mus musculus 264-269 33000252-0 2020 [Retracted] Glycogen synthase kinase-3beta is required for epithelial-mesenchymal transition and barrier dysfunction in mouse podocytes under high glucose conditions. Glucose 147-154 glycogen synthase kinase 3 beta Mus musculus 12-42 33168035-7 2020 RESULTS: Our data shows that the simultaneous use of SB431542 (TGF-beta inhibitor), Chir9901 (GSK3 inhibitor), and Bpv (PTEN inhibitor) resulted in a 50-fold increase in the number of CD34+CD38- cells. 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide 53-61 glycogen synthase kinase 3 beta Mus musculus 94-98 33168035-7 2020 RESULTS: Our data shows that the simultaneous use of SB431542 (TGF-beta inhibitor), Chir9901 (GSK3 inhibitor), and Bpv (PTEN inhibitor) resulted in a 50-fold increase in the number of CD34+CD38- cells. bromopyruvate 115-118 glycogen synthase kinase 3 beta Mus musculus 94-98 32827692-7 2020 Moreover, HGF treatment obviously prevented inactivation of the protein kinase B (Akt)-glycogen synthase kinase 3 beta (GSK3beta)-transcription factor EB (TFEB) axis in high glucose-stimulated podocytes, which was associated with improved lysosome function and autophagy. Glucose 174-181 glycogen synthase kinase 3 beta Mus musculus 87-118 33192176-0 2020 Isoorientin Inhibits Inflammation in Macrophages and Endotoxemia Mice by Regulating Glycogen Synthase Kinase 3beta. homoorientin 0-11 glycogen synthase kinase 3 beta Mus musculus 84-114 33192176-2 2020 We previously found isoorientin is an inhibitor of glycogen synthase kinase 3beta (GSK3beta) in vitro. homoorientin 20-31 glycogen synthase kinase 3 beta Mus musculus 51-81 32960565-5 2020 Overall, the simultaneous modulation of 6h on multiple dysfunctions of disease network highlights this structural distinctively bisindole-substituted aminopyrazole could be useful prototype for the discovery of innovative therapeutic agents to tackle AD and other GSK-3 associated complex neurological syndromes. 3-aminopyrazole 150-163 glycogen synthase kinase 3 beta Mus musculus 264-269 33066035-8 2020 Although morphine administration induced analgesia when glycogen synthase kinase 3beta (GSK3beta) was in an inactive state due to serine 9 phosphorylation, repeated morphine administration suppressed this phosphorylation event. Morphine 9-17 glycogen synthase kinase 3 beta Mus musculus 56-86 33081685-12 2021 Memantine treatment decreased GSK3B protein expression levels in tumor tissue samples. Memantine 0-9 glycogen synthase kinase 3 beta Mus musculus 30-35 33066035-8 2020 Although morphine administration induced analgesia when glycogen synthase kinase 3beta (GSK3beta) was in an inactive state due to serine 9 phosphorylation, repeated morphine administration suppressed this phosphorylation event. Serine 130-136 glycogen synthase kinase 3 beta Mus musculus 56-86 32812777-10 2020 Finally, SB treatment reduced GSK3 marker, pTau in adult primary enteric neuronal cells. Antimony 9-11 glycogen synthase kinase 3 beta Mus musculus 30-34 33023073-5 2020 Gene heatmaps for IPA canonical pathways showed a novel role for GSK-3 in GP6 signaling pathways associated with capacitation for 60 min. ipa 18-21 glycogen synthase kinase 3 beta Mus musculus 65-70 32640867-5 2020 Biochemical characterization revealed that NPD13432 inhibited GSK3alpha and GSK3beta with IC50 values of 92 nM and 310 nM, respectively, suggesting that the compound promotes self-renewal in mESCs by inhibiting GSK3. npd13432 43-51 glycogen synthase kinase 3 beta Mus musculus 62-66 32698955-9 2020 CONCLUSION: Dual inhibition of GSK3B and HDACs via APCS-540 showed potent anti-tumor activity in vitro and in vivo, suggesting that APCS-540 may provide a novel treatment option for ovarian cancer, including the platinum-resistant disease. Platinum 212-220 glycogen synthase kinase 3 beta Mus musculus 31-36 32855722-13 2020 CA also suppressed the activation of AKT and glycogen synthase kinase 3 beta (GSK3beta) in mice challenged with AB. ab 112-114 glycogen synthase kinase 3 beta Mus musculus 45-76 32540877-7 2020 Specifically, high glucose induces tau hyper-phosphorylation via glucose-responsive kinases GSK3, PKA, PKC, and CDK5. Glucose 19-26 glycogen synthase kinase 3 beta Mus musculus 92-96 32673674-5 2020 First, an 81-kinase screening was carried out and results showed that PT109 potently inhibited c-Jun N-terminal kinases and Serum and glucocorticoid-inducible kinase 1, which are the important signaling molecules involved in neurogenesis, neuroprotection and neuroinflammation and mildly inhibit glycogen synthase kinase-3beta as well as protein kinase C gamma, both are involved in AD pathological processes. platinum 109 70-75 glycogen synthase kinase 3 beta Mus musculus 296-326 32540877-7 2020 Specifically, high glucose induces tau hyper-phosphorylation via glucose-responsive kinases GSK3, PKA, PKC, and CDK5. Glucose 65-72 glycogen synthase kinase 3 beta Mus musculus 92-96 32531667-3 2020 The aim of this study was to investigate whether curcumin could improve chronic kidney disease (CKD)-induced muscle atrophy and mitochondrial dysfunction by inhibiting glycogen synthase kinase-3beta (GSK-3beta) activity. Curcumin 49-57 glycogen synthase kinase 3 beta Mus musculus 168-198 32653611-6 2020 Consequently, poncirin increased GLUT-4 expression level by activating the IRS-1/PI3K/Akt/GSK-3 signaling pathway. poncirin 14-22 glycogen synthase kinase 3 beta Mus musculus 90-95 32680958-7 2020 Thus, Gsk3 N-terminal serine phosphorylation inhibits liver innate immune activation but suppresses hepatocyte autophagy in response to inflammation. Serine 22-28 glycogen synthase kinase 3 beta Mus musculus 6-10 32417177-10 2020 also reversed the STZ-induced increased expression of inducible nitric oxide synthase (iNOS) and glycogen synthase kinase 3 beta (GSK3beta) in the PFC and HC. Streptozocin 18-21 glycogen synthase kinase 3 beta Mus musculus 97-128 32171837-5 2020 Western blot results showed that CS@Se can attenuate excessive phosphorylation of tau (Ser396/Ser404) by regulating the expression of glycogen synthase kinase-3 beta (GSK-3beta). Cesium 33-35 glycogen synthase kinase 3 beta Mus musculus 134-165 32573072-7 2020 The NK cell expression of T-bet was up-regulated by thalidomide treatment and the down-regulation of glycogen synthase kinase 3b expression was observed in thalidomide-treated NK cells. Thalidomide 156-167 glycogen synthase kinase 3 beta Mus musculus 101-128 31951013-13 2020 We also found that miR-124/PTPN1 abnormalities induced activation of glycogen synthase kinase 3 (GSK-3) and inactivation of protein phosphatase 2A (PP2A) by promoting tyrosine phosphorylation, implicating an imbalance in tau kinase/phosphatase. Tyrosine 167-175 glycogen synthase kinase 3 beta Mus musculus 69-95 31951013-13 2020 We also found that miR-124/PTPN1 abnormalities induced activation of glycogen synthase kinase 3 (GSK-3) and inactivation of protein phosphatase 2A (PP2A) by promoting tyrosine phosphorylation, implicating an imbalance in tau kinase/phosphatase. Tyrosine 167-175 glycogen synthase kinase 3 beta Mus musculus 97-102 32660121-7 2020 Furthermore, regorafenib-injected 5x FAD mice displayed significantly reduced tau phosphorylation at T212 and S214 (AT100) due to the downregulation of glycogen synthase kinase-3 beta (GSK3beta) activity. regorafenib 13-24 glycogen synthase kinase 3 beta Mus musculus 152-183 32729236-0 2020 GSK3 inhibition with low dose lithium supplementation augments murine muscle fatigue resistance and specific force production. Lithium 30-37 glycogen synthase kinase 3 beta Mus musculus 0-4 32729236-3 2020 Glycogen synthase kinase 3 (GSK3) is a serine/threonine kinase that antagonizes calcineurin by re-phosphorylating NFAT preventing its entry into the nucleus. Serine 39-45 glycogen synthase kinase 3 beta Mus musculus 0-26 32729236-3 2020 Glycogen synthase kinase 3 (GSK3) is a serine/threonine kinase that antagonizes calcineurin by re-phosphorylating NFAT preventing its entry into the nucleus. Serine 39-45 glycogen synthase kinase 3 beta Mus musculus 28-32 32729236-4 2020 Here, we tested whether GSK3 inhibition in vivo with low dose lithium chloride (LiCl) supplementation (10 mg kg-1 day-1 for 6 weeks) in male C57BL/6J mice would enhance muscle fatigue resistance in soleus and extensor digitorum longus (EDL) muscles by activating NFAT and augmenting PGC-1alpha and MHC I expression. Lithium Chloride 62-78 glycogen synthase kinase 3 beta Mus musculus 24-28 32729236-4 2020 Here, we tested whether GSK3 inhibition in vivo with low dose lithium chloride (LiCl) supplementation (10 mg kg-1 day-1 for 6 weeks) in male C57BL/6J mice would enhance muscle fatigue resistance in soleus and extensor digitorum longus (EDL) muscles by activating NFAT and augmenting PGC-1alpha and MHC I expression. Lithium Chloride 80-84 glycogen synthase kinase 3 beta Mus musculus 24-28 32729236-5 2020 LiCl treatment inhibited GSK3 by elevating Ser9 phosphorylation in soleus (+1.8-fold, p = .007) and EDL (+1.3-fold p = .04) muscles. Lithium Chloride 0-4 glycogen synthase kinase 3 beta Mus musculus 25-29 32729236-10 2020 Altogether, our findings show the skleletal muscle contractile benefits of LiCl-mediated GSK3 inhibition in mice. Lithium Chloride 75-79 glycogen synthase kinase 3 beta Mus musculus 89-93 32695123-5 2020 Firstly, it is already clear that GSK-3 phosphorylation of SARs CoV1 N protein on key serine residues is needed for viral replication such that small molecule inhibitors (SMIs) of GSK-3 can inhibit viral replication. Serine 86-92 glycogen synthase kinase 3 beta Mus musculus 34-39 32695123-5 2020 Firstly, it is already clear that GSK-3 phosphorylation of SARs CoV1 N protein on key serine residues is needed for viral replication such that small molecule inhibitors (SMIs) of GSK-3 can inhibit viral replication. Serine 86-92 glycogen synthase kinase 3 beta Mus musculus 180-185 32695123-9 2020 My hypothesis is that the repurposing of low-cost inhibitors of GSK-3 such as lithium will limit SARS-CoV2 infections by both reducing viral replication and potentiating the immune response against the virus. Lithium 78-85 glycogen synthase kinase 3 beta Mus musculus 64-69 32561809-0 2020 Publisher Correction: 6-Bromoindirubin-3"-oxime intercepts GSK3 signaling to promote and enhance skeletal muscle differentiation affecting miR-206 expression in mice. 6-bromoindirubin-3'-oxime 22-47 glycogen synthase kinase 3 beta Mus musculus 59-63 31679397-1 2020 Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups. Lithium Chloride 409-413 glycogen synthase kinase 3 beta Mus musculus 90-120 32517647-2 2020 However, whether tolfenamic acid can regulate the major tau protein kinase, glycogen synthase kinase-3beta (GSK-3beta), or tau protein phosphatase, protein phosphatase 2A (PP2A), further inhibiting hyperphosphorylation of tau, remains unknown. tolfenamic acid 17-32 glycogen synthase kinase 3 beta Mus musculus 76-106 32581704-6 2020 We found that Gsk3b DeltaDat , but not Gsk3a DeltaDat , showed significant resistance to MPTP insult, revealing non-redundancy of GSK-3alpha and GSK-3beta in PD pathogenesis. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 89-93 glycogen synthase kinase 3 beta Mus musculus 14-19 32357113-8 2020 SR-9009 administration was sufficient to normalize cardiac glycogen synthesis rates, cardiomyocyte size, interstitial fibrosis, and contractility in CBK hearts (without influencing mitochondrial complex activities, nor normalizing substrate oxidation and Akt/mTOR/GSK3b signaling). SR9009 0-7 glycogen synthase kinase 3 beta Mus musculus 264-269 32533502-8 2020 Furthermore, fucoidan increased the expression of nuclear factor erythroid-2 related factor 2 (Nrf2), Glycogen synthase kinase3beta (GSK-3beta), and heme oxygenase (HO-1). fucoidan 13-21 glycogen synthase kinase 3 beta Mus musculus 102-131 31827236-7 2020 Supplementation with exogenous S1P significantly reversed the activation of the PERK-eIF2alpha-ATF4 pathway and ATF6 during ER stress as well as the activation of GSK3beta, ASK1, and JNK during MPT. sphingosine 1-phosphate 31-34 glycogen synthase kinase 3 beta Mus musculus 163-171 31679397-1 2020 Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups. Lithium Chloride 53-69 glycogen synthase kinase 3 beta Mus musculus 90-120 31679397-1 2020 Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups. Lithium Chloride 71-75 glycogen synthase kinase 3 beta Mus musculus 90-120 31679397-1 2020 Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups. Lithium Chloride 409-413 glycogen synthase kinase 3 beta Mus musculus 90-120 31679397-1 2020 Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups. Lithium Chloride 409-413 glycogen synthase kinase 3 beta Mus musculus 90-120 31877332-0 2020 MiR-202-5p attenuates neurological deficits and neuronal injury in MCAO model rats and OGD-induced injury in Neuro-2a cells by targeting eIF4E-mediated induction of autophagy and inhibition of Akt/GSK-3beta pathway. CHD4 protein, human 0-10 glycogen synthase kinase 3 beta Mus musculus 197-206 32295843-8 2020 Diabetes diminished inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser-9 in the retina of WT mice but not in REDD1-deficient mice. Serine 95-98 glycogen synthase kinase 3 beta Mus musculus 50-80 32434848-4 2020 Targets of lithium include paralogs of glycogen synthase kinase 3 (GSK3), and nonselective small-molecule inhibitors of these enzymes improved disease phenotypes in a fragile X syndrome mouse model. Lithium 11-18 glycogen synthase kinase 3 beta Mus musculus 39-65 32434848-4 2020 Targets of lithium include paralogs of glycogen synthase kinase 3 (GSK3), and nonselective small-molecule inhibitors of these enzymes improved disease phenotypes in a fragile X syndrome mouse model. Lithium 11-18 glycogen synthase kinase 3 beta Mus musculus 67-71 32227985-7 2020 Moreover, brains from QTC-4-MeOBnE treated mice had significant decrease in acetylcholinesterase activity and glycogen synthase kinase-3beta levels, but an increase in brain-derived neurotrophic factor and Bcl-2 expression levels. qtc-4-meobne 22-34 glycogen synthase kinase 3 beta Mus musculus 110-140 32414166-5 2020 CRS induced activation of glycogen synthase kinase-3beta and regulated development and DNA damage responses, and reductions in the extracellular-signal-regulated kinase pathway activity were also reversed by rubrofusarin treatment. rubrofusarin 208-220 glycogen synthase kinase 3 beta Mus musculus 26-56 32156176-3 2020 The creation of similar but larger lesions in rat molars shows that the adenosine triphosphate (ATP)-competitive GSK-3 inhibitor, CHIR99021 (CHIR), and the ATP noncompetitive inhibitor, Tideglusib (TG), can equally enhance reparative dentine formation to fully repair an area of dentine damage up to 10 times larger, mimicking the size of small lesions in humans. Adenosine Triphosphate 72-94 glycogen synthase kinase 3 beta Mus musculus 113-118 32156176-3 2020 The creation of similar but larger lesions in rat molars shows that the adenosine triphosphate (ATP)-competitive GSK-3 inhibitor, CHIR99021 (CHIR), and the ATP noncompetitive inhibitor, Tideglusib (TG), can equally enhance reparative dentine formation to fully repair an area of dentine damage up to 10 times larger, mimicking the size of small lesions in humans. Adenosine Triphosphate 96-99 glycogen synthase kinase 3 beta Mus musculus 113-118 31892408-2 2020 GSK-3beta (glycogen synthase kinase-3beta) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D2 receptor (D2R)-mediated signaling to affect dopamine-dependent behaviors. Cyclic AMP 69-73 glycogen synthase kinase 3 beta Mus musculus 0-9 32333225-3 2020 Our results indicated that oral administration of MG136-pMG36e-GLP-1 significantly reduced lipopolysaccharide (LPS)-induced memory impairment and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor dysfunction through the toll-like receptor4 (TLR4)/nuclear factor-kappa B (NFkappaB) and protein kinase B (AKT)/Glycogen synthase kinase-3beta (GSK3beta) signaling pathway. mg136-pmg36e 50-62 glycogen synthase kinase 3 beta Mus musculus 324-354 32340354-2 2020 LiCl affects the activity of the glycogen synthase kinase 3 (GSK3), and mice deficient for GSK3beta showed a reduction in the urine concentration capability. Lithium Chloride 0-4 glycogen synthase kinase 3 beta Mus musculus 33-59 32340354-2 2020 LiCl affects the activity of the glycogen synthase kinase 3 (GSK3), and mice deficient for GSK3beta showed a reduction in the urine concentration capability. Lithium Chloride 0-4 glycogen synthase kinase 3 beta Mus musculus 61-65 32340354-5 2020 LiCl and the inhibitor of GSK3 (SB216763) induced a decrease in the aquaporin-2 (Aqp2) protein level. SB 216763 32-40 glycogen synthase kinase 3 beta Mus musculus 26-30 31892408-2 2020 GSK-3beta (glycogen synthase kinase-3beta) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D2 receptor (D2R)-mediated signaling to affect dopamine-dependent behaviors. Cyclic AMP 69-73 glycogen synthase kinase 3 beta Mus musculus 11-41 31892408-2 2020 GSK-3beta (glycogen synthase kinase-3beta) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D2 receptor (D2R)-mediated signaling to affect dopamine-dependent behaviors. Cyclic AMP 75-105 glycogen synthase kinase 3 beta Mus musculus 0-9 31892408-2 2020 GSK-3beta (glycogen synthase kinase-3beta) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D2 receptor (D2R)-mediated signaling to affect dopamine-dependent behaviors. Cyclic AMP 75-105 glycogen synthase kinase 3 beta Mus musculus 11-41 31892408-2 2020 GSK-3beta (glycogen synthase kinase-3beta) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D2 receptor (D2R)-mediated signaling to affect dopamine-dependent behaviors. Dopamine 119-127 glycogen synthase kinase 3 beta Mus musculus 0-9 31892408-2 2020 GSK-3beta (glycogen synthase kinase-3beta) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D2 receptor (D2R)-mediated signaling to affect dopamine-dependent behaviors. Dopamine 119-127 glycogen synthase kinase 3 beta Mus musculus 11-41 31892408-2 2020 GSK-3beta (glycogen synthase kinase-3beta) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D2 receptor (D2R)-mediated signaling to affect dopamine-dependent behaviors. Dopamine 175-183 glycogen synthase kinase 3 beta Mus musculus 0-9 31892408-2 2020 GSK-3beta (glycogen synthase kinase-3beta) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D2 receptor (D2R)-mediated signaling to affect dopamine-dependent behaviors. Dopamine 175-183 glycogen synthase kinase 3 beta Mus musculus 11-41 31892408-10 2020 Indeed, D2R-GSK-3beta-/- mice also exhibited a resistance of working memory impairment induced by injection of NMDAR antagonist MK-801. Dizocilpine Maleate 128-134 glycogen synthase kinase 3 beta Mus musculus 12-21 32087034-3 2020 Lithium can inhibit GSK3 however, therapeutic doses used in treating bipolar disorder can have toxic effects. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 20-24 32087034-12 2020 In this study, we sought to determine whether feeding mice low-dose lithium, a natural GSK3 inhibitor, would improve left ventricular SERCA function by altering the SERCA2a:PLN ratio. Lithium 68-75 glycogen synthase kinase 3 beta Mus musculus 87-91 32087034-6 2020 Using left ventricles from wild-type mice, we found sub-therapeutic lithium feeding for six weeks decreased GSK3 activity and increased cardiac SERCA function compared to control-fed mice. Lithium 68-75 glycogen synthase kinase 3 beta Mus musculus 108-112 32087034-14 2020 GSK3 activity was significantly reduced in LiCl-fed vs. control-fed mice. Lithium Chloride 43-47 glycogen synthase kinase 3 beta Mus musculus 0-4 31951826-7 2020 Furthermore, LiCl treatment decreased the death of mature oligodendrocytes (OLGs) in ICH mice, which may have been attributed to the enhanced expression of brain-derived neurotrophic factor (BDNF) regulated by the LiCl-induced inhibition of glycogen synthase kinase-3beta (GSK-3beta). Lithium Chloride 214-218 glycogen synthase kinase 3 beta Mus musculus 241-271 32087034-17 2020 Future studies in murine preclinical models will determine whether GSK3 inhibition via low-dose lithium could be a potential therapeutic strategy for DCM and HF. Lithium 96-103 glycogen synthase kinase 3 beta Mus musculus 67-71 31927145-12 2020 Levels of p-Akt and phosphorylated glycogen synthase kinase-3beta measured by a homogeneous time-resolved fluorescence assay were significantly lower in STZ-treated mice than in HFuD-fed mice, suggesting a greater inhibition of brain insulin signaling by STZ than HFuD, although both levels were significantly decreased in these groups compared with controls. Streptozocin 255-258 glycogen synthase kinase 3 beta Mus musculus 35-65 31825818-6 2020 Genetic ablation of TNF-alpha suppressed the obesity-promoted elevation of Wnt signaling, as indicated by decreased levels of phospho-GSK3beta and active beta-catenin, two key components within the Wnt pathway (P<.05). phosphorylleucylphenylalanine 126-133 glycogen synthase kinase 3 beta Mus musculus 134-142 31951826-7 2020 Furthermore, LiCl treatment decreased the death of mature oligodendrocytes (OLGs) in ICH mice, which may have been attributed to the enhanced expression of brain-derived neurotrophic factor (BDNF) regulated by the LiCl-induced inhibition of glycogen synthase kinase-3beta (GSK-3beta). Lithium Chloride 13-17 glycogen synthase kinase 3 beta Mus musculus 241-271 31927145-12 2020 Levels of p-Akt and phosphorylated glycogen synthase kinase-3beta measured by a homogeneous time-resolved fluorescence assay were significantly lower in STZ-treated mice than in HFuD-fed mice, suggesting a greater inhibition of brain insulin signaling by STZ than HFuD, although both levels were significantly decreased in these groups compared with controls. Streptozocin 153-156 glycogen synthase kinase 3 beta Mus musculus 35-65 31638285-6 2020 Boehmite increased hDPC viability, ALP activity, AKT/GSK3ss/ss-catenin pathway activity, anagen-related gene expression, and VEGF secretion; moreover, it accelerated hair re-growth in a catagen-anagen transition model via upregulation of beta-catenin signaling and follicular cell proliferation. aluminum oxide hydroxide 0-8 glycogen synthase kinase 3 beta Mus musculus 53-57 32001318-7 2020 Moreover, theophylline increased the protein expression levels of microphthalmia-associated transcription factor (MITF), tyrosinase, and tyrosinase-related protein 1 (TRP-1), and the level of phosphorylated extracellular regulated protein kinase (p-ERK) and phosphorylated glycogen synthase kinase-3beta (p-GSK3beta) were also increased. Theophylline 10-22 glycogen synthase kinase 3 beta Mus musculus 273-303 31918291-12 2020 Immunohistochemical and immunofluorescence data demonstrated that, compared with the model group, blebbistatin intervention reduced expression of NMMHCIIA, TF, GSK3beta, p65, and p-p65 in carotid-artery endothelia in the CAL-induced AT model, but it increased levels of p-GSK3beta. blebbistatin 98-110 glycogen synthase kinase 3 beta Mus musculus 160-168 31503067-0 2020 Pharmacological inhibition of glycogen synthase kinase 3 increases operant alcohol self-administration in a manner associated with altered pGSK-3beta, protein interacting with C kinase and GluA2 protein expression in the reward pathway of male C57BL/6J mice. Alcohols 75-82 glycogen synthase kinase 3 beta Mus musculus 30-56 31503067-1 2020 Glycogen synthase kinase 3 (GSK-3) is a constitutively active serine-threonine kinase that regulates numerous signaling pathways and has been implicated in neurodegenerative and neuropsychiatric diseases. Serine 62-68 glycogen synthase kinase 3 beta Mus musculus 0-26 31503067-1 2020 Glycogen synthase kinase 3 (GSK-3) is a constitutively active serine-threonine kinase that regulates numerous signaling pathways and has been implicated in neurodegenerative and neuropsychiatric diseases. Serine 62-68 glycogen synthase kinase 3 beta Mus musculus 28-33 31503067-2 2020 Alcohol exposure increases GSK-3beta (ser9) phosphorylation (pGSK-3beta); however, few studies have investigated whether GSK-3 regulates the positive reinforcing effects of alcohol, which drive repetitive drug use. Alcohols 0-7 glycogen synthase kinase 3 beta Mus musculus 27-32 31503067-11 2020 We conclude that GSK-3 inhibition increased the reinforcing effects of alcohol in mice. Alcohols 71-78 glycogen synthase kinase 3 beta Mus musculus 17-22 31503067-13 2020 Given prior results showing that AMPA receptor activity regulates alcohol self-administration, we propose that signaling through the GSK-3/PICK1/GluA2 molecular pathway drives the positive reinforcing effects of the drug, which are required for abuse liability. Alcohols 66-73 glycogen synthase kinase 3 beta Mus musculus 133-138 31918291-12 2020 Immunohistochemical and immunofluorescence data demonstrated that, compared with the model group, blebbistatin intervention reduced expression of NMMHCIIA, TF, GSK3beta, p65, and p-p65 in carotid-artery endothelia in the CAL-induced AT model, but it increased levels of p-GSK3beta. blebbistatin 98-110 glycogen synthase kinase 3 beta Mus musculus 272-280 31918291-14 2020 Overall, our data demonstrated that blebbistatin could inhibit TF expression and AT development in arterial endothelia (at least in part) via GSK3beta/NF-kappaB signaling. blebbistatin 36-48 glycogen synthase kinase 3 beta Mus musculus 142-150 31908108-8 2020 Since ketamine/xylazine also had a marked impact on other key molecular signaling pathways involving the MAP/microtubule affinity-regulating kinase (MARK), extracellular signal-regulated kinase (ERK), and glycogen synthase kinase-3 (GSK3), our study calls for high caution and careful monitoring when using this anesthetic agent in laboratory animal settings across all fields of biological sciences in order to avoid artifactual results. Xylazine 15-23 glycogen synthase kinase 3 beta Mus musculus 205-231 31773824-7 2020 Inhibition of GSK3beta by LiCl showed a gradual decrease in the levels of 78 kDa. Lithium Chloride 26-30 glycogen synthase kinase 3 beta Mus musculus 14-22 31908108-8 2020 Since ketamine/xylazine also had a marked impact on other key molecular signaling pathways involving the MAP/microtubule affinity-regulating kinase (MARK), extracellular signal-regulated kinase (ERK), and glycogen synthase kinase-3 (GSK3), our study calls for high caution and careful monitoring when using this anesthetic agent in laboratory animal settings across all fields of biological sciences in order to avoid artifactual results. Ketamine 6-14 glycogen synthase kinase 3 beta Mus musculus 205-231 32096189-19 2020 Fluoxetine could effectively lower the expressions of GSK-3b and APC in the hippocampus (p<0.01) and increase the expressions of DVL-1 and b-catenin (p<0.01) in model group. Fluoxetine 0-10 glycogen synthase kinase 3 beta Mus musculus 54-60 31908108-8 2020 Since ketamine/xylazine also had a marked impact on other key molecular signaling pathways involving the MAP/microtubule affinity-regulating kinase (MARK), extracellular signal-regulated kinase (ERK), and glycogen synthase kinase-3 (GSK3), our study calls for high caution and careful monitoring when using this anesthetic agent in laboratory animal settings across all fields of biological sciences in order to avoid artifactual results. Ketamine 6-14 glycogen synthase kinase 3 beta Mus musculus 233-237 31908108-8 2020 Since ketamine/xylazine also had a marked impact on other key molecular signaling pathways involving the MAP/microtubule affinity-regulating kinase (MARK), extracellular signal-regulated kinase (ERK), and glycogen synthase kinase-3 (GSK3), our study calls for high caution and careful monitoring when using this anesthetic agent in laboratory animal settings across all fields of biological sciences in order to avoid artifactual results. Xylazine 15-23 glycogen synthase kinase 3 beta Mus musculus 233-237 31881477-8 2020 Consequently, dioscin increased phosphorylation levels of STAT3, PI3K, AKT, GSK-3beta, and FoxO1 and decreased gene levels of PEPCK, G6Pase, SREBP-1c, FAS, ACC, and SCD1, leading to an increase in glycogen synthesis and a decrease in gluconeogenesis and lipogenesis. dioscin 14-21 glycogen synthase kinase 3 beta Mus musculus 76-85 31916204-8 2020 Moreover, edaravone substantially increased the expression of PSD-95 and pSer9-glycogen synthase kinase-3beta (pSer9-GSK3beta) as demonstrated by Western blotting assay. edaravone 10-19 glycogen synthase kinase 3 beta Mus musculus 117-125 31596966-10 2020 CHIR99021 (GSK3beta inhibitor) treatment increased calcium deposition in WT and Ocn-/- VSMCs (1 muM; p < 0.001). Chir 99021 0-9 glycogen synthase kinase 3 beta Mus musculus 11-19 31596966-10 2020 CHIR99021 (GSK3beta inhibitor) treatment increased calcium deposition in WT and Ocn-/- VSMCs (1 muM; p < 0.001). Calcium 51-58 glycogen synthase kinase 3 beta Mus musculus 11-19 31808502-8 2020 Furthermore, we found that GA promoted oligodendrocyte maturation through modulating GSK-3beta signaling pathways. Glycyrrhizic Acid 27-29 glycogen synthase kinase 3 beta Mus musculus 85-94 31783102-0 2020 Glycogen Synthase Kinase 3beta in the Ventral Hippocampus is Important for Cocaine Reward and Object Location Memory. Cocaine 75-82 glycogen synthase kinase 3 beta Mus musculus 0-30 31959776-2 2020 AKT1 activity is also required for lithium, a GSK3 inhibitor, to modulate mood-related behaviors. Lithium 35-42 glycogen synthase kinase 3 beta Mus musculus 46-50 31618623-8 2020 In addition, SRT2104 treatment ameliorated CUMS-induced SIRT1 decreased expression in the hippocampus coincides with the up-regulation phosphorylation levels of GSK3beta and PTEN. SRT2104 13-20 glycogen synthase kinase 3 beta Mus musculus 161-169 31783102-2 2020 Glycogen synthase kinase 3 beta (GSK3beta) has been linked to the maintenance of synaptic plasticity, contextual memory retrieval, and is involved in the reconsolidation of cocaine-associated contextual memory. Cocaine 173-180 glycogen synthase kinase 3 beta Mus musculus 0-31 31936236-4 2020 We established that IGF-1 induced BNIP3 expression through a known AKT serine/threonine kinase 1 (AKT)-mediated inhibitory phosphorylation on Glycogen Synthase Kinase-3beta (GSK-3beta), leading to activation of Nuclear Factor Erythroid 2-related Factor 2 (NFE2L2/Nrf2) and acting through the downstream transcriptional regulators Nuclear Respiratory Factor-1 (NRF1) and Hypoxia-inducible Factor 1 subunit alpha (HIF-1alpha). Serine 71-77 glycogen synthase kinase 3 beta Mus musculus 142-172 31952248-4 2020 Furthermore, GHP supplementation increased muscle glycogen content in diabetic mice, which was probably due to the regulation of glycogen synthase kinase 3 beta and glycogen synthase. ghp 13-16 glycogen synthase kinase 3 beta Mus musculus 129-182 31900153-0 2020 Dopamine D3 receptor and GSK3beta signaling mediate deficits in novel object recognition memory within dopamine transporter knockdown mice. Dopamine 103-111 glycogen synthase kinase 3 beta Mus musculus 25-33 31900153-6 2020 Total or phospho-GSK3 and -ERK1/2 signals in various brain regions were measured by Western blot analyses. phosphorylleucylphenylalanine 9-16 glycogen synthase kinase 3 beta Mus musculus 17-21 32038114-9 2020 TMF treatment also decreased pTau expression, inhibited phosphonuclear factor-kappa B (pNF-kB) and inhibited glycogen synthase kinase 3 (GSK-3) activity by increasing GSK3 phosphorylation (pGSK3). 5,6,7,4'-tetramethoxyflavanone 0-3 glycogen synthase kinase 3 beta Mus musculus 109-135 31906440-0 2020 GSK-3beta-Targeting Fisetin Promotes Melanogenesis in B16F10 Melanoma Cells and Zebrafish Larvae through beta-Catenin Activation. fisetin 20-27 glycogen synthase kinase 3 beta Mus musculus 0-9 32038114-9 2020 TMF treatment also decreased pTau expression, inhibited phosphonuclear factor-kappa B (pNF-kB) and inhibited glycogen synthase kinase 3 (GSK-3) activity by increasing GSK3 phosphorylation (pGSK3). 5,6,7,4'-tetramethoxyflavanone 0-3 glycogen synthase kinase 3 beta Mus musculus 137-142 32038114-9 2020 TMF treatment also decreased pTau expression, inhibited phosphonuclear factor-kappa B (pNF-kB) and inhibited glycogen synthase kinase 3 (GSK-3) activity by increasing GSK3 phosphorylation (pGSK3). 5,6,7,4'-tetramethoxyflavanone 0-3 glycogen synthase kinase 3 beta Mus musculus 167-171 31710934-0 2020 Piperine regulates glycogen synthase kinase-3beta-related signaling and attenuates cognitive decline in D-galactose-induced aging mouse model. piperine 0-8 glycogen synthase kinase 3 beta Mus musculus 19-49 30689763-7 2020 Lansoprazole decreased myocardial levels of phosphorylated Akt, phosphorylated glycogen synthase kinase 3beta, and active beta-catenin in TAC mice and in angiotensin II-stimulated cardiomyocytes. Lansoprazole 0-12 glycogen synthase kinase 3 beta Mus musculus 79-109 31914663-9 2020 Inhibition of calcineurin by FK506 results in an increase in the net phosphorylation and a consequent decrease in catalytic activity of sperm GSK3. Tacrolimus 29-34 glycogen synthase kinase 3 beta Mus musculus 142-146 32741833-10 2020 Our data also showed downregulation of the tau kinases glycogen synthase kinase 3beta and cyclin dependent kinase-5 in DFP treated mice and an increase in the methylation of the catalytic subunit of protein phosphatase 2A. Deferiprone 119-122 glycogen synthase kinase 3 beta Mus musculus 55-85 31789395-6 2020 Pre-treatment with LiCl, which is known to inactivate glycogen synthase kinase 3beta (GSK3beta) by inducing the phosphorylation of the Ser-9 site, resulted in an increased phospho-GSK3beta expression accompanied by beta-catenin that was initially reduced by TQ, and the recovery of the expression and activity of tyrosinase was also confirmed. Lithium Chloride 19-23 glycogen synthase kinase 3 beta Mus musculus 54-84 31789395-6 2020 Pre-treatment with LiCl, which is known to inactivate glycogen synthase kinase 3beta (GSK3beta) by inducing the phosphorylation of the Ser-9 site, resulted in an increased phospho-GSK3beta expression accompanied by beta-catenin that was initially reduced by TQ, and the recovery of the expression and activity of tyrosinase was also confirmed. Serine 135-138 glycogen synthase kinase 3 beta Mus musculus 54-84 31710934-11 2020 Moreover, piperine also reversed D-Gal-induced GSK-3beta activation through modulating PKC and PI3K/AKT pathways in senescent mouse hippocampus, suggesting GSK-3beta-related signaling might be involved in the benefits of piperine against D-Gal-induced cognitive decline in mice. piperine 10-18 glycogen synthase kinase 3 beta Mus musculus 47-56 31710934-11 2020 Moreover, piperine also reversed D-Gal-induced GSK-3beta activation through modulating PKC and PI3K/AKT pathways in senescent mouse hippocampus, suggesting GSK-3beta-related signaling might be involved in the benefits of piperine against D-Gal-induced cognitive decline in mice. piperine 10-18 glycogen synthase kinase 3 beta Mus musculus 156-165 31710934-11 2020 Moreover, piperine also reversed D-Gal-induced GSK-3beta activation through modulating PKC and PI3K/AKT pathways in senescent mouse hippocampus, suggesting GSK-3beta-related signaling might be involved in the benefits of piperine against D-Gal-induced cognitive decline in mice. Galactose 33-38 glycogen synthase kinase 3 beta Mus musculus 47-56 31710934-11 2020 Moreover, piperine also reversed D-Gal-induced GSK-3beta activation through modulating PKC and PI3K/AKT pathways in senescent mouse hippocampus, suggesting GSK-3beta-related signaling might be involved in the benefits of piperine against D-Gal-induced cognitive decline in mice. Galactose 33-38 glycogen synthase kinase 3 beta Mus musculus 156-165 31682812-7 2019 Inhibition of GSK3beta by LiCl rescued the influence of melatonin on differentiation efficiency, Myomaker, but not Myomxier in C2C12 cells. Lithium Chloride 26-30 glycogen synthase kinase 3 beta Mus musculus 14-22 31713882-6 2020 In addition, MK-801-induced increases in phosphorylated Akt and GSK-3beta expression levels in the prefrontal cortex were reversed by HCE (30, 100 or 300 mg/kg). Dizocilpine Maleate 13-19 glycogen synthase kinase 3 beta Mus musculus 64-73 31713882-7 2020 CONCLUSIONS: These results imply that HCE ameliorates MK-801-induced dysfunctions in prepulse inhibition, social interactions and cognitive function, partly by regulating the Akt and GSK-3beta signalling pathways. Dizocilpine Maleate 54-60 glycogen synthase kinase 3 beta Mus musculus 183-192 31706979-8 2020 Mechanistically, SFN prevented T2D-induced cardiomyopathy not only by improving AMPK-mediated lipid metabolic pathways, but also enhancing NRF2 activation via AMPK/AKT/GSK3beta pathway. sulforaphane 17-20 glycogen synthase kinase 3 beta Mus musculus 168-176 31706979-10 2020 CONCLUSIONS: AMPK is indispensable for the SFN-induced prevention of cardiomyopathy in T2D, and the activation of NRF2 by SFN is mediated by AMPK/AKT/GSK3beta signaling pathways. sulforaphane 122-125 glycogen synthase kinase 3 beta Mus musculus 150-158 31535657-11 2020 These results confirm that sevoflurane has less effect on cognitive impairment than isoflurane, which may be related to expression of D1 dopamine receptors and catechol-O-methyltransferase and phosphorylation of glycogen synthase kinase-3beta in the hippocampus. Sevoflurane 27-38 glycogen synthase kinase 3 beta Mus musculus 212-242 31535657-11 2020 These results confirm that sevoflurane has less effect on cognitive impairment than isoflurane, which may be related to expression of D1 dopamine receptors and catechol-O-methyltransferase and phosphorylation of glycogen synthase kinase-3beta in the hippocampus. Isoflurane 84-94 glycogen synthase kinase 3 beta Mus musculus 212-242 31861323-5 2019 The phosphorylation of GSK3beta (Ser9) and anti-apoptotic protein Bcl2 expression levels were significantly downregulated in Prx II knockdown HT22 cells, which suggests that Prx II knockdown HT22 cells were more susceptible to alcohol-induced apoptosis. Ethanol 227-234 glycogen synthase kinase 3 beta Mus musculus 23-31 31861323-6 2019 Scavenging the alcohol-induced ROS with NAC significantly decreased the intracellular ROS levels, as well as the phosphorylation level of GSK3beta in Prx II knockdown HT22 cells. Ethanol 15-22 glycogen synthase kinase 3 beta Mus musculus 138-146 31682812-7 2019 Inhibition of GSK3beta by LiCl rescued the influence of melatonin on differentiation efficiency, Myomaker, but not Myomxier in C2C12 cells. Melatonin 56-65 glycogen synthase kinase 3 beta Mus musculus 14-22 31920532-8 2019 However, genetic brain 5-HT deficiency blocks HFD-induced reductions in forced swim immobility and prevents HFD-induced increases in hippocampal GSK3beta phosphorylation despite having no significant effects on HFD-induced changes in body weight or anxiety-like behavior. Serotonin 23-27 glycogen synthase kinase 3 beta Mus musculus 145-153 31831767-0 2019 Glycogen Synthase Kinase-3beta Inhibition with 9-ING-41 Attenuates the Progression of Pulmonary Fibrosis. 3-(5-fluorobenzofuran-3-yl)-4-(5-methyl-5H-(1,3)dioxolo(4,5-f)indol-7-yl)-pyrrole-2,5-dione 47-55 glycogen synthase kinase 3 beta Mus musculus 0-30 31831767-5 2019 These same mediators enhanced GSK-3beta activation via phosphorylation of tyrosine-216 (p-Y216). SK-216 74-86 glycogen synthase kinase 3 beta Mus musculus 30-39 31831767-6 2019 Inhibition of GSK-3beta signaling with the novel inhibitor 9-ING-41 blocked the induction of myofibroblast markers; alpha-SMA and Col-1 and reduced morphological changes of myofibroblast differentiation. 3-(5-fluorobenzofuran-3-yl)-4-(5-methyl-5H-(1,3)dioxolo(4,5-f)indol-7-yl)-pyrrole-2,5-dione 59-67 glycogen synthase kinase 3 beta Mus musculus 14-23 31562948-5 2019 Mechanistically, HML was found to inhibit Akt activation, subsequently decreasing GSK-3 and Bad phosphorylation, promoting apoptotic induction. humulene 17-20 glycogen synthase kinase 3 beta Mus musculus 82-87 31792344-0 2019 6-Bromoindirubin-3"-oxime intercepts GSK3 signaling to promote and enhance skeletal muscle differentiation affecting miR-206 expression in mice. 6-bromoindirubin-3'-oxime 0-25 glycogen synthase kinase 3 beta Mus musculus 37-41 31815045-11 2019 DSF/Cu2+ upregulated PD-L1 expression by inhibiting PARP1 activity and enhancing GSK3beta phosphorylation at Ser9 and ultimately inhibited T cell infiltration. Copper 4-8 glycogen synthase kinase 3 beta Mus musculus 81-89 31619538-4 2019 GSK3beta deficiency in mouse embryonic fibroblasts significantly reduces polyinosinic:polycytidylic acid-induced IFN-beta and IFN-stimulated gene expression, which is caused by diminished phosphorylation of Src at tyrosine 416. Poly I-C 73-104 glycogen synthase kinase 3 beta Mus musculus 0-8 31619538-4 2019 GSK3beta deficiency in mouse embryonic fibroblasts significantly reduces polyinosinic:polycytidylic acid-induced IFN-beta and IFN-stimulated gene expression, which is caused by diminished phosphorylation of Src at tyrosine 416. Tyrosine 214-222 glycogen synthase kinase 3 beta Mus musculus 0-8 31852639-1 2019 OBJECTIVE: To investigate the role of the protein-serine-threonine kinase (AKT)/glycogen synthase kinase 3beta (GSK3beta) signaling pathway in nicotinic acetylcholine receptors (nAChRs) aggregation disorder on skeletal muscle cell membranes induced by sepsis. Acetylcholine 153-166 glycogen synthase kinase 3 beta Mus musculus 80-110 31693697-9 2019 Testosterone supplementation inhibited GSK3alpha in the myocytes in a PI3K/AKT pathway dependent manner; on the other hand GSK3beta gene expression was reduced in the skeletal muscle upon testosterone supplementation. Testosterone 188-200 glycogen synthase kinase 3 beta Mus musculus 123-131 31662443-11 2019 Collectively, these findings suggest that CXCL12 interacts with CXCR4 and then activates the GSK-3beta/beta-cateninT120/TCF21 signaling pathway to inhibit ABCA1-dependent cholesterol efflux from macrophages and aggravate atherosclerosis. Cholesterol 171-182 glycogen synthase kinase 3 beta Mus musculus 93-102 31394202-6 2019 We further confirmed that the activation or inhibition of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta) significantly changed Abeta/p75NTR-mediated p-tau levels in neurons. p-tau 181-186 glycogen synthase kinase 3 beta Mus musculus 95-125 31642668-10 2019 Pterostilbene induced CAT expression was associated with inhibition of Akt, PRAS40, and GSK-3beta signaling activation and upregulation of PTEN. pterostilbene 0-13 glycogen synthase kinase 3 beta Mus musculus 88-97 31815045-11 2019 DSF/Cu2+ upregulated PD-L1 expression by inhibiting PARP1 activity and enhancing GSK3beta phosphorylation at Ser9 and ultimately inhibited T cell infiltration. seryl-seryl-seryl-arginine 109-113 glycogen synthase kinase 3 beta Mus musculus 81-89 31815045-13 2019 In addition, we observed negative associations between PARP1 and p-GSK3beta (Ser9) or PD-L1 expression in tumor tissue samples from HCC patients. seryl-seryl-seryl-arginine 77-81 glycogen synthase kinase 3 beta Mus musculus 67-75 31815045-14 2019 Through in vitro and in vivo studies, we found that DSF/Cu2+ could restrain GSK3beta activity by inhibiting PARP1, leading to the upregulation of PD-L1 expression. Copper 56-60 glycogen synthase kinase 3 beta Mus musculus 76-84 31420527-1 2019 Previous research has demonstrated that activity of glycogen synthase kinase-3 (GSK3) is necessary for the rewarding effects of cocaine. Cocaine 128-135 glycogen synthase kinase 3 beta Mus musculus 52-78 31461543-10 2019 The latter involves GSK3beta inhibitory serine 9 phosphorylation downstream of Akt activation but not HDAC6 activity. Serine 40-46 glycogen synthase kinase 3 beta Mus musculus 20-28 31486092-0 2019 p-Synephrine exhibits anti-adipogenic activity by activating the Akt/GSK3beta signaling pathway in 3T3-L1 adipocytes. Synephrine 0-12 glycogen synthase kinase 3 beta Mus musculus 69-77 31486092-3 2019 p-Synephrine treatment markedly activated the protein kinase B (PKB/Akt) pathway and sequentially inhibited glycogen synthase kinase 3beta (GSK3beta) activity. Synephrine 0-12 glycogen synthase kinase 3 beta Mus musculus 108-138 31486092-3 2019 p-Synephrine treatment markedly activated the protein kinase B (PKB/Akt) pathway and sequentially inhibited glycogen synthase kinase 3beta (GSK3beta) activity. Synephrine 0-12 glycogen synthase kinase 3 beta Mus musculus 140-148 31486092-4 2019 Inhibition of GSK3beta activity by LiCl was found to partially ameliorate the above-mentioned effects. Lithium Chloride 35-39 glycogen synthase kinase 3 beta Mus musculus 14-22 31420527-1 2019 Previous research has demonstrated that activity of glycogen synthase kinase-3 (GSK3) is necessary for the rewarding effects of cocaine. Cocaine 128-135 glycogen synthase kinase 3 beta Mus musculus 80-84 31483951-8 2019 Rho A gene depletion partially diminishes GSK3beta induction of podocytes by glucose. Glucose 77-84 glycogen synthase kinase 3 beta Mus musculus 42-50 30499878-8 2019 Our results demonstrated that hypercholesterolemia attenuated RIPC-induced cardioprotection against I/R injury by alteration of PTEN/Akt/GSK3beta signals, and inhibition of PTEN rescued RIPC-induced cardioprotection in the presence of hypercholesterolemia. ripc 62-66 glycogen synthase kinase 3 beta Mus musculus 137-145 31671858-2 2019 Lithium, a common medication for bipolar disorder, inhibits GSK3 via Mg+ competition and increased Ser21 (GSK3alpha) or Ser9 (GSK3beta) phosphorylation, leading to enhanced myoblast fusion and myogenic differentiation. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 126-134 31666560-5 2019 Ouabain administration also caused activation of Akt, deactivation of GSK3beta and activation of ERK1/2 in the striatum of ouabain-treated mice. Ouabain 0-7 glycogen synthase kinase 3 beta Mus musculus 70-78 31671858-0 2019 A Low-Therapeutic Dose of Lithium Inhibits GSK3 and Enhances Myoblast Fusion in C2C12 Cells. Lithium 26-33 glycogen synthase kinase 3 beta Mus musculus 43-47 31671858-2 2019 Lithium, a common medication for bipolar disorder, inhibits GSK3 via Mg+ competition and increased Ser21 (GSK3alpha) or Ser9 (GSK3beta) phosphorylation, leading to enhanced myoblast fusion and myogenic differentiation. Magnesium 69-71 glycogen synthase kinase 3 beta Mus musculus 60-64 31671858-2 2019 Lithium, a common medication for bipolar disorder, inhibits GSK3 via Mg+ competition and increased Ser21 (GSK3alpha) or Ser9 (GSK3beta) phosphorylation, leading to enhanced myoblast fusion and myogenic differentiation. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 60-64 31671858-3 2019 However, previous studies demonstrating the effect of lithium on GSK3 have used concentrations up to 10 mM, which greatly exceeds concentrations measured in the serum of patients being treated for bipolar disorder (0.5-1.2 mM). Lithium 54-61 glycogen synthase kinase 3 beta Mus musculus 65-69 31671858-5 2019 C2C12 myotubes differentiated for three days in media containing 0.5 mM lithium chloride (LiCl) had significantly higher GSK3beta (ser9) and GSK3alpha (ser21) phosphorylation compared with control myotubes differentiated in the same media without LiCl (+2-2.5 fold, p < 0.05), a result associated with an increase in total beta-catenin. Lithium Chloride 72-88 glycogen synthase kinase 3 beta Mus musculus 121-129 31671858-5 2019 C2C12 myotubes differentiated for three days in media containing 0.5 mM lithium chloride (LiCl) had significantly higher GSK3beta (ser9) and GSK3alpha (ser21) phosphorylation compared with control myotubes differentiated in the same media without LiCl (+2-2.5 fold, p < 0.05), a result associated with an increase in total beta-catenin. Lithium Chloride 90-94 glycogen synthase kinase 3 beta Mus musculus 121-129 31671858-6 2019 To further demonstrate that 0.5 mM LiCl inhibited GSK3 activity, we also developed a novel GSK3-specific activity assay. Lithium Chloride 35-39 glycogen synthase kinase 3 beta Mus musculus 50-54 31671858-6 2019 To further demonstrate that 0.5 mM LiCl inhibited GSK3 activity, we also developed a novel GSK3-specific activity assay. Lithium Chloride 35-39 glycogen synthase kinase 3 beta Mus musculus 91-95 31671858-7 2019 Using this enzyme-linked spectrophotometric assay, we showed that 0.5 mM LiCl-treated myotubes had significantly reduced GSK3 activity (-86%, p < 0.001). Lithium Chloride 73-77 glycogen synthase kinase 3 beta Mus musculus 121-125 31736967-5 2019 Administration of an alpha7-nAChR agonist PHA-543613 induced activation of PI3K/AKT/GSK-3beta, and reversed changes in pro-inflammatory and anti-inflammatory factors, Nrf-2 and HO-1. N-(1-azabicyclo(2.2.2)oct-3-yl)furo(2,3-c)pyridine-5-carboxamide 42-52 glycogen synthase kinase 3 beta Mus musculus 84-93 31749684-8 2019 Interestingly, the levels of phosphorylated GSK-3beta (Ser9), which inhibits the activity of GSK-3beta, decreased along the same time course as the levels of GluR2 increased in ACC during development. seryl-seryl-seryl-arginine 55-59 glycogen synthase kinase 3 beta Mus musculus 44-53 31875823-0 2019 [The role of GSK3beta in adipose tissue inflammation induced by bisphenol-A in high fat diet fed mice]. bisphenol A 64-75 glycogen synthase kinase 3 beta Mus musculus 13-21 31875823-1 2019 OBJECTIVE: To study the effect of glycogen synthase kinase 3beta(GSK3beta) in BPA-induced adipose tissue inflammation in high fat diet(HFD) fed mice. 4-boronophenylalanine-fructose 78-81 glycogen synthase kinase 3 beta Mus musculus 34-64 31875823-1 2019 OBJECTIVE: To study the effect of glycogen synthase kinase 3beta(GSK3beta) in BPA-induced adipose tissue inflammation in high fat diet(HFD) fed mice. 4-boronophenylalanine-fructose 78-81 glycogen synthase kinase 3 beta Mus musculus 65-73 31875823-44 2019 CONCLUSION: GSK3beta inhibitor can down-regulate BPA-induced adipose tissue inflammation, inflammatory cytokine expression and upregulate GSK3beta-S9 phosphorylation in HFD-fed mice, suggesting that BPA exposure may regulate the expression of inflammatory cytokines mediating adipose tissue inflammation by affecting the degree of phosphorylation of GSK3beta-S9. 4-boronophenylalanine-fructose 49-52 glycogen synthase kinase 3 beta Mus musculus 12-20 31875823-44 2019 CONCLUSION: GSK3beta inhibitor can down-regulate BPA-induced adipose tissue inflammation, inflammatory cytokine expression and upregulate GSK3beta-S9 phosphorylation in HFD-fed mice, suggesting that BPA exposure may regulate the expression of inflammatory cytokines mediating adipose tissue inflammation by affecting the degree of phosphorylation of GSK3beta-S9. 4-boronophenylalanine-fructose 199-202 glycogen synthase kinase 3 beta Mus musculus 12-20 31749684-8 2019 Interestingly, the levels of phosphorylated GSK-3beta (Ser9), which inhibits the activity of GSK-3beta, decreased along the same time course as the levels of GluR2 increased in ACC during development. seryl-seryl-seryl-arginine 55-59 glycogen synthase kinase 3 beta Mus musculus 93-102 31499069-5 2019 KEY FINDINGS: We conclude that XQ-1H preserved the motor functions, limited apoptosis, and concomitantly promoted neurogenesis-related protein expression by Wnt signaling-dependently compromising GSK3beta/Caspase-3 activity and enhancing the expression of Wnt1/beta-catenin/Neuro D1/Cyclin D1 and Bcl-xL. xq-1h 31-36 glycogen synthase kinase 3 beta Mus musculus 196-204 31376787-3 2019 Chrysin reduced weight loss, attenuated clinical signs and blunted the EAE-induced increase in histone deacetylase (HDCA) activity, glycogen synthase kinase-3beta (GSK-3beta) levels and pro-inflammatory cytokine levels as well as in the EAE-induced decrease in histone acetyltransferases 3 and 4 (HAT3, HAT4). EAE 71-74 glycogen synthase kinase 3 beta Mus musculus 132-162 30576423-8 2019 This FUNDC2/AKT/GSK-3beta/cGMP axis also regulates clot retraction of platelet-rich plasma. Cyclic GMP 26-30 glycogen synthase kinase 3 beta Mus musculus 16-25 31229551-0 2019 2,5-Dimethylcelecoxib prevents isoprenaline-induced cardiomyocyte hypertrophy and cardiac fibroblast activation by inhibiting Akt-mediated GSK-3 phosphorylation. 2,5-dimethylcelecoxib 0-21 glycogen synthase kinase 3 beta Mus musculus 139-144 31229551-0 2019 2,5-Dimethylcelecoxib prevents isoprenaline-induced cardiomyocyte hypertrophy and cardiac fibroblast activation by inhibiting Akt-mediated GSK-3 phosphorylation. Isoproterenol 31-43 glycogen synthase kinase 3 beta Mus musculus 139-144 31229551-1 2019 We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative that is unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3) and prolonged the lifespan of heart failure mice with genetic dilated cardiomyopathy or transverse aortic constriction-induced left ventricular hypertrophy. 2,5-dimethylcelecoxib 28-49 glycogen synthase kinase 3 beta Mus musculus 176-202 31229551-1 2019 We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative that is unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3) and prolonged the lifespan of heart failure mice with genetic dilated cardiomyopathy or transverse aortic constriction-induced left ventricular hypertrophy. 2,5-dimethylcelecoxib 28-49 glycogen synthase kinase 3 beta Mus musculus 204-209 31229551-1 2019 We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative that is unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3) and prolonged the lifespan of heart failure mice with genetic dilated cardiomyopathy or transverse aortic constriction-induced left ventricular hypertrophy. dm-celecoxib 51-63 glycogen synthase kinase 3 beta Mus musculus 176-202 31229551-1 2019 We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative that is unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3) and prolonged the lifespan of heart failure mice with genetic dilated cardiomyopathy or transverse aortic constriction-induced left ventricular hypertrophy. dm-celecoxib 51-63 glycogen synthase kinase 3 beta Mus musculus 204-209 31229551-4 2019 DM-celecoxib suppressed isoprenaline-induced neonatal rat cardiomyocyte hypertrophy by the inhibition of Akt phosphorylation resulting in the activation of GSK-3 and the inhibition of beta-catenin and mammalian target of rapamycin (mTOR). dm-celecoxib 0-12 glycogen synthase kinase 3 beta Mus musculus 156-161 31229551-4 2019 DM-celecoxib suppressed isoprenaline-induced neonatal rat cardiomyocyte hypertrophy by the inhibition of Akt phosphorylation resulting in the activation of GSK-3 and the inhibition of beta-catenin and mammalian target of rapamycin (mTOR). Isoproterenol 24-36 glycogen synthase kinase 3 beta Mus musculus 156-161 31540917-6 2019 The GSK-3 inhibitor CHIR-98014 similarly downregulated SHH-driven proliferation. Chir 98014 20-30 glycogen synthase kinase 3 beta Mus musculus 4-9 31361029-0 2019 Activation of GSK3beta induced by recall of cocaine reward memories is dependent on GluN2A/B NMDA receptor signaling. Cocaine 44-51 glycogen synthase kinase 3 beta Mus musculus 14-22 31361029-2 2019 Our previous study demonstrated that GSK3beta activity is highly induced during cocaine memory reactivation, and that reconsolidation of cocaine reward memory is attenuated by inhibition of GSK3beta. Cocaine 80-87 glycogen synthase kinase 3 beta Mus musculus 37-45 31361029-2 2019 Our previous study demonstrated that GSK3beta activity is highly induced during cocaine memory reactivation, and that reconsolidation of cocaine reward memory is attenuated by inhibition of GSK3beta. Cocaine 137-144 glycogen synthase kinase 3 beta Mus musculus 190-198 31361029-9 2019 Administration of the GluN2A- and GluN2B-NMDA receptor antagonists, NVP-AAM077 and ifenprodil, respectively, immediately following recall abrogated an established cocaine place preference, while preventing the activation of GSK3beta in the amygdala, nucleus accumbens, and hippocampus during cocaine memory reactivation. ifenprodil 83-93 glycogen synthase kinase 3 beta Mus musculus 224-232 31361029-10 2019 PP1 inhibition with okadaic acid also blocked the activation of GSK3beta and attenuated a previously established cocaine place preference. Okadaic Acid 20-32 glycogen synthase kinase 3 beta Mus musculus 64-72 31361029-11 2019 These findings suggest that the dephosphorylation of GSK3beta that occurred upon activation of cocaine-associated reward memories may be initiated by the activation of PP1 during the induction of NMDA receptor-dependent reconsolidation of cocaine mnemonic traces. Cocaine 95-102 glycogen synthase kinase 3 beta Mus musculus 53-61 31251996-0 2019 Ketamine-induced regulation of TrkB-GSK3beta signaling is accompanied by slow EEG oscillations and sedation but is independent of hydroxynorketamine metabolites. Ketamine 0-8 glycogen synthase kinase 3 beta Mus musculus 36-44 31251996-0 2019 Ketamine-induced regulation of TrkB-GSK3beta signaling is accompanied by slow EEG oscillations and sedation but is independent of hydroxynorketamine metabolites. 6-Hydroxynorketamine 130-148 glycogen synthase kinase 3 beta Mus musculus 36-44 31251996-2 2019 Among molecular mechanisms, activation of BDNF receptor TrkB along with the inhibition of GSK3beta (glycogen synthase kinase 3beta) are considered as critical molecular level determinants for ketamine"s antidepressant effects. Ketamine 192-200 glycogen synthase kinase 3 beta Mus musculus 90-98 31251996-2 2019 Among molecular mechanisms, activation of BDNF receptor TrkB along with the inhibition of GSK3beta (glycogen synthase kinase 3beta) are considered as critical molecular level determinants for ketamine"s antidepressant effects. Ketamine 192-200 glycogen synthase kinase 3 beta Mus musculus 100-130 31251996-4 2019 However, we have shown that nitrous oxide, another NMDAR blocking anesthetic and a putative rapid-acting antidepressant, evokes TrkB-GSK3beta signaling alterations during rebound slow EEG (electroencephalogram) oscillations. Nitrous Oxide 28-41 glycogen synthase kinase 3 beta Mus musculus 133-141 31251996-10 2019 recapitulated the effects of ketamine on TrkB and GSK3beta phosphorylation while cis-HNK at a dose of 20 mg/kg produced negligible acute effects on TrkB-GSK3beta signaling or slow oscillations. Ketamine 29-37 glycogen synthase kinase 3 beta Mus musculus 50-58 31251996-11 2019 These findings suggest that the acute effects of ketamine on TrkB-GSK3beta signaling are by no means restricted to subanesthetic (i.e. antidepressant) doses and that cis-HNK is not responsible for these effects. Ketamine 49-57 glycogen synthase kinase 3 beta Mus musculus 66-74 31158442-15 2019 The underlying mechanisms of the beneficial effects of ASE may be associated with the increase of glycogen synthesis, the inhibition of AGEs production, the upregulation of IRS2, PI3K, AKT, and GLUT4 protein and mRNA expression, and the downregulation of GSK3beta protein and mRNA expression. ase 55-58 glycogen synthase kinase 3 beta Mus musculus 255-263 30576423-9 2019 CONCLUSION: FUNDC2 positively regulates platelet functions via AKT/GSK-3beta/cGMP signalling pathways, which provides new insight for platelet-related diseases. Cyclic GMP 77-81 glycogen synthase kinase 3 beta Mus musculus 67-76 33597499-2 2019 The ubiquitous serine/threonine kinase, glycogen synthase kinase3beta (GSK3beta) is a crucial regulator of the balance between pro- and anti-inflammatory cytokine productions in the inflammatory response to pathogenic infections. Serine 15-21 glycogen synthase kinase 3 beta Mus musculus 40-69 31410155-6 2019 SB216763, an inhibitor of glycogen synthase kinase-3beta, that reduces the phosphorylation of beta-catenin, inhibited the T3-induced osteocalcin release. SB 216763 0-8 glycogen synthase kinase 3 beta Mus musculus 26-56 31296061-8 2019 Furthermore, uridine affected the levels of 10 fatty acids, lipid and glucose gene (FASN, LCAT, PC, PEPCK, GSK3beta, and GLUT2; P < .05) depending on the timing of administration (P < .05). Uridine 13-20 glycogen synthase kinase 3 beta Mus musculus 107-115 31233346-0 2019 Isorhynchophylline exerts antidepressant-like effects in mice via modulating neuroinflammation and neurotrophins: involvement of the PI3K/Akt/GSK-3beta signaling pathway. rhyncophylline 0-18 glycogen synthase kinase 3 beta Mus musculus 142-151 31233346-7 2019 Western blotting analysis showed that CUMS markedly suppressed the levels of phosphorylated GSK-3beta (Ser9) and phosphorylated Akt (Ser473) but significantly enhanced the translocation of NF-kappaB p65 from cytosol to nuclei in the hippocampus and cerebral cortex of the mice. cums 38-42 glycogen synthase kinase 3 beta Mus musculus 92-101 31497228-5 2019 We showed that bFGF and LIF are indispensable for the derivation and maintenance of rbES; whereas the 3i medium containing inhibitors to the MEK (PD0325901), GSK3 (CHIR99021) and PKC (Go6983) were necessary for deriving domed rbES. 3i medium 102-111 glycogen synthase kinase 3 beta Mus musculus 158-162 31125824-7 2019 When the GSK-3 inhibitor was combined with DOX increased more expression levels of Nrf2 mRNA and restored levels of GSH-Px and SOD-1 mRNA similar to those in the control group. Doxorubicin 43-46 glycogen synthase kinase 3 beta Mus musculus 9-14 31125824-0 2019 Protective properties of glycogen synthase kinase-3 inhibition against doxorubicin-induced oxidative damage to mouse ovarian reserve. Doxorubicin 71-82 glycogen synthase kinase 3 beta Mus musculus 25-51 31125824-7 2019 When the GSK-3 inhibitor was combined with DOX increased more expression levels of Nrf2 mRNA and restored levels of GSH-Px and SOD-1 mRNA similar to those in the control group. Glutathione 116-119 glycogen synthase kinase 3 beta Mus musculus 9-14 31125824-4 2019 The present study assessed whether GSK-3 inhibition confers protection to the ovary against DOX-induced oxidative stress damage. Doxorubicin 92-95 glycogen synthase kinase 3 beta Mus musculus 35-40 31125824-16 2019 Given these results, we suggest that GSK-3/Nrf2 is a promising protective pathway against doxorubicin-induced oxidative damage to the ovaries of females at reproductive ages. Doxorubicin 90-101 glycogen synthase kinase 3 beta Mus musculus 37-42 31125824-5 2019 An intraperitoneal injection of DOX was used to induce oxidative damage in the mouse ovary, while the inhibition of GSK-3 was achieved by the administration of SB216763, a small and potent GSK-3 inhibitor. SB 216763 160-168 glycogen synthase kinase 3 beta Mus musculus 116-121 31125824-5 2019 An intraperitoneal injection of DOX was used to induce oxidative damage in the mouse ovary, while the inhibition of GSK-3 was achieved by the administration of SB216763, a small and potent GSK-3 inhibitor. SB 216763 160-168 glycogen synthase kinase 3 beta Mus musculus 189-194 30887567-5 2019 In a molecular mechanism study, platycodin D induced beta-catenin nuclear accumulation by upregulating GSK3beta phosphorylation. platycodin D 32-44 glycogen synthase kinase 3 beta Mus musculus 103-111 31825015-2 2019 Glycogen synthase kinase 3 (GSK3) is a multi-functional serine/threonine kinase existing as two distinct but related isoforms (alpha and beta). cholecystokinin C-terminal flanking peptide 56-62 glycogen synthase kinase 3 beta Mus musculus 0-26 31825015-2 2019 Glycogen synthase kinase 3 (GSK3) is a multi-functional serine/threonine kinase existing as two distinct but related isoforms (alpha and beta). cholecystokinin C-terminal flanking peptide 56-62 glycogen synthase kinase 3 beta Mus musculus 28-32 31825015-2 2019 Glycogen synthase kinase 3 (GSK3) is a multi-functional serine/threonine kinase existing as two distinct but related isoforms (alpha and beta). glycyl-threonine 63-72 glycogen synthase kinase 3 beta Mus musculus 0-26 31825015-2 2019 Glycogen synthase kinase 3 (GSK3) is a multi-functional serine/threonine kinase existing as two distinct but related isoforms (alpha and beta). glycyl-threonine 63-72 glycogen synthase kinase 3 beta Mus musculus 28-32 30604872-0 2019 Extracellular enzymatically synthesized glycogen promotes osteogenesis by activating osteoblast differentiation via Akt/GSK-3beta signaling pathway. Glycogen 40-48 glycogen synthase kinase 3 beta Mus musculus 120-129 31175886-0 2019 Modification of GSK3beta/beta-catenin signaling on saikosaponins-d-induced inhibition of neural progenitor cell proliferation and adult neurogenesis. saikosaponin D 51-66 glycogen synthase kinase 3 beta Mus musculus 16-24 31175886-7 2019 Treatment with SB216763, a specific inhibitor for GSK3beta activation, we showed that inactivation GSK3beta improved the beta-catenin signaling by inhibiting degradation complex comprising Axin and APC and attenuated SSd-induced toxicity in NPCs. SB 216763 15-23 glycogen synthase kinase 3 beta Mus musculus 50-58 31175886-7 2019 Treatment with SB216763, a specific inhibitor for GSK3beta activation, we showed that inactivation GSK3beta improved the beta-catenin signaling by inhibiting degradation complex comprising Axin and APC and attenuated SSd-induced toxicity in NPCs. SB 216763 15-23 glycogen synthase kinase 3 beta Mus musculus 99-107 31304751-0 2019 Neuroprotective Effects of Ginsenoside Rg1 against Hyperphosphorylated Tau-Induced Diabetic Retinal Neurodegeneration via Activation of IRS-1/Akt/GSK3beta Signaling. Ginsenosides 27-38 glycogen synthase kinase 3 beta Mus musculus 146-154 31304751-0 2019 Neuroprotective Effects of Ginsenoside Rg1 against Hyperphosphorylated Tau-Induced Diabetic Retinal Neurodegeneration via Activation of IRS-1/Akt/GSK3beta Signaling. uridine triacetate 71-74 glycogen synthase kinase 3 beta Mus musculus 146-154 31034777-9 2019 Administration of the selective GSK3beta inhibitor AR-A014418 abolished the effects of lenti-CXCL1, and the CXCR2 inhibitor SB265610 prevented chronic stress-induced depression-like behaviors, inhibited GSK3beta activity, blocked apoptosis pathways, and restored BDNF expression. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 51-61 glycogen synthase kinase 3 beta Mus musculus 32-40 31034777-9 2019 Administration of the selective GSK3beta inhibitor AR-A014418 abolished the effects of lenti-CXCL1, and the CXCR2 inhibitor SB265610 prevented chronic stress-induced depression-like behaviors, inhibited GSK3beta activity, blocked apoptosis pathways, and restored BDNF expression. 1-(2-bromophenyl)-3-(7-cyano-3H-benzotriazol-4-yl)urea 124-132 glycogen synthase kinase 3 beta Mus musculus 203-211 31199069-10 2019 In addition, the MH treatment of DCM mice significantly improved their insulin resistance levels by activation of GSK-3beta. 4-O-methylhonokiol 17-19 glycogen synthase kinase 3 beta Mus musculus 114-123 31250637-6 2019 The activation of intracellular signaling Protein kinase B (PKB), also known as AKT, was inhibited while glycogen synthase kinase 3 (GSK3) was activated by NaB in both in vivo and in vitro studies. nab 156-159 glycogen synthase kinase 3 beta Mus musculus 105-131 31296906-0 2019 Identification of GSK3beta inhibitor kenpaullone as a temozolomide enhancer against glioblastoma. kenpaullone 37-48 glycogen synthase kinase 3 beta Mus musculus 18-26 31296906-0 2019 Identification of GSK3beta inhibitor kenpaullone as a temozolomide enhancer against glioblastoma. Temozolomide 54-66 glycogen synthase kinase 3 beta Mus musculus 18-26 31250637-6 2019 The activation of intracellular signaling Protein kinase B (PKB), also known as AKT, was inhibited while glycogen synthase kinase 3 (GSK3) was activated by NaB in both in vivo and in vitro studies. nab 156-159 glycogen synthase kinase 3 beta Mus musculus 133-137 31028988-5 2019 SRPC treatment improved glucose metabolism via activation of the IR/IRS-2/PI3K/PKB/GSK-3beta signaling pathway (which is related to glycogen synthesis) and enhanced glucose transport through insulin signaling cascade-induced GLUT4 translocation. Glycogen 132-140 glycogen synthase kinase 3 beta Mus musculus 83-92 30980919-6 2019 Moreover, other DGK isozymes, DGKeta and zeta, as well as glucose uptake-related proteins, such as protein kinase C (PKC) alpha, PKCzeta, Akt and glycogen synthase kinase 3beta, failed to be stabilized by myristic acid. Glucose 58-65 glycogen synthase kinase 3 beta Mus musculus 146-176 31179549-9 2019 In pilocarpine-treated mice, protein levels of the PI3K/Akt/GSK-3beta/eIF2alpha/ATF4 pathway were increased during the chronic phase of the model, consistent with previous findings in the hippocampus of patients with epilepsy. Pilocarpine 3-14 glycogen synthase kinase 3 beta Mus musculus 60-69 30954605-4 2019 Leptin may be protective against the development of AD as it can inactivate GSK-3beta through the phosphorylation of Ser-9, leading to the reduction of tau phosphorylation. Serine 117-120 glycogen synthase kinase 3 beta Mus musculus 76-85 30887599-9 2019 Inhibitory signaling of epimagnolin on cell proliferation of lung cancer cells was observed mainly in mTOR-Akt-p70S6K and mTOR-Akt-GSK3beta-AP-1, which was similar to that shown in JB6 Cl41 cells. magnolin 24-35 glycogen synthase kinase 3 beta Mus musculus 131-139 31232699-6 2019 Moreover, GSPs increased phosphorylation levels of phosphatidylinositol 3-kinase (PI3K), Akt and glycogen synthase kinase 3beta (GSK-3beta) at its Ser9. Grape Seed Proanthocyanidins 10-14 glycogen synthase kinase 3 beta Mus musculus 97-127 31185702-5 2019 However, fucoidan-mediated NFATc1 inactivation was greatly reversed by kenpaullone, a GSK3beta inhibitor. kenpaullone 71-82 glycogen synthase kinase 3 beta Mus musculus 86-94 30885574-0 2019 Effect of CAPE-pNO2 against type 2 diabetes mellitus via the AMPK/GLUT4/ GSK3beta/PPARalpha pathway in HFD/STZ-induced diabetic mice. cape-pno2 10-19 glycogen synthase kinase 3 beta Mus musculus 73-81 30885574-7 2019 Besides, CAPE-pNO2 enhanced the expression of phosphorylation-AMP-activated protein kinas (p-AMPK) (Thr172), GLUT4, peroxisome proliferator-activated receptor-alpha (PPARalpha) and p-Akt (Ser473), and inhibited the expression of glycogen synthase kinase 3beta (GSK3beta) and p-JNK (Thr183/Tyr185) in liver. cape-pno2 9-18 glycogen synthase kinase 3 beta Mus musculus 229-259 30885574-7 2019 Besides, CAPE-pNO2 enhanced the expression of phosphorylation-AMP-activated protein kinas (p-AMPK) (Thr172), GLUT4, peroxisome proliferator-activated receptor-alpha (PPARalpha) and p-Akt (Ser473), and inhibited the expression of glycogen synthase kinase 3beta (GSK3beta) and p-JNK (Thr183/Tyr185) in liver. cape-pno2 9-18 glycogen synthase kinase 3 beta Mus musculus 261-269 30885574-9 2019 It suggested that CAPE-pNO2 ameliorated type 2 diabetes mellitus by effectively protecting islet beta cell and improving the insulin resistance via the AMPK/GLUT4/GSK3beta/PPARalpha pathway. cape-pno2 18-27 glycogen synthase kinase 3 beta Mus musculus 163-171 30913518-8 2019 Moreover, Nrf2 knockdown increased the Glu4 protein level and decreased AKT and GSK3beta protein phosphorylation in M1 macrophages, suggesting multiple roles for Nrf2 in regulating glucose metabolism in macrophages. Glucose 181-188 glycogen synthase kinase 3 beta Mus musculus 80-88 30711399-4 2019 GSK3beta transgenic mice performed significantly better than wild-type mice and transgene shutdown with doxycycline normalizes the values in latency to fall in rotarod test. Doxycycline 104-115 glycogen synthase kinase 3 beta Mus musculus 0-8 30975482-2 2019 Lithium (Li) is also a GSK3 antagonist and can be incorporated into bioactive glasses (BG), which can be used clinically in dental and bone repair applications and tuned to quickly release their constituent ions. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 23-27 31086208-7 2019 In addition, QTC-4-MeOBnE pretreatment abolished the up-regulation of AChE activity and the overexpression of GSK 3beta and genes involved in amyloid cascade such as BACE-1, protein precursor amyloid, u-secretase, induced by STZ. qtc-4-meobne 13-25 glycogen synthase kinase 3 beta Mus musculus 110-119 30288695-8 2019 Notably, phosphorylation of BDNF receptor TrkB and GSK3beta (glycogen synthase kinase 3beta) became regulated only gradually upon N2O discontinuation, during a brain state dominated by slow EEG activity. Nitrous Oxide 130-133 glycogen synthase kinase 3 beta Mus musculus 51-59 30288695-8 2019 Notably, phosphorylation of BDNF receptor TrkB and GSK3beta (glycogen synthase kinase 3beta) became regulated only gradually upon N2O discontinuation, during a brain state dominated by slow EEG activity. Nitrous Oxide 130-133 glycogen synthase kinase 3 beta Mus musculus 61-91 30288695-10 2019 The correlation between ongoing slow EEG oscillations and TrkB-GSK3beta signaling was further strengthened utilizing medetomidine, a hypnotic-sedative agent that facilitates slow oscillations directly through the activation of alpha2-adrenergic autoreceptors. Medetomidine 117-129 glycogen synthase kinase 3 beta Mus musculus 63-71 31086208-7 2019 In addition, QTC-4-MeOBnE pretreatment abolished the up-regulation of AChE activity and the overexpression of GSK 3beta and genes involved in amyloid cascade such as BACE-1, protein precursor amyloid, u-secretase, induced by STZ. Streptozocin 225-228 glycogen synthase kinase 3 beta Mus musculus 110-119 31022582-6 2019 Because glycogen synthase kinase-3 (GSK-3) seems to be one of the most promising targets, therefore, we have tested the capacity of lithium carbonate, a classical inhibitor of GSK-3, for treatment of dementia resulting from mild chronic cerebral hypoperfusion in mice. Lithium Carbonate 132-149 glycogen synthase kinase 3 beta Mus musculus 176-181 30824102-4 2019 Western blot analysis indicated that the up-regulated IRS1-PI3K-Akt phosphorylation followed by the down-regulated FoxO1/GSK 3beta phosphorylation contributed to the enhanced glycogen synthesis and the decreased gluconeogenesis by GXG, suggesting that the response of insulin-mediated IRS1-PI3K-Akt-FoxO1/GSK 3beta signaling to GXG might be the required mechanism for GXG-ameliorated development of type 2 diabetes. Glycogen 175-183 glycogen synthase kinase 3 beta Mus musculus 121-130 30824102-4 2019 Western blot analysis indicated that the up-regulated IRS1-PI3K-Akt phosphorylation followed by the down-regulated FoxO1/GSK 3beta phosphorylation contributed to the enhanced glycogen synthesis and the decreased gluconeogenesis by GXG, suggesting that the response of insulin-mediated IRS1-PI3K-Akt-FoxO1/GSK 3beta signaling to GXG might be the required mechanism for GXG-ameliorated development of type 2 diabetes. Glycogen 175-183 glycogen synthase kinase 3 beta Mus musculus 305-314 30824102-4 2019 Western blot analysis indicated that the up-regulated IRS1-PI3K-Akt phosphorylation followed by the down-regulated FoxO1/GSK 3beta phosphorylation contributed to the enhanced glycogen synthesis and the decreased gluconeogenesis by GXG, suggesting that the response of insulin-mediated IRS1-PI3K-Akt-FoxO1/GSK 3beta signaling to GXG might be the required mechanism for GXG-ameliorated development of type 2 diabetes. 4-(2,6-difluorophenyl)-2,4-dioxobutanoic acid 231-234 glycogen synthase kinase 3 beta Mus musculus 121-130 30824102-4 2019 Western blot analysis indicated that the up-regulated IRS1-PI3K-Akt phosphorylation followed by the down-regulated FoxO1/GSK 3beta phosphorylation contributed to the enhanced glycogen synthesis and the decreased gluconeogenesis by GXG, suggesting that the response of insulin-mediated IRS1-PI3K-Akt-FoxO1/GSK 3beta signaling to GXG might be the required mechanism for GXG-ameliorated development of type 2 diabetes. 4-(2,6-difluorophenyl)-2,4-dioxobutanoic acid 328-331 glycogen synthase kinase 3 beta Mus musculus 121-130 31123706-8 2019 GSK3beta inhibition with lithium chloride improves muscle size and strength in an LGMD1D preclinical mouse model. Lithium Chloride 25-41 glycogen synthase kinase 3 beta Mus musculus 0-8 30711629-10 2019 MET phosphorylated and activated GSK3B at tyrosine 56, which decreased the expression of PDL1 by liver cancer cells. Tyrosine 42-50 glycogen synthase kinase 3 beta Mus musculus 33-38 30821572-6 2019 Liver glycogen was depleted after 2 h of cold exposure, and blood glucose decreased after 4 h. Glycogen synthase kinase 3beta (GSK3beta) phosphorylation continued to increase to promote hepatic glycogen synthesis. Glycogen 194-202 glycogen synthase kinase 3 beta Mus musculus 95-125 30526118-8 2019 Finally, the study demonstrated that improved glucose metabolism by rAAV-MPRO pretreatment might be due to the activation of the PI3K/Akt/GSK3beta pathway and spurring Glut4 transposition from the cytoplasm to the cytomembrane in C2C12 cells. Glucose 46-53 glycogen synthase kinase 3 beta Mus musculus 138-146 31141608-13 2019 Hydrogen peroxide addition to culture medium increased REDD1 expression and attenuated Akt/GSK3 phosphorylation in a REDD1-dependent manner. Hydrogen Peroxide 0-17 glycogen synthase kinase 3 beta Mus musculus 91-95 31141608-14 2019 In REDD1-deficient cells exposed to hyperglycemic conditions, expression of a dominant negative Akt or constitutively active GSK3 increased the mitochondrial membrane potential and promoted ROS. Reactive Oxygen Species 190-193 glycogen synthase kinase 3 beta Mus musculus 125-129 31141608-16 2019 Specifically, hyperglycemia-induced REDD1 activates a ROS-generating feedback loop that includes Akt/GSK3. Reactive Oxygen Species 54-57 glycogen synthase kinase 3 beta Mus musculus 101-105 31123706-11 2019 GSK3beta inhibition with lithium chloride may be a therapeutic option in LGMD1D. Lithium Chloride 25-41 glycogen synthase kinase 3 beta Mus musculus 0-8 30482847-7 2019 These analyses combined with functional assays uncovered the differential regulation of Akt and Gsk3b by SH-BC-893 (vacuolating) and C2-ceramide (non-vacuolating). CHEMBL4440140 105-114 glycogen synthase kinase 3 beta Mus musculus 96-101 31001473-8 2019 Further, based on in silico predicted activation of GSK3beta in CSCs, we found that tideglusib, an irreversible inhibitor of the kinase, exhibited marked anti-growth effects in the cultured CSCs. tideglusib 84-94 glycogen synthase kinase 3 beta Mus musculus 52-60 30791983-1 2019 Lithium, a well-known inhibitor of glycogen synthase kinase-3beta (GSK3beta), can improve bone formation by activating the Wnt/beta-catenin signalling pathway. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 35-65 30649326-2 2019 Glycogen synthase kinase-3beta is involved in various cognitive and behavioral processes associated with methamphetamine exposure. Methamphetamine 105-120 glycogen synthase kinase 3 beta Mus musculus 0-30 30649326-3 2019 This study aims to investigate the protective effects of the glycogen synthase kinase-3beta inhibitor lithium chloride on adolescent methamphetamine exposure-induced long-term alterations in emotion, cognition, behavior, and molecule and hippocampal ultrastructure in adulthood. Lithium Chloride 102-118 glycogen synthase kinase 3 beta Mus musculus 61-91 30649326-3 2019 This study aims to investigate the protective effects of the glycogen synthase kinase-3beta inhibitor lithium chloride on adolescent methamphetamine exposure-induced long-term alterations in emotion, cognition, behavior, and molecule and hippocampal ultrastructure in adulthood. Methamphetamine 133-148 glycogen synthase kinase 3 beta Mus musculus 61-91 30649326-8 2019 RESULTS: Adolescent methamphetamine exposure induced long-term alterations in locomotor activity, novel spatial exploration, and social recognition memory; increases in glycogen synthase kinase-3beta activity in dorsal hippocampus; and decreases in excitatory synapse density and postsynaptic density thickness in CA1. Methamphetamine 20-35 glycogen synthase kinase 3 beta Mus musculus 169-199 30649326-12 2019 CONCLUSIONS: Hyperactive glycogen synthase kinase-3beta contributes to adolescent chronic methamphetamine exposure-induced behavioral and hippocampal impairments in adulthood. Methamphetamine 90-105 glycogen synthase kinase 3 beta Mus musculus 25-55 30649326-13 2019 Our results suggest glycogen synthase kinase-3beta may be a potential target for the treatment of deficits in adulthood associated with adolescent methamphetamine abuse. Methamphetamine 147-162 glycogen synthase kinase 3 beta Mus musculus 20-50 30674062-8 2019 Tat-induced death of immature OLs was rescued by the GSK3beta inhibitors valproic acid or SB415286, supporting involvement of GSK3beta signaling. Valproic Acid 73-86 glycogen synthase kinase 3 beta Mus musculus 53-61 31182913-5 2019 Additionally, nitroxoline downregulated the expressions of phospho-PI3 kinase, phospho-Akt (Thr308), phospho-Akt (Ser473), phospho-GSK-3beta, Bcl-2, and Bcl-xL. nitroxoline 14-25 glycogen synthase kinase 3 beta Mus musculus 131-140 30654094-0 2019 The inhibitor of glycerol 3-phosphate acyltransferase FSG67 blunts liver regeneration after acetaminophen overdose by altering GSK3beta and Wnt/beta-catenin signaling. Glycerol 17-25 glycogen synthase kinase 3 beta Mus musculus 127-135 30654094-3 2019 Here, we hypothesized that PA inhibits glycogen synthase kinase-3beta (GSK3beta), a component of canonical Wnt/beta-catenin signaling, after APAP overdose. Phosphatidic Acids 27-29 glycogen synthase kinase 3 beta Mus musculus 71-79 30654094-3 2019 Here, we hypothesized that PA inhibits glycogen synthase kinase-3beta (GSK3beta), a component of canonical Wnt/beta-catenin signaling, after APAP overdose. Acetaminophen 141-145 glycogen synthase kinase 3 beta Mus musculus 71-79 30654094-10 2019 Our data indicate PA and lysoPA may support recovery after APAP overdose by inhibiting GSK3beta. Acetaminophen 59-63 glycogen synthase kinase 3 beta Mus musculus 87-95 30482847-7 2019 These analyses combined with functional assays uncovered the differential regulation of Akt and Gsk3b by SH-BC-893 (vacuolating) and C2-ceramide (non-vacuolating). N-acetylsphingosine 133-144 glycogen synthase kinase 3 beta Mus musculus 96-101 30906318-9 2019 The stimulatory effect of MEM on CRS-induced tau phosphorylation was correlated with increased activities of AKT, JNK, and GSK3beta, inactivation of PP2A, and downregulation of Pin1 and HSP70. Chromium 33-36 glycogen synthase kinase 3 beta Mus musculus 123-131 30775809-7 2019 In addition, acute CCl 4 -exposed mice showed reduced functional proteins of glucose transporter 2 (GLUT2), insulin receptor beta, insulin receptor substrate 1, glycogen synthase kinase 3beta (GSK3beta), p-AKT Ser473 associated with AKT signaling pathway in liver cells, whereas acute CCl 4 exposure downregulated the endogenous expressions of the insulin and glucagon hormonal proteins in the pancreas. Carbon Tetrachloride 19-24 glycogen synthase kinase 3 beta Mus musculus 161-191 30775809-7 2019 In addition, acute CCl 4 -exposed mice showed reduced functional proteins of glucose transporter 2 (GLUT2), insulin receptor beta, insulin receptor substrate 1, glycogen synthase kinase 3beta (GSK3beta), p-AKT Ser473 associated with AKT signaling pathway in liver cells, whereas acute CCl 4 exposure downregulated the endogenous expressions of the insulin and glucagon hormonal proteins in the pancreas. Carbon Tetrachloride 19-24 glycogen synthase kinase 3 beta Mus musculus 193-201 30775809-8 2019 Taken together, the current findings highlight that CCl 4 impaired insulin-dependent glucose homeostasis through modulating hepatocellular AKT signaling pathway in acute CCl 4 exposure and GLUT2/GSK3beta pathway in chronic CCl 4 -exposed liver cells. Cefaclor 52-55 glycogen synthase kinase 3 beta Mus musculus 195-203 30775809-8 2019 Taken together, the current findings highlight that CCl 4 impaired insulin-dependent glucose homeostasis through modulating hepatocellular AKT signaling pathway in acute CCl 4 exposure and GLUT2/GSK3beta pathway in chronic CCl 4 -exposed liver cells. Carbon Tetrachloride 52-57 glycogen synthase kinase 3 beta Mus musculus 195-203 30699850-2 2019 Although Glycogen synthase kinase 3 beta (GSK3beta) has been suggested to play a role in the pathophysiology of BD since it is inhibited by lithium, it remains unknown how GSK3beta activity might be involved. Lithium 140-147 glycogen synthase kinase 3 beta Mus musculus 9-40 30699850-2 2019 Although Glycogen synthase kinase 3 beta (GSK3beta) has been suggested to play a role in the pathophysiology of BD since it is inhibited by lithium, it remains unknown how GSK3beta activity might be involved. Lithium 140-147 glycogen synthase kinase 3 beta Mus musculus 42-50 30699850-7 2019 Furthermore, specific knockout of GSK3beta in the MSNs of the indirect pathway significantly suppressed amphetamine-induced hyperlocomotion. Amphetamine 104-115 glycogen synthase kinase 3 beta Mus musculus 34-42 30699850-13 2019 Moreover, our data also suggest lithium may exert its effect on BD through a GSK3beta-independent mechanism, in addition to the GSK3beta inhibition-mediated mechanism. Lithium 32-39 glycogen synthase kinase 3 beta Mus musculus 77-85 30728291-4 2019 By studying human and mouse cells with defective or absent TSC2, we show that complete loss of TSC2 causes an increase in glycogen synthesis through mTORC1 hyperactivation and subsequent inactivation of glycogen synthase kinase 3beta (GSK3beta), a negative regulator of glycogen synthesis. Glycogen 122-130 glycogen synthase kinase 3 beta Mus musculus 203-233 30858693-7 2019 Results: Mechanistically, D206008 inhibited beta-catenin degradation by enhancing the phosphorylation of Akt and glycogen synthase kinase-3beta (GSK-3beta), which increased the accumulation of beta-catenin in the cytoplasm. d206008 26-33 glycogen synthase kinase 3 beta Mus musculus 113-143 30858693-7 2019 Results: Mechanistically, D206008 inhibited beta-catenin degradation by enhancing the phosphorylation of Akt and glycogen synthase kinase-3beta (GSK-3beta), which increased the accumulation of beta-catenin in the cytoplasm. d206008 26-33 glycogen synthase kinase 3 beta Mus musculus 145-154 30721232-7 2019 Yet, GSK-3 inhibition modestly reduced RU24969-induced PPI deficits. 5-methoxy 3-(1,2,3,6-tetrahydro-4-pyridinyl)1H indole 39-46 glycogen synthase kinase 3 beta Mus musculus 5-10 30741414-8 2019 Our findings suggest that galangin protects against cardiac remodeling through decreasing inflammatory responses and apoptosis, which are associated with inhibition of the MEK1/2-ERK1/2-GATA4 and PI3K-AKT-GSK3beta signals. galangin 26-34 glycogen synthase kinase 3 beta Mus musculus 205-213 30412805-3 2019 Specifically, the halogenated derivative 6-bromo indirubin-3"-oxime (6BIO) possesses increased selectivity against GSK-3. 6-bromoindirubin-3'-oxime 41-67 glycogen synthase kinase 3 beta Mus musculus 115-120 30858693-0 2019 Amine derivatives of furocoumarin induce melanogenesis by activating Akt/GSK-3beta/beta-catenin signal pathway. Amines 0-5 glycogen synthase kinase 3 beta Mus musculus 73-82 30858693-0 2019 Amine derivatives of furocoumarin induce melanogenesis by activating Akt/GSK-3beta/beta-catenin signal pathway. Furocoumarins 21-33 glycogen synthase kinase 3 beta Mus musculus 73-82 30537677-0 2019 Dexamethasone induces osteoblast apoptosis through ROS-PI3K/AKT/GSK3beta signaling pathway. Dexamethasone 0-13 glycogen synthase kinase 3 beta Mus musculus 64-72 30688489-7 2019 In this line, we observed that both biochemical and motor learning impairments were prevented in Akt3-deficent mice by chronic treatments with lithium, a well-known GSK-3 inhibitor. Lithium 143-150 glycogen synthase kinase 3 beta Mus musculus 165-170 30537677-0 2019 Dexamethasone induces osteoblast apoptosis through ROS-PI3K/AKT/GSK3beta signaling pathway. Reactive Oxygen Species 51-54 glycogen synthase kinase 3 beta Mus musculus 64-72 30537677-3 2019 This study aimed to explore the effects of phosphatidylinositol 3-kinase/Protein kinase 3 (PI3K/AKT) and glycogen synthase kinase 3beta (GSK3beta) on Dex-induced osteoblasts apoptosis. Dexamethasone 150-153 glycogen synthase kinase 3 beta Mus musculus 105-135 30537677-3 2019 This study aimed to explore the effects of phosphatidylinositol 3-kinase/Protein kinase 3 (PI3K/AKT) and glycogen synthase kinase 3beta (GSK3beta) on Dex-induced osteoblasts apoptosis. Dexamethasone 150-153 glycogen synthase kinase 3 beta Mus musculus 137-145 30537677-7 2019 The expressions of PI3K/AKT and GSK3beta in osteoblasts and MC3T3-E1 cells after Dex treatment were analyzed using western blotting and qRT-PCR, respectively. Dexamethasone 81-84 glycogen synthase kinase 3 beta Mus musculus 32-40 30537677-8 2019 Then the effects of GSK3beta knockdown on Dex-induced apoptosis of osteoblasts were explored. Dexamethasone 42-45 glycogen synthase kinase 3 beta Mus musculus 20-28 30537677-14 2019 The expressions of GSK3beta in osteoblasts and MC3T3-E1 cells were obviously up-regulated after Dex treatment. Dexamethasone 96-99 glycogen synthase kinase 3 beta Mus musculus 19-27 30537677-15 2019 Knockdown of GSK3beta alleviated Dex-induced osteoblast and MC3T3-E1 cell apoptosis by decreasing the expressions of Bax, cleaved-caspase 3, cleaved-caspase 9 and increasing the expression of Bcl-2. Dexamethasone 33-36 glycogen synthase kinase 3 beta Mus musculus 13-21 30537677-16 2019 CONCLUSION: Our research verified that Dex induced osteoblasts apoptosis by ROS-PI3K/AKT/GSK3beta signaling pathway. Dexamethasone 39-42 glycogen synthase kinase 3 beta Mus musculus 89-97 30537677-16 2019 CONCLUSION: Our research verified that Dex induced osteoblasts apoptosis by ROS-PI3K/AKT/GSK3beta signaling pathway. Reactive Oxygen Species 76-79 glycogen synthase kinase 3 beta Mus musculus 89-97 31119045-7 2019 We also found that higher expression of pSer9-GSK-3beta induced higher levels of ROS, and observed that abnormality of mitochondrial respiratory chain complex I/III function induced the dysfunction of GSK-3beta-induced electron transport chain, naturally disturbing the ROS level. Reactive Oxygen Species 270-273 glycogen synthase kinase 3 beta Mus musculus 201-210 30292770-2 2019 Glutamate results in the activation of an enzyme called glycogen synthase kinase-3 (GSK-3) acting through N-methyl-d-aspartate (NMDA) receptors. Glutamic Acid 0-9 glycogen synthase kinase 3 beta Mus musculus 56-82 30292770-2 2019 Glutamate results in the activation of an enzyme called glycogen synthase kinase-3 (GSK-3) acting through N-methyl-d-aspartate (NMDA) receptors. Glutamic Acid 0-9 glycogen synthase kinase 3 beta Mus musculus 84-89 30292770-4 2019 It has been reported that lithium acts as an inhibitor of GSK-3 and inhibit the enzyme GSK-3 in an uncompetitive manner. Lithium 26-33 glycogen synthase kinase 3 beta Mus musculus 58-63 30292770-4 2019 It has been reported that lithium acts as an inhibitor of GSK-3 and inhibit the enzyme GSK-3 in an uncompetitive manner. Lithium 26-33 glycogen synthase kinase 3 beta Mus musculus 87-92 30292770-10 2019 Glutamate acting through the NMDA receptor has been found to regulate the expression of enzyme neuronal nitric oxide synthase (nNOS), which is responsible for the release of nitric oxide (NO), suggesting a possible link between NO and GSK-3 also. Glutamic Acid 0-9 glycogen synthase kinase 3 beta Mus musculus 235-240 30292770-10 2019 Glutamate acting through the NMDA receptor has been found to regulate the expression of enzyme neuronal nitric oxide synthase (nNOS), which is responsible for the release of nitric oxide (NO), suggesting a possible link between NO and GSK-3 also. Nitric Oxide 104-116 glycogen synthase kinase 3 beta Mus musculus 235-240 30292770-15 2019 Therefore, it is suggested that NO signaling pathway influence the anxiolytic like activity of lithium in mice, further suggesting the link between the GSK-3 and NO signaling in the regulation of anxiety related behavior. Lithium 95-102 glycogen synthase kinase 3 beta Mus musculus 152-157 31119045-9 2019 Furthermore, we found that the expression of pSer535-eIF2B promoted the expression of NKG2D ligands (Mult-1 and Rae1) following by expression of pSer9-GSK-3beta and generation of ROS. Reactive Oxygen Species 179-182 glycogen synthase kinase 3 beta Mus musculus 151-160 31119045-10 2019 Conclusions: The PI3K/Akt/GSK-3beta/ROS/eIF2B pathway could regulate NK cell activity and sensitivity of tumor cells to NK cells, which resulted in breast cancer growth and lung metastasis. Reactive Oxygen Species 36-39 glycogen synthase kinase 3 beta Mus musculus 26-35 30711516-14 2019 SA-49-induced MITF translocation acted through activation of PKCalpha and subsequently suppression of GSK3beta activity. N-[3-(dimethylamino)-2-methylpropyl]-N-(2,6-dimethylphenyl)-2-phenylacetamide 0-5 glycogen synthase kinase 3 beta Mus musculus 102-110 30535296-11 2019 This phenotype is reversed by the end of the third week (G18.5) despite a smaller placental transfer zone, probably based on GSK3beta-mediated increased glucose mobilization in the placenta and hence an increased glucose supply to the fetus. Glucose 153-160 glycogen synthase kinase 3 beta Mus musculus 125-133 30535296-11 2019 This phenotype is reversed by the end of the third week (G18.5) despite a smaller placental transfer zone, probably based on GSK3beta-mediated increased glucose mobilization in the placenta and hence an increased glucose supply to the fetus. Glucose 213-220 glycogen synthase kinase 3 beta Mus musculus 125-133 31119045-0 2019 The PI3K/Akt/GSK-3beta/ROS/eIF2B pathway promotes breast cancer growth and metastasis via suppression of NK cell cytotoxicity and tumor cell susceptibility. Reactive Oxygen Species 23-26 glycogen synthase kinase 3 beta Mus musculus 13-22 31119045-6 2019 Nevertheless, LY290042, which attenuates p-GSK-3beta formation by inhibiting the PI3K/Akt pathway, reversed these effects. LY 290042 14-22 glycogen synthase kinase 3 beta Mus musculus 43-52 30407505-10 2019 Furthermore, rhodomyrtone inhibited the increase of glycogen synthase kinase-3beta activity and reversed the decrease of brain-derived neurotrophic factor and postsynaptic density protein 95 in chronic unpredictable mild stress mice. rhodomyrtone 13-25 glycogen synthase kinase 3 beta Mus musculus 52-82 31119045-7 2019 We also found that higher expression of pSer9-GSK-3beta induced higher levels of ROS, and observed that abnormality of mitochondrial respiratory chain complex I/III function induced the dysfunction of GSK-3beta-induced electron transport chain, naturally disturbing the ROS level. Reactive Oxygen Species 81-84 glycogen synthase kinase 3 beta Mus musculus 46-55 31119045-7 2019 We also found that higher expression of pSer9-GSK-3beta induced higher levels of ROS, and observed that abnormality of mitochondrial respiratory chain complex I/III function induced the dysfunction of GSK-3beta-induced electron transport chain, naturally disturbing the ROS level. Reactive Oxygen Species 81-84 glycogen synthase kinase 3 beta Mus musculus 201-210 31119045-7 2019 We also found that higher expression of pSer9-GSK-3beta induced higher levels of ROS, and observed that abnormality of mitochondrial respiratory chain complex I/III function induced the dysfunction of GSK-3beta-induced electron transport chain, naturally disturbing the ROS level. Reactive Oxygen Species 270-273 glycogen synthase kinase 3 beta Mus musculus 46-55 30094601-7 2019 In CD group, the PostC reduced infarct size (CD-I/R: 52.14 +- 2.8 vs. CD-PostC: 36.58 +- 1.8, P < 0.05) and increased phosphorylation of GSK3beta (CD-PostC: 2.341 +- 1.03 vs. CD-Baseline: 0.923 +- 0.41 AUOD, P < 0.05), and this cardioprotection was abolished in HFD-exposed mice. Cadmium 3-5 glycogen synthase kinase 3 beta Mus musculus 140-148 30094601-7 2019 In CD group, the PostC reduced infarct size (CD-I/R: 52.14 +- 2.8 vs. CD-PostC: 36.58 +- 1.8, P < 0.05) and increased phosphorylation of GSK3beta (CD-PostC: 2.341 +- 1.03 vs. CD-Baseline: 0.923 +- 0.41 AUOD, P < 0.05), and this cardioprotection was abolished in HFD-exposed mice. postc 17-22 glycogen synthase kinase 3 beta Mus musculus 140-148 29257917-10 2019 PDK1-deficient mice showed higher aggregation when PI3K-Akt-Gsk3beta signaling was blocked by the Gsk3beta-inhibitor SB216763. SB 216763 117-125 glycogen synthase kinase 3 beta Mus musculus 60-68 30774348-0 2019 Hyperbaric oxygen therapy attenuates neuronal apoptosis induced by traumatic brain injury via Akt/GSK3beta/beta-catenin pathway. Oxygen 11-17 glycogen synthase kinase 3 beta Mus musculus 98-106 30669571-0 2019 Fucoidan-Fucoxanthin Ameliorated Cardiac Function via IRS1/GRB2/ SOS1, GSK3beta/CREB Pathways and Metabolic Pathways in Senescent Mice. fucoidan-fucoxanthin 0-20 glycogen synthase kinase 3 beta Mus musculus 71-79 30669571-8 2019 Treatment with fucoidan and fucoxanthin reduced the expression levels of SOS1 and GRB2 while increasing GSK3beta, CREB and IRS1 proteins expression in the aging process. fucoidan 15-23 glycogen synthase kinase 3 beta Mus musculus 104-112 30669571-8 2019 Treatment with fucoidan and fucoxanthin reduced the expression levels of SOS1 and GRB2 while increasing GSK3beta, CREB and IRS1 proteins expression in the aging process. fucoxanthin 28-39 glycogen synthase kinase 3 beta Mus musculus 104-112 30626440-7 2019 The increase in insulin stimulated glucose oxidation was accompanied by activation of the IRS-1/Akt/AS160/GSK-3beta pathway, an increase in GLUT4 expression and a reduction in pyruvate dehydrogenase phosphorylation. Glucose 35-42 glycogen synthase kinase 3 beta Mus musculus 106-115 31155593-0 2019 Adenosine N1-Oxide Exerts Anti-inflammatory Effects through the PI3K/Akt/GSK-3beta Signaling Pathway and Promotes Osteogenic and Adipocyte Differentiation. adenosine N(1)-oxide 0-18 glycogen synthase kinase 3 beta Mus musculus 73-82 30417494-0 2019 Pyruvic acid/ethyl pyruvate inhibits melanogenesis in B16F10 melanoma cells through PI3K/AKT, GSK3beta, and ROS-ERK signaling pathways. Pyruvic Acid 0-12 glycogen synthase kinase 3 beta Mus musculus 94-102 30417494-0 2019 Pyruvic acid/ethyl pyruvate inhibits melanogenesis in B16F10 melanoma cells through PI3K/AKT, GSK3beta, and ROS-ERK signaling pathways. ethyl pyruvate 13-27 glycogen synthase kinase 3 beta Mus musculus 94-102 30417494-8 2019 PA and EP induced GSK3beta phosphorylation and activated PI3K/AKT signaling, leading to decreased melanin synthesis. Pyruvic Acid 0-2 glycogen synthase kinase 3 beta Mus musculus 18-26 30417494-8 2019 PA and EP induced GSK3beta phosphorylation and activated PI3K/AKT signaling, leading to decreased melanin synthesis. Melanins 98-105 glycogen synthase kinase 3 beta Mus musculus 18-26 29779175-0 2019 Anthocyanins Improve Hippocampus-Dependent Memory Function and Prevent Neurodegeneration via JNK/Akt/GSK3beta Signaling in LPS-Treated Adult Mice. Anthocyanins 0-12 glycogen synthase kinase 3 beta Mus musculus 101-109 30668392-13 2019 Furthermore, yangonin modulated blood glucose homeostasis through regulation of gluconeogenesis-related gene phosphoenol pyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), and glycogen synthesis-related gene glycogen synthase kinase 3beta (GSK3beta) and pyruvate dehydrogenase (PDase). yangonin 13-21 glycogen synthase kinase 3 beta Mus musculus 224-254 30668392-13 2019 Furthermore, yangonin modulated blood glucose homeostasis through regulation of gluconeogenesis-related gene phosphoenol pyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase), and glycogen synthesis-related gene glycogen synthase kinase 3beta (GSK3beta) and pyruvate dehydrogenase (PDase). yangonin 13-21 glycogen synthase kinase 3 beta Mus musculus 256-264 30678114-12 2019 The neuroprotective mechanism of ST extract against MPTP-induced Parkinsonism might be related to decreasing GSK-3beta phosphorylation and restoring the activities of striatal antioxidant defenses to restore the nigrostriatal dopaminergic function and decrease alpha-synuclein accumulation. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 52-56 glycogen synthase kinase 3 beta Mus musculus 109-118 29978469-5 2019 Both of the gedatolisib-resistant cell lines expressed high levels of active glycogen synthase kinase 3-beta (GSK3beta) and harbored the same frameshift mutation (c.465_466insC; H155fs*) in TCF7, which encodes a positive transcriptional regulator of the WNT/beta-catenin signaling pathway. gedatolisib 12-23 glycogen synthase kinase 3 beta Mus musculus 77-108 29978469-5 2019 Both of the gedatolisib-resistant cell lines expressed high levels of active glycogen synthase kinase 3-beta (GSK3beta) and harbored the same frameshift mutation (c.465_466insC; H155fs*) in TCF7, which encodes a positive transcriptional regulator of the WNT/beta-catenin signaling pathway. gedatolisib 12-23 glycogen synthase kinase 3 beta Mus musculus 110-118 29978469-6 2019 Inhibition of GSK3beta activity in gedatolisib-resistant cells by siRNA-mediated knockdown or treatment with a GSK3beta-specific inhibitor effectively reduced the activity of molecules downstream of mTOR and also decreased signaling through the WNT/beta-catenin pathway. gedatolisib 35-46 glycogen synthase kinase 3 beta Mus musculus 14-22 29978469-6 2019 Inhibition of GSK3beta activity in gedatolisib-resistant cells by siRNA-mediated knockdown or treatment with a GSK3beta-specific inhibitor effectively reduced the activity of molecules downstream of mTOR and also decreased signaling through the WNT/beta-catenin pathway. gedatolisib 35-46 glycogen synthase kinase 3 beta Mus musculus 111-119 29978469-7 2019 Notably, GSK3beta inhibition rendered the resistant cell lines sensitive to gedatolisib cytotoxicity, both in vitro and in a mouse xenograft model. gedatolisib 76-87 glycogen synthase kinase 3 beta Mus musculus 9-17 29978469-8 2019 Taken together, these data demonstrate that aberrant regulation of WNT/beta-catenin signaling and active GSK3beta induced by the TCF7 frameshift mutation cause resistance to the dual PI3K/mTOR inhibitor gedatolisib. gedatolisib 203-214 glycogen synthase kinase 3 beta Mus musculus 105-113 30502054-7 2019 FINDINGS: Higher GSK3beta activity decreased the progression of kainic acid induced epileptogenesis. Kainic Acid 64-75 glycogen synthase kinase 3 beta Mus musculus 17-25 30502054-8 2019 At the biochemical level, higher GSK3beta activity increased the expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) channel 4 under basal conditions and in the epileptic mouse brain and decreased phosphorylation of the glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluA1 at Serine 831 under basal conditions. Nucleotides, Cyclic 107-124 glycogen synthase kinase 3 beta Mus musculus 33-41 30502054-8 2019 At the biochemical level, higher GSK3beta activity increased the expression of hyperpolarization-activated cyclic nucleotide-gated (HCN) channel 4 under basal conditions and in the epileptic mouse brain and decreased phosphorylation of the glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluA1 at Serine 831 under basal conditions. Serine 340-346 glycogen synthase kinase 3 beta Mus musculus 33-41 29257917-10 2019 PDK1-deficient mice showed higher aggregation when PI3K-Akt-Gsk3beta signaling was blocked by the Gsk3beta-inhibitor SB216763. SB 216763 117-125 glycogen synthase kinase 3 beta Mus musculus 98-106 31453129-9 2019 In vitro experiments, flavonoids contained in these kampo medicines, inhibited GSK-3beta activity in concentration-dependent manners. Flavonoids 22-32 glycogen synthase kinase 3 beta Mus musculus 79-88 30544623-9 2018 We also present evidence that GSK3 inhibition in GM/DCs reduced C/EBPbeta DNA binding activity and increased expression of costimulatory molecules in GM/DCs and their production of IL-10. gm 49-51 glycogen synthase kinase 3 beta Mus musculus 30-34 30321530-0 2018 Curcumin ameliorates scopolamine-induced mice memory retrieval deficit and restores hippocampal p-Akt and p-GSK-3beta. Curcumin 0-8 glycogen synthase kinase 3 beta Mus musculus 108-117 30321530-14 2018 Overall, these findings showed that pre-test scopolamine administration disrupts memory retrieval along with the diminished Akt and GSK-3beta phosphorylation in hippocampus while curcumin administration prevented those changes. Scopolamine 45-56 glycogen synthase kinase 3 beta Mus musculus 132-141 30544623-9 2018 We also present evidence that GSK3 inhibition in GM/DCs reduced C/EBPbeta DNA binding activity and increased expression of costimulatory molecules in GM/DCs and their production of IL-10. gm 150-152 glycogen synthase kinase 3 beta Mus musculus 30-34 30144430-1 2018 BACKGROUND & AIMS: Growth, progression, and drug resistance of pancreatic ductal adenocarcinomas (PDACs) have been associated with increased levels and activity of glycogen synthase kinase 3 beta (GSK3B) and histone deacetylases (HDACs). Adenosine Monophosphate 12-15 glycogen synthase kinase 3 beta Mus musculus 168-199 30069702-7 2018 Moreover, MOB1 was found to be a novel substrate for GSK3beta that is phosphorylated on serine 146 and degraded via the ubiquitin-proteasome system (UPS). Serine 88-94 glycogen synthase kinase 3 beta Mus musculus 53-61 30546306-0 2018 Isoorientin Ameliorates APAP-Induced Hepatotoxicity via Activation Nrf2 Antioxidative Pathway: The Involvement of AMPK/Akt/GSK3beta. homoorientin 0-11 glycogen synthase kinase 3 beta Mus musculus 123-131 30343259-0 2018 Anti-inflammatory effects of isoalantolactone on LPS-stimulated BV2 microglia cells through activating GSK-3beta-Nrf2 signaling pathway. isoalantolactone 29-45 glycogen synthase kinase 3 beta Mus musculus 103-112 30343259-8 2018 Furthermore, ISO increased the level of phosphorylated GSK-3beta, the upstream molecule of Nrf2. isoalantolactone 13-16 glycogen synthase kinase 3 beta Mus musculus 55-64 30389400-11 2018 Chronic catecholamine stimulation was followed by an enhanced expression of GSK3beta, whereas the phosphorylation at Ser9 was lower in TG as compared to the corresponding WT group. Catecholamines 8-21 glycogen synthase kinase 3 beta Mus musculus 76-84 30188517-2 2018 We previously identified glycogen synthase kinase 3-beta (Gsk3b) as a member of a highly ethanol-responsive gene network in mouse medial prefrontal cortex (mPFC). Ethanol 89-96 glycogen synthase kinase 3 beta Mus musculus 25-56 30188517-2 2018 We previously identified glycogen synthase kinase 3-beta (Gsk3b) as a member of a highly ethanol-responsive gene network in mouse medial prefrontal cortex (mPFC). Ethanol 89-96 glycogen synthase kinase 3 beta Mus musculus 58-63 30188517-5 2018 Stereotactic viral vector gene delivery overexpression of Gsk3b in mouse mPFC increased 2-bottle choice ethanol consumption, which was blocked by lithium, a known GSK3B inhibitor. Ethanol 104-111 glycogen synthase kinase 3 beta Mus musculus 58-63 30188517-5 2018 Stereotactic viral vector gene delivery overexpression of Gsk3b in mouse mPFC increased 2-bottle choice ethanol consumption, which was blocked by lithium, a known GSK3B inhibitor. Ethanol 104-111 glycogen synthase kinase 3 beta Mus musculus 163-168 30188517-5 2018 Stereotactic viral vector gene delivery overexpression of Gsk3b in mouse mPFC increased 2-bottle choice ethanol consumption, which was blocked by lithium, a known GSK3B inhibitor. Lithium 146-153 glycogen synthase kinase 3 beta Mus musculus 58-63 30188517-5 2018 Stereotactic viral vector gene delivery overexpression of Gsk3b in mouse mPFC increased 2-bottle choice ethanol consumption, which was blocked by lithium, a known GSK3B inhibitor. Lithium 146-153 glycogen synthase kinase 3 beta Mus musculus 163-168 30296514-7 2018 Moreover, paeonol increased the denosine 5"-monophosphate-activated protein kinase (AMPK) phosphorylation and decreased the activations of glycogen synthase kinase-3 (GSK-3), protein kinase RNA-like ER kinase (PERK), inositol-requiring protein-1 (IRE1), c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). paeonol 10-17 glycogen synthase kinase 3 beta Mus musculus 139-165 30296514-7 2018 Moreover, paeonol increased the denosine 5"-monophosphate-activated protein kinase (AMPK) phosphorylation and decreased the activations of glycogen synthase kinase-3 (GSK-3), protein kinase RNA-like ER kinase (PERK), inositol-requiring protein-1 (IRE1), c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). paeonol 10-17 glycogen synthase kinase 3 beta Mus musculus 167-172 30296514-9 2018 Taken together, these findings indicate that paeonol could protect kidney form Pb-induced injury by inhibiting oxidative stress, ER stress and inflammation via the AMPK and GSK-3 pathway. paeonol 45-52 glycogen synthase kinase 3 beta Mus musculus 173-178 30296514-9 2018 Taken together, these findings indicate that paeonol could protect kidney form Pb-induced injury by inhibiting oxidative stress, ER stress and inflammation via the AMPK and GSK-3 pathway. Lead 79-81 glycogen synthase kinase 3 beta Mus musculus 173-178 30546306-0 2018 Isoorientin Ameliorates APAP-Induced Hepatotoxicity via Activation Nrf2 Antioxidative Pathway: The Involvement of AMPK/Akt/GSK3beta. 4-amino-N-acetyl-N-methylaniline 24-28 glycogen synthase kinase 3 beta Mus musculus 123-131 30546306-12 2018 In summary, Iso ameliorated APAP-induced hepatotoxicity by activating Nrf2 via the AMPK/Akt/GSK3beta pathway. 4-amino-N-acetyl-N-methylaniline 28-32 glycogen synthase kinase 3 beta Mus musculus 92-100 30555565-9 2018 Re-phosphorylation of GSK3beta induced by LiCl treatment restored differentiation of BMMSCs and attenuated skeletal deformities in Alpl +/- mice. Lithium Chloride 42-46 glycogen synthase kinase 3 beta Mus musculus 22-30 30061174-0 2018 Tamoxifen attenuates dialysate-induced peritoneal fibrosis by inhibiting GSK-3beta/beta-catenin axis activation. Tamoxifen 0-9 glycogen synthase kinase 3 beta Mus musculus 73-82 30061174-5 2018 Mouse peritoneal mesothelial cells (mPMCs) were cultured in 4.25% glucose or 4.25% glucose plus Tamoxifen for 48 h. Tamoxifen inhibited epithelial-to-mesenchymal transition (EMT) as well as phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), nuclear beta-catenin, and Snail induced by exposure to HG. Tamoxifen 116-125 glycogen synthase kinase 3 beta Mus musculus 209-239 30061174-5 2018 Mouse peritoneal mesothelial cells (mPMCs) were cultured in 4.25% glucose or 4.25% glucose plus Tamoxifen for 48 h. Tamoxifen inhibited epithelial-to-mesenchymal transition (EMT) as well as phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), nuclear beta-catenin, and Snail induced by exposure to HG. Tamoxifen 116-125 glycogen synthase kinase 3 beta Mus musculus 241-250 30061174-7 2018 In conclusion, Tamoxifen significantly attenuated EMT during peritoneal epithelial fibrosis, in part by inhibiting GSK-3beta/beta-catenin activation. Tamoxifen 15-24 glycogen synthase kinase 3 beta Mus musculus 115-124 30218672-9 2018 Moreover, donepezil can also improve PCP-induced schizophrenia-like cognitive deficits by inhibiting neuronal apoptosis and regulating synaptic plasticity, which was possible through the up-regulation of p-Akt, p-GSK-3beta, Bcl-2 and the down-regulation of Bax, Caspase-3. Donepezil 10-19 glycogen synthase kinase 3 beta Mus musculus 213-222 30218672-9 2018 Moreover, donepezil can also improve PCP-induced schizophrenia-like cognitive deficits by inhibiting neuronal apoptosis and regulating synaptic plasticity, which was possible through the up-regulation of p-Akt, p-GSK-3beta, Bcl-2 and the down-regulation of Bax, Caspase-3. Phencyclidine 37-40 glycogen synthase kinase 3 beta Mus musculus 213-222 30293796-0 2018 Discovery and anti-inflammatory evaluation of benzothiazepinones (BTZs) as novel non-ATP competitive inhibitors of glycogen synthase kinase-3beta (GSK-3beta). benzothiazepinones 46-64 glycogen synthase kinase 3 beta Mus musculus 115-145 30138894-11 2018 In general, the protective effect of rutin on the liver of T2DM may be mediated by facilitating signal transduction and activated state of insulin IRS-2/PI3K/Akt/GSK-3beta signal pathway, promoting hepatocyte proliferation, reducing blood glucose level and generation of AGEs. Rutin 37-42 glycogen synthase kinase 3 beta Mus musculus 162-171 30171855-0 2018 Isoliquiritigenin inhibits mouse S180 tumors with a new mechanism that regulates autophagy by GSK-3beta/TNF-alpha pathway. isoliquiritigenin 0-17 glycogen synthase kinase 3 beta Mus musculus 94-103 30217816-9 2018 Moreover, the GSK-3beta inhibitor lithium or siRNA-mediated GSK-3beta knockdown diminished the effects of IGF-1 on the Bmal-1 promoter. Lithium 34-41 glycogen synthase kinase 3 beta Mus musculus 14-23 30293796-0 2018 Discovery and anti-inflammatory evaluation of benzothiazepinones (BTZs) as novel non-ATP competitive inhibitors of glycogen synthase kinase-3beta (GSK-3beta). benzothiazepinones 46-64 glycogen synthase kinase 3 beta Mus musculus 147-156 30293796-0 2018 Discovery and anti-inflammatory evaluation of benzothiazepinones (BTZs) as novel non-ATP competitive inhibitors of glycogen synthase kinase-3beta (GSK-3beta). btzs 66-70 glycogen synthase kinase 3 beta Mus musculus 115-145 30293796-0 2018 Discovery and anti-inflammatory evaluation of benzothiazepinones (BTZs) as novel non-ATP competitive inhibitors of glycogen synthase kinase-3beta (GSK-3beta). btzs 66-70 glycogen synthase kinase 3 beta Mus musculus 147-156 30293796-0 2018 Discovery and anti-inflammatory evaluation of benzothiazepinones (BTZs) as novel non-ATP competitive inhibitors of glycogen synthase kinase-3beta (GSK-3beta). Adenosine Triphosphate 85-88 glycogen synthase kinase 3 beta Mus musculus 115-145 30293796-0 2018 Discovery and anti-inflammatory evaluation of benzothiazepinones (BTZs) as novel non-ATP competitive inhibitors of glycogen synthase kinase-3beta (GSK-3beta). Adenosine Triphosphate 85-88 glycogen synthase kinase 3 beta Mus musculus 147-156 30293796-3 2018 In this paper, we designed and synthesized a series of new BTZ derivatives as non-ATP competitive GSK-3beta inhibitors. btz 59-62 glycogen synthase kinase 3 beta Mus musculus 98-107 30293796-3 2018 In this paper, we designed and synthesized a series of new BTZ derivatives as non-ATP competitive GSK-3beta inhibitors. Adenosine Triphosphate 82-85 glycogen synthase kinase 3 beta Mus musculus 98-107 30293796-4 2018 Kinetic analysis revealed two typical compounds 6j and 3j showed the different non-ATP competitive mechanism of substrate competition or allosteric modulation to GSK-3beta, respectively. Adenosine Triphosphate 83-86 glycogen synthase kinase 3 beta Mus musculus 162-171 30237424-10 2018 Surprisingly, decreasing GSK-3 activity, either via overexpression of GSK-3beta-DN or through the use of specific GSK-3 inhibitors, also exacerbated hippocampal damage and increased seizure severity during status epilepticus. gsk- 25-29 glycogen synthase kinase 3 beta Mus musculus 70-75 30118183-2 2018 Stimulation of these pathways inhibits GSK-3 to modulate diverse downstream effectors that include transcription factors, nutrient sensors, glycogen synthesis, mitochondrial function, circadian rhythm, and cell fate. Glycogen 140-148 glycogen synthase kinase 3 beta Mus musculus 39-44 30224063-8 2018 A western blot analysis revealed that LH dose-dependently increased the expression of Runx2 and beta-catenin, and promoted phosphorylation of glycogen synthase kinase-3beta in vitro. Luteinizing Hormone 38-40 glycogen synthase kinase 3 beta Mus musculus 142-172 30233733-12 2018 Fentanyl pretreatment significantly reduced the LPS-induced elevation of TLR4 at mRNA and protein levels as well as p-GSK-3beta protein levels in BV-2 cells. Fentanyl 0-8 glycogen synthase kinase 3 beta Mus musculus 118-127 30233733-13 2018 In conclusion, fentanyl pretreatment protects BV-2 cells from LPS-induced neuroinflammation by inhibiting TLR4 expression and GSK-3beta activation. Fentanyl 15-23 glycogen synthase kinase 3 beta Mus musculus 126-135 30556043-6 2018 Analysis of livers from Phb1 KO mice demonstrated an activation of the WNT-beta-catenin pathway as determined by phosphorylation of glycogen synthase kinase 3 (GSK3)betaserine [Ser]9 and protein kinase B (AKT)Ser473. betaserine 165-175 glycogen synthase kinase 3 beta Mus musculus 160-164 30556043-6 2018 Analysis of livers from Phb1 KO mice demonstrated an activation of the WNT-beta-catenin pathway as determined by phosphorylation of glycogen synthase kinase 3 (GSK3)betaserine [Ser]9 and protein kinase B (AKT)Ser473. Serine 177-180 glycogen synthase kinase 3 beta Mus musculus 160-164 30250248-0 2018 Proscillaridin A exerts anti-tumor effects through GSK3beta activation and alteration of microtubule dynamics in glioblastoma. Proscillaridin 0-16 glycogen synthase kinase 3 beta Mus musculus 51-59 30129879-10 2018 RESULTS: TA1 (7 and 11 mug/kg) significantly reduced the number of mice showing convulsions and increased their latency of onset, restored pentylenetrazole-induced reduction of hippocampal c-fos levels, activated the PI3K/AKT, and reduced GSK-3beta activity. pentylenetrazole 139-155 glycogen synthase kinase 3 beta Mus musculus 239-248 30237424-10 2018 Surprisingly, decreasing GSK-3 activity, either via overexpression of GSK-3beta-DN or through the use of specific GSK-3 inhibitors, also exacerbated hippocampal damage and increased seizure severity during status epilepticus. 3beta-dn 74-82 glycogen synthase kinase 3 beta Mus musculus 25-30 30071197-11 2018 GSK-3beta specific inhibitor, CHIR99021, attenuated sevoflurane-induced cell cycle arrest and abnormality of neurogenesis in neural stem cells. Sevoflurane 52-63 glycogen synthase kinase 3 beta Mus musculus 0-9 30231545-6 2018 This was accompanied by significantly increased activation levels of the glucose metabolism regulators 160 kDa AKT substrate (AS160), 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2), and glycogen synthase kinase-3beta (GSK3beta). Glucose 73-80 glycogen synthase kinase 3 beta Mus musculus 202-232 30231545-6 2018 This was accompanied by significantly increased activation levels of the glucose metabolism regulators 160 kDa AKT substrate (AS160), 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2), and glycogen synthase kinase-3beta (GSK3beta). Glucose 73-80 glycogen synthase kinase 3 beta Mus musculus 234-242 29427083-0 2018 Fluoxetine Inhibits Natural Decay of Long-Term Memory via Akt/GSK-3beta Signaling. Fluoxetine 0-10 glycogen synthase kinase 3 beta Mus musculus 62-71 29574946-4 2018 Intracellular cAMP levels were found to be significantly lower in sperm lacking GSK3alpha or GSK3beta. Cyclic AMP 14-18 glycogen synthase kinase 3 beta Mus musculus 93-101 29574946-5 2018 A similar outcome was observed when sperm cells were treated with SB216763, a GSK3 inhibitor. SB 216763 66-74 glycogen synthase kinase 3 beta Mus musculus 78-82 29574946-8 2018 PDE activity assay also showed that hyperactivated PDE4 contributes in lowering of cAMP levels in GSK3alpha null sperm suggesting that in wild-type sperm PDE4 activity is kept in check by GSK3. Cyclic AMP 83-87 glycogen synthase kinase 3 beta Mus musculus 98-102 29574946-9 2018 Conversely, PKA being triggered by cAMP, affected GSK3 activity through increasing its phosphorylation. Cyclic AMP 35-39 glycogen synthase kinase 3 beta Mus musculus 50-54 30125581-0 2018 Dioscin ameliorates cardiac hypertrophy through inhibition of the MAPK and Akt/GSK3beta/mTOR pathways. dioscin 0-7 glycogen synthase kinase 3 beta Mus musculus 79-87 30125581-5 2018 In addition, dioscin blocked the activation of the MAPK and Akt/GSK3beta/mTOR pathways and nuclear accumulation of p-Akt1 in AngII-infused mice. dioscin 13-20 glycogen synthase kinase 3 beta Mus musculus 64-72 30125581-6 2018 In vitro, dioscin inhibited the activation of the MAPK and Akt/GSK3beta/mTOR pathways and nuclear translocation of p-Akt1 and thus alleviated the hypertrophic growth. dioscin 10-17 glycogen synthase kinase 3 beta Mus musculus 63-71 30125581-7 2018 Our study demonstrated dioscin protects against AngII-induced cardiac hypertrophy via inhibition of the MAPK and Akt/GSK3beta/mTOR pathways and is a potential therapeutic candidate. dioscin 23-30 glycogen synthase kinase 3 beta Mus musculus 117-125 30026270-7 2018 These anti-inflammatory effects of GSK3 inhibition were found to be driven, at least in part, by inhibiting production of apoptosis inhibitor of macrophage in macrophages via inactivating STAT3 to reduce free fatty acid and chemokine level produced from VAT to suppress the migration/chemotaxis of macrophages and monocytes. Fatty Acids, Nonesterified 204-219 glycogen synthase kinase 3 beta Mus musculus 35-39 29883716-6 2018 RESULTS: In vitro, both knock-down as well as pharmacological inhibition of GSK-3beta not only increased expression levels of important constituents of the PGC-1 signaling network, but also potentiated myogenic differentiation-associated increases in mitochondrial respiration, mitochondrial DNA copy number, oxidative phosphorylation (OXPHOS) protein abundance and the activity of key enzymes involved in the Krebs cycle and fatty acid beta-oxidation. krebs 410-415 glycogen synthase kinase 3 beta Mus musculus 76-85 29883716-6 2018 RESULTS: In vitro, both knock-down as well as pharmacological inhibition of GSK-3beta not only increased expression levels of important constituents of the PGC-1 signaling network, but also potentiated myogenic differentiation-associated increases in mitochondrial respiration, mitochondrial DNA copy number, oxidative phosphorylation (OXPHOS) protein abundance and the activity of key enzymes involved in the Krebs cycle and fatty acid beta-oxidation. Fatty Acids 426-436 glycogen synthase kinase 3 beta Mus musculus 76-85 29427083-5 2018 Fluoxetine altered Akt/glycogen synthase kinase-3beta (GSK-3beta)/beta-catenin signaling in the hippocampus. Fluoxetine 0-10 glycogen synthase kinase 3 beta Mus musculus 23-53 29427083-5 2018 Fluoxetine altered Akt/glycogen synthase kinase-3beta (GSK-3beta)/beta-catenin signaling in the hippocampus. Fluoxetine 0-10 glycogen synthase kinase 3 beta Mus musculus 55-64 29427083-6 2018 Late short- and long-term pharmacological inhibition of GSK-3beta mimicked the effect of fluoxetine on memory persistence. Fluoxetine 89-99 glycogen synthase kinase 3 beta Mus musculus 56-65 29427083-9 2018 These results demonstrate that GSK-3beta might be a key molecule in memory decay process, and fluoxetine extends the period of long-term memory maintenance via Akt/GSK-3beta signaling. Fluoxetine 94-104 glycogen synthase kinase 3 beta Mus musculus 164-173 30165626-9 2018 In contrast, STI-571 abrogated phosphorylation of GSK3beta-Tyr216 induced by MPP+ in SN4741 cells and in primary midbrain neurons. mangion-purified polysaccharide (Candida albicans) 77-81 glycogen synthase kinase 3 beta Mus musculus 50-58 29981415-5 2018 Further analysis revealed that METH exposure obviously disrupted insulin signalling, resulted in brain insulin resistance, which manifested as downregulation of the insulin receptor substrate-1, AKTser 473, and GSK3beta activation. Methamphetamine 31-35 glycogen synthase kinase 3 beta Mus musculus 211-219 29753049-15 2018 This study provides the first evidence of the antidepressive-like effects of creatine in Ass1-40-treated mice, which were accompanied by hippocampal inhibition of GSK-3beta and modulation of antioxidant defenses. Creatine 77-85 glycogen synthase kinase 3 beta Mus musculus 163-172 29981415-6 2018 Notably, the linkage between p-tau expression and insulin signalling can be partially verified by treatment with the insulin-sensitizing drug rosiglitazone and GSK3beta inhibitor TWS119 which specifically reversed METH-induced hyperphosphorylation of tau. Methamphetamine 214-218 glycogen synthase kinase 3 beta Mus musculus 160-168 29753049-5 2018 Moreover, we addressed the participation of the intracellular signaling pathway mediated by glycogen synthase kinase-3beta (GSK-3beta)/nuclear factor erythroid-2-related factor 2 (Nrf2) in the creatine effects. Creatine 193-201 glycogen synthase kinase 3 beta Mus musculus 92-122 29698694-6 2018 The cross-generational effects appeared to be mediated via disruption of the balance between GSK3 and p-GKS3 by nicotine. Nicotine 112-120 glycogen synthase kinase 3 beta Mus musculus 93-97 29753049-5 2018 Moreover, we addressed the participation of the intracellular signaling pathway mediated by glycogen synthase kinase-3beta (GSK-3beta)/nuclear factor erythroid-2-related factor 2 (Nrf2) in the creatine effects. Creatine 193-201 glycogen synthase kinase 3 beta Mus musculus 124-133 29753049-12 2018 However, Ass1-40-infused mice treated with creatine (0.01 mg/kg) presented increased phosphorylation of GSK-3beta(Ser9) and HO-1 immunocontent in the hippocampus. Creatine 43-51 glycogen synthase kinase 3 beta Mus musculus 104-113 29753049-13 2018 Fluoxetine per se increased GSK-3beta(Ser9) phosphorylation, but did not alter HO-1 levels. Fluoxetine 0-10 glycogen synthase kinase 3 beta Mus musculus 28-37 30150769-6 2018 In this study, we aimed to evaluate whether the use of FUS-induced BBB opening to enhance GSK-3 inhibitor delivery, which would bring additive effect of Abeta plaque clearance by FUS with the reduction of Abeta plaque synthesis by GSK-3 inhibitor in an AD mice model. fusarubin 55-58 glycogen synthase kinase 3 beta Mus musculus 90-95 30150769-6 2018 In this study, we aimed to evaluate whether the use of FUS-induced BBB opening to enhance GSK-3 inhibitor delivery, which would bring additive effect of Abeta plaque clearance by FUS with the reduction of Abeta plaque synthesis by GSK-3 inhibitor in an AD mice model. fusarubin 55-58 glycogen synthase kinase 3 beta Mus musculus 231-236 30150769-6 2018 In this study, we aimed to evaluate whether the use of FUS-induced BBB opening to enhance GSK-3 inhibitor delivery, which would bring additive effect of Abeta plaque clearance by FUS with the reduction of Abeta plaque synthesis by GSK-3 inhibitor in an AD mice model. fusarubin 179-182 glycogen synthase kinase 3 beta Mus musculus 90-95 30075764-10 2018 Also, we found that GSK-3beta serine-9 phosphorylation increased in Hepa1-6 spheroids. Serine 30-36 glycogen synthase kinase 3 beta Mus musculus 20-29 30046097-7 2018 These changes were rescued by inhibition of glycogen synthase kinase 3 (GSK3) with lithium or CHIR99021, a highly selective GSK3 inhibitor. Lithium 83-90 glycogen synthase kinase 3 beta Mus musculus 44-70 29979973-4 2018 Here we show a single pharmacological GSK3 inhibitor, 6-bromoindirubin-3"-oxime (BIO), in combination with leukemia inhibition factor (LIF), promoted generation of stable NOD ESC lines at >80% efficiency. 6-bromoindirubin-3'-oxime 54-79 glycogen synthase kinase 3 beta Mus musculus 38-42 29529390-4 2018 GSK-3beta inhibition by SB216763 treatment aggravated liver fibrosis and elevated the expression of osteopontin (OPN) in the BDL mouse model. SB 216763 24-32 glycogen synthase kinase 3 beta Mus musculus 0-9 30046097-7 2018 These changes were rescued by inhibition of glycogen synthase kinase 3 (GSK3) with lithium or CHIR99021, a highly selective GSK3 inhibitor. Lithium 83-90 glycogen synthase kinase 3 beta Mus musculus 72-76 29039022-10 2018 Metformin globally normalized the increased glycogen synthase kinase 3beta activity induced by chronic treatment of L-DOPA in a manner associated with Akt activation in unilaterally 6-OHDA-lesioned mice. Metformin 0-9 glycogen synthase kinase 3 beta Mus musculus 44-74 29452207-1 2018 BACKGROUND & AIMS: Glycogen synthase kinase 3beta (Gsk3beta [Gsk3b]) is a ubiquitously expressed kinase with distinctive functions in different types of cells. Adenosine Monophosphate 12-15 glycogen synthase kinase 3 beta Mus musculus 23-53 29452207-1 2018 BACKGROUND & AIMS: Glycogen synthase kinase 3beta (Gsk3beta [Gsk3b]) is a ubiquitously expressed kinase with distinctive functions in different types of cells. Adenosine Monophosphate 12-15 glycogen synthase kinase 3 beta Mus musculus 55-63 29452207-1 2018 BACKGROUND & AIMS: Glycogen synthase kinase 3beta (Gsk3beta [Gsk3b]) is a ubiquitously expressed kinase with distinctive functions in different types of cells. Adenosine Monophosphate 12-15 glycogen synthase kinase 3 beta Mus musculus 55-60 30021941-9 2018 Moreover, activation of caspases, increase of inflammatory factors, and phosphorylation of ERK and GSK3 were inhibited by 6-MSITC. 6-(Methylsulfinyl)hexyl isothiocyanate 122-129 glycogen synthase kinase 3 beta Mus musculus 99-103 29976922-8 2018 Interestingly, Zscan4 is repressed in mESCs cultured in 2i (inhibitors of Mek and Gsk3beta signaling) media, associated with shorter telomeres and increased chromosome instability. zscan4 15-21 glycogen synthase kinase 3 beta Mus musculus 82-90 29039022-10 2018 Metformin globally normalized the increased glycogen synthase kinase 3beta activity induced by chronic treatment of L-DOPA in a manner associated with Akt activation in unilaterally 6-OHDA-lesioned mice. Levodopa 116-122 glycogen synthase kinase 3 beta Mus musculus 44-74 29039022-10 2018 Metformin globally normalized the increased glycogen synthase kinase 3beta activity induced by chronic treatment of L-DOPA in a manner associated with Akt activation in unilaterally 6-OHDA-lesioned mice. Oxidopamine 182-188 glycogen synthase kinase 3 beta Mus musculus 44-74 29730167-6 2018 KEY FINDINGS: SP was found to prevent hepatocyte death due to ethanol-induced oxidative stress by upregulating Akt/GSK-3beta activation in vitro. Ethanol 62-69 glycogen synthase kinase 3 beta Mus musculus 115-124 29557914-11 2018 GM6001 pretreatment suppressed SDC-1 shedding, alleviated renal inflammation and tubular apoptosis, and upregulated phosphorylation of the c-Met/AKT/GSK-3beta pathway. N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide 0-6 glycogen synthase kinase 3 beta Mus musculus 149-158 29398139-10 2018 At the molecular level, on a CD, CM-GSK-3alpha compensated for the loss of CM-GSK-3beta, as evident by significantly reduced GSK-3alphas21 phosphorylation (activation) resulting in a preserved canonical beta-catenin ubiquitination pathway and cardiac function. Cadmium 29-31 glycogen synthase kinase 3 beta Mus musculus 36-41 29765479-8 2018 Moreover, evodiamine increased the activity of AKT/GSK-3beta signalling pathway and inhibited the activity of nuclear factor kappaB. evodiamine 10-20 glycogen synthase kinase 3 beta Mus musculus 51-60 29789524-6 2018 Our in vivo study also showed that hirsutine effectively inhibits tumor growth in a A549 xenograft mouse model through ROCK1/PTEN/PI3K/Akt signaling-mediated GSK3beta dephosphorylation and apoptosis. hirsutine 35-44 glycogen synthase kinase 3 beta Mus musculus 158-166 29891841-0 2018 PQQ ameliorates D-galactose induced cognitive impairments by reducing glutamate neurotoxicity via the GSK-3beta/Akt signaling pathway in mouse. PQQ Cofactor 0-3 glycogen synthase kinase 3 beta Mus musculus 102-111 29891841-10 2018 In addition, PQQ reduced the up-regulated expression of p-Akt by D-gal and maintained the activity of GSK-3beta, resulting in a down-regulation of p-Tau level in hippocampus. PQQ Cofactor 13-16 glycogen synthase kinase 3 beta Mus musculus 102-111 29891841-11 2018 PQQ modulated memory ability partly via Akt/GSK-3beta pathway. PQQ Cofactor 0-3 glycogen synthase kinase 3 beta Mus musculus 44-53 29665406-0 2018 SN56 neuronal cell death after 24 h and 14 days chlorpyrifos exposure through glutamate transmission dysfunction, increase of GSK-3beta enzyme, beta-amyloid and tau protein levels. Chlorpyrifos 48-60 glycogen synthase kinase 3 beta Mus musculus 126-135 29530582-11 2018 Administration with lithium (non-selective GSK-3beta inhibitor) activated GSK-3beta/mTOR/p70S6K signalling in stroke-affected Hspa12a-/- mice. Lithium 20-27 glycogen synthase kinase 3 beta Mus musculus 43-52 29482106-1 2018 GS87 is a novel, highly specific GSK3 inhibitor, which has shown to induce extensive differentiation of acute myeloid leukemia (AML) cells in early mouse studies and has great potential for therapeutic advancement. 4-(5-{[(3-phenyl-1,2,4-oxadiazol-5-yl)methyl]sulfanyl}-1,3,4-oxadiazol-2-yl)pyridine 0-4 glycogen synthase kinase 3 beta Mus musculus 33-37 29530582-11 2018 Administration with lithium (non-selective GSK-3beta inhibitor) activated GSK-3beta/mTOR/p70S6K signalling in stroke-affected Hspa12a-/- mice. Lithium 20-27 glycogen synthase kinase 3 beta Mus musculus 74-83 29670081-9 2018 In seipin-nKO mice, the phosphorylation of GSK3beta was increased at Tyr216 and was reduced at Ser9, which was corrected by the PPARgamma agonist rosiglitazone. Rosiglitazone 146-159 glycogen synthase kinase 3 beta Mus musculus 43-51 29548997-10 2018 Finally, FTY720 significantly inhibited activation of PI3K/Akt/GSK3beta/p65 signaling, which further reduced the expression levels of adhesion molecules in bEND.3 cells treated with B6.MRL-lpr mouse serum. Fingolimod Hydrochloride 9-15 glycogen synthase kinase 3 beta Mus musculus 63-71 29670081-10 2018 The increased IL-6 level in seipin-nKO mice was sensitive to rosiglitazone and GSK3beta inhibitor AR-A014418. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 98-108 glycogen synthase kinase 3 beta Mus musculus 79-87 29700285-9 2018 Furthermore, inhibition of GSK3beta by LiCl abolished the suppression of cell growth, migration, and invasion mediated by HOXA4. Lithium Chloride 39-43 glycogen synthase kinase 3 beta Mus musculus 27-35 29353218-0 2018 Sulforaphane prevents angiotensin II-induced cardiomyopathy by activation of Nrf2 via stimulating the Akt/GSK-3ss/Fyn pathway. sulforaphane 0-12 glycogen synthase kinase 3 beta Mus musculus 106-111 29127434-4 2018 BRD7 mediates phosphorylation of GSK3beta at the Serine 9 residue and this effect on GSK3beta occurs even in the absence of AKT activity. Serine 49-55 glycogen synthase kinase 3 beta Mus musculus 33-41 29127434-4 2018 BRD7 mediates phosphorylation of GSK3beta at the Serine 9 residue and this effect on GSK3beta occurs even in the absence of AKT activity. Serine 49-55 glycogen synthase kinase 3 beta Mus musculus 85-93 29353218-7 2018 Up-regulation and activation of Nrf2 by SFN is accompanied by activation of Akt, inhibition of glycogen synthase kinase (GSK)-3beta, and accumulation of Fyn in nuclei. sulforaphane 40-43 glycogen synthase kinase 3 beta Mus musculus 95-131 29642438-9 2018 Sesamol increased glycogen synthase kinase 3 beta (GSK3beta), protein kinase B (AKT), and extracellular signal-related kinase (ERK) phosphorylation, thus inhibiting the transcription of MITF. sesamol 0-7 glycogen synthase kinase 3 beta Mus musculus 18-49 29642438-9 2018 Sesamol increased glycogen synthase kinase 3 beta (GSK3beta), protein kinase B (AKT), and extracellular signal-related kinase (ERK) phosphorylation, thus inhibiting the transcription of MITF. sesamol 0-7 glycogen synthase kinase 3 beta Mus musculus 51-59 29331582-3 2018 The drug lithium has actions on GSK3, and also on inositol metabolism. Lithium 9-16 glycogen synthase kinase 3 beta Mus musculus 32-36 29670521-3 2018 The ELISA and Western-blot analysis revealed that xanthohumol (Xn) inhibited Abeta accumulation and APP processing, and that Xn ameliorated tau hyperphosphorylation via PP2A, GSK3beta pathways in N2a/APP cells. xanthohumol 125-127 glycogen synthase kinase 3 beta Mus musculus 175-183 29331582-4 2018 While it is suspected that lithium"s inhibition of GSK3 causes rhythm changes, it is not known if inositol polyphosphates can also affect the circadian clock. Lithium 27-34 glycogen synthase kinase 3 beta Mus musculus 51-55 29331582-7 2018 The IP6 effect on amplitude was attenuated by selective siRNA knockdown of GSK3B and pharmacological blockade of AKT kinase. Phytic Acid 4-7 glycogen synthase kinase 3 beta Mus musculus 75-80 29599817-8 2018 The mRNA expression levels of GSK3beta and DKK1 in the WYHZTL formula and XAV-939-treated group were significantly higher than those in the BLM group, while Wnt1, beta-catenin, TCF4, cyclin D1, survivin, VEGF, CTGF, FN1, collagen I/III were decreased. XAV939 74-81 glycogen synthase kinase 3 beta Mus musculus 30-38 29121589-6 2018 DMF induces the NRF2 transcriptional through a mechanism that involves KEAP1 but also PI3K/AKT/GSK-3-dependent pathways. Dimethyl Fumarate 0-3 glycogen synthase kinase 3 beta Mus musculus 95-100 29121589-9 2018 This study reveals neuroprotective effects of DMF beyond disruption of the KEAP1/NRF2 axis by inhibiting GSK3 in a mouse model of tauopathy. Dimethyl Fumarate 46-49 glycogen synthase kinase 3 beta Mus musculus 105-109 29599817-9 2018 Compared with BLM group, the protein expression levels of GSK3beta and DKK1 in the WYHZTL formula and XAV-939-treated group were upregulated, while Wnt1, beta-catenin, cyclin D1, survivin, CTGF, FN1, collagen I/III were downregulated. XAV939 102-105 glycogen synthase kinase 3 beta Mus musculus 58-66 29504933-2 2018 Enzymatic activity of GSK3 is inhibited by N-terminal serine phosphorylation. Serine 54-60 glycogen synthase kinase 3 beta Mus musculus 22-26 29509689-0 2018 Novel Furocoumarin Derivatives Stimulate Melanogenesis in B16 Melanoma Cells by Up-Regulation of MITF and TYR Family via Akt/GSK3beta/beta-Catenin Signaling Pathways. Furocoumarins 6-18 glycogen synthase kinase 3 beta Mus musculus 125-133 29555900-4 2018 We demonstrate that GSK3 is tyrosine phosphorylated (pY) in mouse neural crest cells and that loss of GSK3 leads to increased pFAK and misregulation of Rac1 and lamellipodin, key regulators of cell migration. Tyrosine 28-36 glycogen synthase kinase 3 beta Mus musculus 20-24 29504933-5 2018 Molecular modeling and/or molecular dynamics simulations indicate that acetylation of GSK3 isoforms would hinder both the adenosine binding and prevent stable interactions of the negatively charged phosphates. Adenosine 122-131 glycogen synthase kinase 3 beta Mus musculus 86-90 29504933-5 2018 Molecular modeling and/or molecular dynamics simulations indicate that acetylation of GSK3 isoforms would hinder both the adenosine binding and prevent stable interactions of the negatively charged phosphates. Phosphates 198-208 glycogen synthase kinase 3 beta Mus musculus 86-90 29504933-6 2018 We found that SIRT2 deacetylates GSK3beta, and thus enhances its binding to ATP. Adenosine Triphosphate 76-79 glycogen synthase kinase 3 beta Mus musculus 33-41 29504933-9 2018 Overall, our study identified lysine acetylation as a novel post-translational modification regulating GSK3 activity. Lysine 30-36 glycogen synthase kinase 3 beta Mus musculus 103-107 29328365-9 2018 Moreover, brain tumor xenograft models revealed that following exposure to IR plus SB216763, a specific GSK3beta inhibitor, tumor growth was markedly inhibited and the survival of mice markedly increased. SB 216763 83-91 glycogen synthase kinase 3 beta Mus musculus 104-112 29452218-6 2018 Treatment with the GSK3 inhibitor TDZD-8 reduced inflammatory cytokine levels, increased tight junction protein levels, and reversed impaired recovery from learned helplessness, demonstrating that prolonged learned helplessness is reversible and is maintained by abnormally active GSK3. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 34-40 glycogen synthase kinase 3 beta Mus musculus 19-23 29452218-6 2018 Treatment with the GSK3 inhibitor TDZD-8 reduced inflammatory cytokine levels, increased tight junction protein levels, and reversed impaired recovery from learned helplessness, demonstrating that prolonged learned helplessness is reversible and is maintained by abnormally active GSK3. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 34-40 glycogen synthase kinase 3 beta Mus musculus 281-285 29328365-11 2018 Our study also suggested that the inhibition of GSK3beta by SB216763 significantly inhibited the proliferation and induced the apoptosis of glioblastoma cells. SB 216763 60-68 glycogen synthase kinase 3 beta Mus musculus 48-56 28357806-2 2018 Our study demonstrated that BP-3 caused neurotoxicity and activated apoptosis via an intrinsic pathway involving the loss of mitochondrial membrane potential and the activation of caspases-9 and -3 and kinases p38/MAPK and Gsk3beta. oxybenzone 28-32 glycogen synthase kinase 3 beta Mus musculus 223-231 29265525-11 2018 Additionally, the protein kinase B/glycogen synthase kinase 3beta (AKT/GSK3beta) signalling pathway was activated after the administration of TPPU. 1-trifluoromethoxyphenyl-3-(1-propionylpiperidine-4-yl)urea 142-146 glycogen synthase kinase 3 beta Mus musculus 35-65 29265525-11 2018 Additionally, the protein kinase B/glycogen synthase kinase 3beta (AKT/GSK3beta) signalling pathway was activated after the administration of TPPU. 1-trifluoromethoxyphenyl-3-(1-propionylpiperidine-4-yl)urea 142-146 glycogen synthase kinase 3 beta Mus musculus 71-79 29054855-7 2018 Genetic modulation studies in cardiomyocytes and cardiac and embryonic fibroblasts revealed that the lack of H-Ras down-regulates the B-RAF/MEK/ERK pathway, which induces the glycogen synthase kinase-3beta-dependent activation of the transcription factor, cAMP response element-binding protein, which is responsible for PKG-Ibeta overexpression in H -ras-/- mouse embryonic fibroblasts. Cyclic AMP 256-260 glycogen synthase kinase 3 beta Mus musculus 175-205 29434807-9 2018 Furthermore, sevoflurane inhibited the phosphorylation of Akt, decreased the phosphorylation of GSK-3beta at ser9 and increased the phosphorylation of CRMP2 at Thr514. Sevoflurane 13-24 glycogen synthase kinase 3 beta Mus musculus 96-105 29434807-10 2018 These results suggest that multiple signaling pathways, including ERK1/2, P38 and Akt/GSK-3beta/CRMP-2 may be involved in sevoflurane-induced neuroapoptosis in the developing brain. Sevoflurane 122-133 glycogen synthase kinase 3 beta Mus musculus 86-95 29218434-0 2018 Inhibition of GSK-3beta Signaling Pathway Rescues Ketamine-Induced Neurotoxicity in Neural Stem Cell-Derived Neurons. Ketamine 50-58 glycogen synthase kinase 3 beta Mus musculus 14-23 29218434-2 2018 In this work, we utilized an in vitro model of neural stem cells-derived neurons (nSCNs) to evaluate the role of GSK-3 signaling pathway in Keta-induced neurotoxicity. Ketamine 140-144 glycogen synthase kinase 3 beta Mus musculus 113-118 29218434-6 2018 The subsequent effects of GSK-3alpha or GSK-3beta downregulation on Keta-induced neurotoxicity, including apoptosis and neurite loss, were then evaluated in nSCNs. Ketamine 68-72 glycogen synthase kinase 3 beta Mus musculus 40-49 29218434-7 2018 Finally, caspase and Akt/ERK signal pathways were further examined by western blot to evaluate the regulatory effect of GSK-3 signaling pathways on Keta-induced neural injury. Ketamine 148-152 glycogen synthase kinase 3 beta Mus musculus 120-125 29218434-9 2018 Keta decreased GSK-3beta phosphorylation, but had no effect on GSK-3alpha phosphorylation. Ketamine 0-4 glycogen synthase kinase 3 beta Mus musculus 15-24 29218434-10 2018 SiRNA-induced GSK-3beta downregulation rescued Keta-induced neurotoxicity in nSCNs by reducing neuronal apoptosis and preventing neurite degeneration. Ketamine 47-51 glycogen synthase kinase 3 beta Mus musculus 14-23 29218434-13 2018 GSK-3beta, not GSK-3alpha, was specifically involved in the process of Keta-induced neurotoxicity in nSCNs. Ketamine 71-75 glycogen synthase kinase 3 beta Mus musculus 0-9 29218434-14 2018 Inhibiting GSK-3beta may be an effective approach to counter toxic effect of ketamine on central neurons in clinical and experimental applications. Ketamine 77-85 glycogen synthase kinase 3 beta Mus musculus 11-20 29267844-6 2018 Flow cytometry results revealed that intracellular calcium (Ca2+) level was changed by nalmefene, western blot analysis showed that nalmefene decreased calmodulin expression and calcium/calmodulin dependent protein kinases II (CaMK II) phosphorylation, thus inhibiting the serine/threonine kinase (AKT)-glycogen synthase kinase-3beta (GSK-3beta) pathway. nalmefene 132-141 glycogen synthase kinase 3 beta Mus musculus 335-344 29267844-8 2018 In conclusion, the anti-tumor effect of nalmefene may be achieved by inhibiting opioid receptor and down-regulating calmodulin expression and CaMK II phosphorylation, thus inhibiting AKT-GSK-3beta pathway and the glycolysis of CT26 cells. nalmefene 40-49 glycogen synthase kinase 3 beta Mus musculus 187-196 29335808-10 2018 Western blot data showed that intracellular PTEN protein level in PFOA-treated adipose was up-regulated, while phosphorylation of AKT, GSK3beta levels were lowered dose-dependently. perfluorooctanoic acid 66-70 glycogen synthase kinase 3 beta Mus musculus 135-143 29307602-9 2018 The activated Akt/GSK-3beta and snail signaling pathway largely accounted for MC-LRinduced TJs toxicity, which could be partially reversed by snail siRNA interference or AKT chemical inhibitor in TM4 cells. microcystin 78-80 glycogen synthase kinase 3 beta Mus musculus 18-27 29557384-10 2018 These findings confirm that the glycogen synthase kinase 3 beta inhibitor, SB216763, promoted the myelination and myotube differentiation through the Wnt/beta-catenin signaling pathway and contributed to nerve remyelination and reduced denervated muscle atrophy after peripheral nerve injury. SB 216763 75-83 glycogen synthase kinase 3 beta Mus musculus 32-63 28621459-7 2018 Moreover, the reduction of nuclear beta-catenin amount and decreased expression of TCF1 and Runx2 were significantly reversed in MACF1-KD cells when treated with lithium chloride, an agonist for beta-catenin by inhibiting GSK-3beta activity. Lithium Chloride 162-178 glycogen synthase kinase 3 beta Mus musculus 222-231 28699662-13 2018 Calycosin increased glycogen synthase kinase 3 beta, glucose transporter 4, and phosphorylated insulin receptor substrates 1 and 2 expressions involved in glucose metabolism. 7,3'-dihydroxy-4'-methoxyisoflavone 0-9 glycogen synthase kinase 3 beta Mus musculus 20-51 27752079-3 2018 Treatment with lithium or a glycogen synthase kinase-3 (GSK3) inhibitor corrects behavioral and neurodevelopmental phenotypes in these animals. Lithium 15-22 glycogen synthase kinase 3 beta Mus musculus 56-60 29146504-11 2018 Consistent with the in vivo observations, minocycline inhibited ethanol-induced the expression of pro-inflammatory cytokines and activation of GSK3beta in a microglia cell line (SIM-9). Ethanol 64-71 glycogen synthase kinase 3 beta Mus musculus 143-151 29146504-12 2018 GSK3beta inhibitor eliminated ethanol activation of pro-inflammatory cytokines in SIM-9 cells. Ethanol 30-37 glycogen synthase kinase 3 beta Mus musculus 0-8 29146504-15 2018 Together, these results suggest that minocycline may ameliorate ethanol neurotoxicity in the developing by alleviating GSK3beta-mediated neuroinflammation. Minocycline 37-48 glycogen synthase kinase 3 beta Mus musculus 119-127 29146504-10 2018 Minocycline blocked ethanol-induced activation of GSK3beta, a key mediator of neuroinflammation and microglial activation in the developing brain. Minocycline 0-11 glycogen synthase kinase 3 beta Mus musculus 50-58 29146504-10 2018 Minocycline blocked ethanol-induced activation of GSK3beta, a key mediator of neuroinflammation and microglial activation in the developing brain. Ethanol 20-27 glycogen synthase kinase 3 beta Mus musculus 50-58 29146504-11 2018 Consistent with the in vivo observations, minocycline inhibited ethanol-induced the expression of pro-inflammatory cytokines and activation of GSK3beta in a microglia cell line (SIM-9). Minocycline 42-53 glycogen synthase kinase 3 beta Mus musculus 143-151 28982059-0 2018 LC-MS/MS determination of tideglusib, a novel GSK-3beta inhibitor in mice plasma and its application to a pharmacokinetic study in mice. tideglusib 26-36 glycogen synthase kinase 3 beta Mus musculus 46-55 29473508-11 2018 In contrast, chronic treatment with tolfenamic acid renders the olfactory bulb resistant to amyloid beta-induced network activity inhibition in vitro and in vivo, which correlates with the inhibition of GSK3beta activation and the protection against amyloid beta-induced olfactory dysfunction. tolfenamic acid 36-51 glycogen synthase kinase 3 beta Mus musculus 203-211 28684297-15 2018 Besides, curcumol also prevented the growth of human colon cancer cells xenografts in nude mouse, accompanied by the reduction of PI3K, Akt, cyclin D1, CDK4, cycln E and significant increase of GSK3beta. curcumol 9-17 glycogen synthase kinase 3 beta Mus musculus 194-202 29129695-0 2018 Tetrahydroxystilbene glucoside modulates amyloid precursor protein processing via activation of AKT-GSK3beta pathway in cells and in APP/PS1 transgenic mice. 2',3',4',5'-tetrahydroxystilbene-2-O-beta-D-glucoside 0-30 glycogen synthase kinase 3 beta Mus musculus 100-108 29129695-3 2018 Here, we determined the effect of Tetrahydroxystilbene glucoside (TSG) on the AKT-GSK3beta pathway. 2',3',4',5'-tetrahydroxystilbene-2-O-beta-D-glucoside 34-64 glycogen synthase kinase 3 beta Mus musculus 82-90 29129695-3 2018 Here, we determined the effect of Tetrahydroxystilbene glucoside (TSG) on the AKT-GSK3beta pathway. tsg 66-69 glycogen synthase kinase 3 beta Mus musculus 82-90 30068273-5 2018 Furthermore, prior exposure to Pb in-vitro also resulted in an increase in alpha-Syn, its phosphorylated forms, as well as an increase in glycogen synthase kinase 3beta (GSK-3beta) and Caspase-3. Lead 31-33 glycogen synthase kinase 3 beta Mus musculus 138-168 29154274-11 2018 Nonetheless, complex AD interactions dictate successful therapeutics harness synergy between Abeta and pTau, possibly through the GSK3 pathway. UNII-042A8N37WH 93-98 glycogen synthase kinase 3 beta Mus musculus 130-134 29399113-0 2018 Geniposide attenuates epilepsy symptoms in a mouse model through the PI3K/Akt/GSK-3beta signaling pathway. geniposide 0-10 glycogen synthase kinase 3 beta Mus musculus 78-87 29399113-2 2018 The results of the current study demonstrate that geniposide attenuates epilepsy in a mouse model through the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3beta (GSK-3beta) signaling pathway. geniposide 50-60 glycogen synthase kinase 3 beta Mus musculus 166-196 29399113-2 2018 The results of the current study demonstrate that geniposide attenuates epilepsy in a mouse model through the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3beta (GSK-3beta) signaling pathway. geniposide 50-60 glycogen synthase kinase 3 beta Mus musculus 198-207 29399113-7 2018 Furthermore, geniposide significantly suppressed the protein expression of activator protein 1, increased the activation of Akt and increased the protein expression of GSK-3beta and PI3K in epilepsy mice (all P<0.01). geniposide 13-23 glycogen synthase kinase 3 beta Mus musculus 168-177 29399113-8 2018 These results suggest that geniposide attenuates epilepsy in mice through the PI3K/Akt/GSK-3beta signaling pathway. geniposide 27-37 glycogen synthase kinase 3 beta Mus musculus 87-96 30149447-6 2018 We also have shown that STZ causes insulin resistance and impairment on phosphoinositide 3-kinase (PI3K) activity in the Neuro-2a cells through protein kinase B (Akt) inactivation by S-nitrosylation, which could upregulate GSK3-beta activity. Streptozocin 24-27 glycogen synthase kinase 3 beta Mus musculus 223-232 29154274-11 2018 Nonetheless, complex AD interactions dictate successful therapeutics harness synergy between Abeta and pTau, possibly through the GSK3 pathway. ptau 103-107 glycogen synthase kinase 3 beta Mus musculus 130-134 27966074-8 2018 We then treated post-septic mice with liraglutide, a GLP-1 receptor agonist with insulinotropic activity, or TDZD-8, a GSK3beta inhibitor, which rescued NOR memory. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 109-115 glycogen synthase kinase 3 beta Mus musculus 119-127 29302212-0 2018 Ethyl linoleate inhibits alpha-MSH-induced melanogenesis through Akt/GSK3beta/beta-catenin signal pathway. ethyl linoleate 0-15 glycogen synthase kinase 3 beta Mus musculus 69-77 29302212-5 2018 We observed that ethyl linoleate inhibited phosphorylation of Akt and glycogen synthase kinase 3beta (GSK3beta) and reduced the level of beta-catenin, suggesting that ethyl linoleate inhibits melanogenesis through Akt/GSK3beta/beta-catenin signal pathway. ethyl linoleate 17-32 glycogen synthase kinase 3 beta Mus musculus 70-100 29302212-5 2018 We observed that ethyl linoleate inhibited phosphorylation of Akt and glycogen synthase kinase 3beta (GSK3beta) and reduced the level of beta-catenin, suggesting that ethyl linoleate inhibits melanogenesis through Akt/GSK3beta/beta-catenin signal pathway. ethyl linoleate 17-32 glycogen synthase kinase 3 beta Mus musculus 102-110 29302212-5 2018 We observed that ethyl linoleate inhibited phosphorylation of Akt and glycogen synthase kinase 3beta (GSK3beta) and reduced the level of beta-catenin, suggesting that ethyl linoleate inhibits melanogenesis through Akt/GSK3beta/beta-catenin signal pathway. ethyl linoleate 17-32 glycogen synthase kinase 3 beta Mus musculus 218-226 29302212-5 2018 We observed that ethyl linoleate inhibited phosphorylation of Akt and glycogen synthase kinase 3beta (GSK3beta) and reduced the level of beta-catenin, suggesting that ethyl linoleate inhibits melanogenesis through Akt/GSK3beta/beta-catenin signal pathway. ethyl linoleate 167-182 glycogen synthase kinase 3 beta Mus musculus 70-100 29302212-5 2018 We observed that ethyl linoleate inhibited phosphorylation of Akt and glycogen synthase kinase 3beta (GSK3beta) and reduced the level of beta-catenin, suggesting that ethyl linoleate inhibits melanogenesis through Akt/GSK3beta/beta-catenin signal pathway. ethyl linoleate 167-182 glycogen synthase kinase 3 beta Mus musculus 102-110 29302212-5 2018 We observed that ethyl linoleate inhibited phosphorylation of Akt and glycogen synthase kinase 3beta (GSK3beta) and reduced the level of beta-catenin, suggesting that ethyl linoleate inhibits melanogenesis through Akt/GSK3beta/beta-catenin signal pathway. ethyl linoleate 167-182 glycogen synthase kinase 3 beta Mus musculus 218-226 29070680-3 2017 Here, we report that an allosteric inhibitor of GSK-3beta, 4-benzyl-2-(naphthalene-1-yl)-1,2,4-thiadiazolidine-3,5-dione (NP12), lessens the magnitude of adverse myocardial remodeling and promotes angiogenesis. tideglusib 59-120 glycogen synthase kinase 3 beta Mus musculus 48-57 29399187-0 2018 Oridonin inhibits migration, invasion, adhesion and TGF-beta1-induced epithelial-mesenchymal transition of melanoma cells by inhibiting the activity of PI3K/Akt/GSK-3beta signaling pathway. oridonin 0-8 glycogen synthase kinase 3 beta Mus musculus 161-170 29058041-9 2018 DHM activated the ERK1/2-CREB pathway and increased glycogen synthase kinase-3 beta (GSK-3beta) phosphorylation at ser-9, with upregulation of BDNF expression, in both hippocampal tissues and cultured hippocampal cells. dihydromyricetin 0-3 glycogen synthase kinase 3 beta Mus musculus 52-83 29058041-9 2018 DHM activated the ERK1/2-CREB pathway and increased glycogen synthase kinase-3 beta (GSK-3beta) phosphorylation at ser-9, with upregulation of BDNF expression, in both hippocampal tissues and cultured hippocampal cells. dihydromyricetin 0-3 glycogen synthase kinase 3 beta Mus musculus 85-94 29058041-9 2018 DHM activated the ERK1/2-CREB pathway and increased glycogen synthase kinase-3 beta (GSK-3beta) phosphorylation at ser-9, with upregulation of BDNF expression, in both hippocampal tissues and cultured hippocampal cells. Serine 115-118 glycogen synthase kinase 3 beta Mus musculus 52-83 29058041-9 2018 DHM activated the ERK1/2-CREB pathway and increased glycogen synthase kinase-3 beta (GSK-3beta) phosphorylation at ser-9, with upregulation of BDNF expression, in both hippocampal tissues and cultured hippocampal cells. Serine 115-118 glycogen synthase kinase 3 beta Mus musculus 85-94 28359686-3 2017 From our previous study, SLM, a carbazole-based fluorophore prevents Abeta aggregation, reduced glycogen synthase kinase-3beta (GSK-3beta) activity and tau hyperphosphorylation in triple transgenic mouse model of AD. carbazole 32-41 glycogen synthase kinase 3 beta Mus musculus 96-126 28359686-3 2017 From our previous study, SLM, a carbazole-based fluorophore prevents Abeta aggregation, reduced glycogen synthase kinase-3beta (GSK-3beta) activity and tau hyperphosphorylation in triple transgenic mouse model of AD. carbazole 32-41 glycogen synthase kinase 3 beta Mus musculus 128-137 29070680-3 2017 Here, we report that an allosteric inhibitor of GSK-3beta, 4-benzyl-2-(naphthalene-1-yl)-1,2,4-thiadiazolidine-3,5-dione (NP12), lessens the magnitude of adverse myocardial remodeling and promotes angiogenesis. tideglusib 122-126 glycogen synthase kinase 3 beta Mus musculus 48-57 29070680-6 2017 Intramyocardial administration of NP12 increased phosphorylation of GSK-3beta, reduced fibrosis, and restored diastolic function in the mice that had experienced an AMI. tideglusib 34-38 glycogen synthase kinase 3 beta Mus musculus 68-77 29244860-2 2017 GSK3 inhibition increases glucose uptake in insulin-insensitive muscle and adipose tissue, while it reduces albuminuria and glomerulosclerosis in acute kidney injury. Glucose 26-33 glycogen synthase kinase 3 beta Mus musculus 0-4 29299155-0 2017 Neuroprotection by aripiprazole against beta-amyloid-induced toxicity by P-CK2alpha activation via inhibition of GSK-3beta. Aripiprazole 19-31 glycogen synthase kinase 3 beta Mus musculus 113-122 29217823-5 2017 LPA administration also strongly blocked the APAP challenge-elicited phosphorylation of JNK, ERK and GSK3beta, which are involved in the pathogenesis of acute liver injury. lysophosphatidic acid 0-3 glycogen synthase kinase 3 beta Mus musculus 101-109 29217823-5 2017 LPA administration also strongly blocked the APAP challenge-elicited phosphorylation of JNK, ERK and GSK3beta, which are involved in the pathogenesis of acute liver injury. Acetaminophen 45-49 glycogen synthase kinase 3 beta Mus musculus 101-109 28679060-7 2017 EGCG induced activation of the PI3K/Akt pathway as evidenced by increased Akt, phospho-Akt, GSK-3beta, phospho-GSK-3beta, and mTORc1 levels. epigallocatechin gallate 0-4 glycogen synthase kinase 3 beta Mus musculus 92-101 28679060-7 2017 EGCG induced activation of the PI3K/Akt pathway as evidenced by increased Akt, phospho-Akt, GSK-3beta, phospho-GSK-3beta, and mTORc1 levels. epigallocatechin gallate 0-4 glycogen synthase kinase 3 beta Mus musculus 111-120 29234273-3 2017 7-bromoindirubin-3-oxime (7Bio), an indirubin derivative derived from indirubin-3-oxime, possesses inhibitory effects against cyclin-dependent kinase-5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta), two pharmacological targets of Alzheimer"s disease (AD). 7-bromoindirubin-3'-oxime 0-24 glycogen synthase kinase 3 beta Mus musculus 163-193 29234273-3 2017 7-bromoindirubin-3-oxime (7Bio), an indirubin derivative derived from indirubin-3-oxime, possesses inhibitory effects against cyclin-dependent kinase-5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta), two pharmacological targets of Alzheimer"s disease (AD). 7-bromoindirubin-3'-oxime 0-24 glycogen synthase kinase 3 beta Mus musculus 195-203 29234273-3 2017 7-bromoindirubin-3-oxime (7Bio), an indirubin derivative derived from indirubin-3-oxime, possesses inhibitory effects against cyclin-dependent kinase-5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta), two pharmacological targets of Alzheimer"s disease (AD). 7-bromoindirubin-3'-oxime 26-30 glycogen synthase kinase 3 beta Mus musculus 163-193 29234273-3 2017 7-bromoindirubin-3-oxime (7Bio), an indirubin derivative derived from indirubin-3-oxime, possesses inhibitory effects against cyclin-dependent kinase-5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta), two pharmacological targets of Alzheimer"s disease (AD). 7-bromoindirubin-3'-oxime 26-30 glycogen synthase kinase 3 beta Mus musculus 195-203 29234273-3 2017 7-bromoindirubin-3-oxime (7Bio), an indirubin derivative derived from indirubin-3-oxime, possesses inhibitory effects against cyclin-dependent kinase-5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta), two pharmacological targets of Alzheimer"s disease (AD). indirubin 7-16 glycogen synthase kinase 3 beta Mus musculus 163-193 29234273-3 2017 7-bromoindirubin-3-oxime (7Bio), an indirubin derivative derived from indirubin-3-oxime, possesses inhibitory effects against cyclin-dependent kinase-5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta), two pharmacological targets of Alzheimer"s disease (AD). indirubin 7-16 glycogen synthase kinase 3 beta Mus musculus 195-203 29182558-0 2017 An Isoxazole Chalcone Derivative Enhances Melanogenesis in B16 Melanoma Cells via the Akt/GSK3beta/beta-Catenin Signaling Pathways. isoxazole chalcone 3-21 glycogen synthase kinase 3 beta Mus musculus 90-98 29234273-3 2017 7-bromoindirubin-3-oxime (7Bio), an indirubin derivative derived from indirubin-3-oxime, possesses inhibitory effects against cyclin-dependent kinase-5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta), two pharmacological targets of Alzheimer"s disease (AD). indirubin-3'-monoxime 7-24 glycogen synthase kinase 3 beta Mus musculus 163-193 29234273-3 2017 7-bromoindirubin-3-oxime (7Bio), an indirubin derivative derived from indirubin-3-oxime, possesses inhibitory effects against cyclin-dependent kinase-5 (CDK5) and glycogen synthase kinase-3beta (GSK3beta), two pharmacological targets of Alzheimer"s disease (AD). indirubin-3'-monoxime 7-24 glycogen synthase kinase 3 beta Mus musculus 195-203 29182558-6 2017 Further investigations revealed that Akt and GSK3beta were the signaling pathways involved in the hyperpigmentation of PMPP. 1,5-pyrimidino-6,9-purinophane 119-123 glycogen synthase kinase 3 beta Mus musculus 45-53 28865114-0 2017 Prenatal Alcohol Exposure Leads to Enhanced Serine 9 Phosphorylation of Glycogen Synthase Kinase-3beta (GSK-3beta) in the Hippocampal Dentate Gyrus of Adult Mouse. Alcohols 9-16 glycogen synthase kinase 3 beta Mus musculus 72-102 29109264-0 2017 Epoxide metabolites of arachidonate and docosahexaenoate function conversely in acute kidney injury involved in GSK3beta signaling. Epoxy Compounds 0-7 glycogen synthase kinase 3 beta Mus musculus 112-120 29109264-0 2017 Epoxide metabolites of arachidonate and docosahexaenoate function conversely in acute kidney injury involved in GSK3beta signaling. Arachidonic Acid 23-35 glycogen synthase kinase 3 beta Mus musculus 112-120 29109264-0 2017 Epoxide metabolites of arachidonate and docosahexaenoate function conversely in acute kidney injury involved in GSK3beta signaling. Docosahexaenoic Acids 40-56 glycogen synthase kinase 3 beta Mus musculus 112-120 29109264-8 2017 In contrast, 19 (20)-EDP dose-dependently promoted H/R-caused apoptosis and worsened the reduction in GSK3beta phosphorylation in mRTECs. 2-ethyl-3,5-dimethylpyrazine 21-24 glycogen synthase kinase 3 beta Mus musculus 102-110 29109264-10 2017 Overall, these epoxide metabolites of ARA and DHA function conversely in I/R-AKI, possibly through their largely different metabolic stability and their opposite effects in modulation of H/R-caused RTEC apoptosis and GSK3beta phosphorylation. Epoxy Compounds 15-22 glycogen synthase kinase 3 beta Mus musculus 217-225 29109264-10 2017 Overall, these epoxide metabolites of ARA and DHA function conversely in I/R-AKI, possibly through their largely different metabolic stability and their opposite effects in modulation of H/R-caused RTEC apoptosis and GSK3beta phosphorylation. Arachidonic Acid 38-41 glycogen synthase kinase 3 beta Mus musculus 217-225 29109264-10 2017 Overall, these epoxide metabolites of ARA and DHA function conversely in I/R-AKI, possibly through their largely different metabolic stability and their opposite effects in modulation of H/R-caused RTEC apoptosis and GSK3beta phosphorylation. Docosahexaenoic Acids 46-49 glycogen synthase kinase 3 beta Mus musculus 217-225 29137190-9 2017 SM70EE also promoted activation of the brain-derived neurotrophic factor/phosphatidylinositol-3 kinase/serine/threonine protein kinase signaling pathway and inhibited glycogen synthase kinase-3beta phosphorylation. sm70ee 0-6 glycogen synthase kinase 3 beta Mus musculus 167-197 29137190-10 2017 These findings suggested that SM70EE ameliorated Abeta1-42-induced cognitive impairments by inhibiting the increased phosphorylation of glycogen synthase kinase-3beta caused by intracerebroventricular injection of Abeta1-42 in mice. sm70ee 30-36 glycogen synthase kinase 3 beta Mus musculus 136-166 28939294-4 2017 Our results demonstrated that MP407 dose-dependently inhibited collagen-induced platelet aggregation, thromboxane B2 (TXB2) production, intracellular Ca2+ mobilization, platelet membrane GPIIb/IIIa expression, and the phosphorylation of Akt, GSK3beta, p38MAPK, and phospho (Ser) PKC substrate (p47). MP407 30-35 glycogen synthase kinase 3 beta Mus musculus 242-250 28939294-8 2017 Therefore, the antiplatelet activity of MP407 may be modulated by cyclic AMP-dependent regulation of Akt, GSK3beta, p38MAPK and VASP phosphorylation. MP407 40-45 glycogen synthase kinase 3 beta Mus musculus 106-114 28939294-8 2017 Therefore, the antiplatelet activity of MP407 may be modulated by cyclic AMP-dependent regulation of Akt, GSK3beta, p38MAPK and VASP phosphorylation. Cyclic AMP 66-76 glycogen synthase kinase 3 beta Mus musculus 106-114 28678521-7 2017 In contrast, wild-type mice treated with the clinically relevant GSK3beta inhibitors, tideglusib and valproate, exhibited significantly decreased alveolar protein concentrations, which was associated with improved lung function and histopathology. tideglusib 86-96 glycogen synthase kinase 3 beta Mus musculus 65-73 28678521-7 2017 In contrast, wild-type mice treated with the clinically relevant GSK3beta inhibitors, tideglusib and valproate, exhibited significantly decreased alveolar protein concentrations, which was associated with improved lung function and histopathology. Valproic Acid 101-110 glycogen synthase kinase 3 beta Mus musculus 65-73 28865114-0 2017 Prenatal Alcohol Exposure Leads to Enhanced Serine 9 Phosphorylation of Glycogen Synthase Kinase-3beta (GSK-3beta) in the Hippocampal Dentate Gyrus of Adult Mouse. Alcohols 9-16 glycogen synthase kinase 3 beta Mus musculus 104-113 28865114-0 2017 Prenatal Alcohol Exposure Leads to Enhanced Serine 9 Phosphorylation of Glycogen Synthase Kinase-3beta (GSK-3beta) in the Hippocampal Dentate Gyrus of Adult Mouse. Serine 44-50 glycogen synthase kinase 3 beta Mus musculus 72-102 28865114-0 2017 Prenatal Alcohol Exposure Leads to Enhanced Serine 9 Phosphorylation of Glycogen Synthase Kinase-3beta (GSK-3beta) in the Hippocampal Dentate Gyrus of Adult Mouse. Serine 44-50 glycogen synthase kinase 3 beta Mus musculus 104-113 28865114-1 2017 BACKGROUND: The goal of this study was to evaluate the expression and serine 9 phosphorylation of glycogen synthase kinase (GSK-3beta) within the adult hippocampal dentate gyrus (DG) in a preclinical mouse model of fetal alcohol spectrum disorders. Serine 70-76 glycogen synthase kinase 3 beta Mus musculus 124-133 28865114-1 2017 BACKGROUND: The goal of this study was to evaluate the expression and serine 9 phosphorylation of glycogen synthase kinase (GSK-3beta) within the adult hippocampal dentate gyrus (DG) in a preclinical mouse model of fetal alcohol spectrum disorders. Alcohols 221-228 glycogen synthase kinase 3 beta Mus musculus 124-133 28865114-2 2017 GSK-3beta is a multifunctional kinase that modulates many hippocampal processes affected by gestational alcohol, including synaptic plasticity and adult neurogenesis. Alcohols 104-111 glycogen synthase kinase 3 beta Mus musculus 0-9 28865114-3 2017 GSK-3beta is a constitutively active kinase that is negatively regulated by phosphorylation at the serine 9 residue. Serine 99-105 glycogen synthase kinase 3 beta Mus musculus 0-9 28543100-9 2017 Moreover, administration of purified syndecan-1, HS, or engineered heparan compounds containing 2-O-sulfate groups rescued Sdc1-/- mice from AILI by potentiating Akt signaling and inhibiting GSK-3beta-mediated apoptosis in hepatocytes. heparan 67-74 glycogen synthase kinase 3 beta Mus musculus 191-200 28764929-13 2017 AURKA-mediated phosphorylation of glycogen synthase kinase 3 beta (GSK3beta) at serine 9 inhibited activation of the RIPK3 and MLKL necrosome. Serine 80-86 glycogen synthase kinase 3 beta Mus musculus 34-65 28764929-13 2017 AURKA-mediated phosphorylation of glycogen synthase kinase 3 beta (GSK3beta) at serine 9 inhibited activation of the RIPK3 and MLKL necrosome. Serine 80-86 glycogen synthase kinase 3 beta Mus musculus 67-75 28778590-7 2017 Ethanol stimulated endoplasmic reticulum (ER) stress and oxidative stress, and activated glycogen synthase kinase 3beta (GSK3beta) and c-Jun N-terminal kinase (JNK) pathways. Ethanol 0-7 glycogen synthase kinase 3 beta Mus musculus 89-119 28543100-9 2017 Moreover, administration of purified syndecan-1, HS, or engineered heparan compounds containing 2-O-sulfate groups rescued Sdc1-/- mice from AILI by potentiating Akt signaling and inhibiting GSK-3beta-mediated apoptosis in hepatocytes. 2-o-sulfate 96-107 glycogen synthase kinase 3 beta Mus musculus 191-200 28866105-0 2017 Dietary phlorizin enhances osteoblastogenic bone formation through enhancing beta-catenin activity via GSK-3beta inhibition in a model of senile osteoporosis. Phlorhizin 8-17 glycogen synthase kinase 3 beta Mus musculus 103-112 29259959-11 2017 Mechanistically, fexaramine blocked the RANKL-triggered p38, extracellular signal-regulated kinase, and glycogen synthase kinase 3beta phosphorylation, resulting in suppressed expression of c-Fos and NF of activated T cells (NFATc1). fexaramine 17-27 glycogen synthase kinase 3 beta Mus musculus 61-134 28866105-10 2017 Finally, phlorizin and phloretin antagonized GSK-3beta induction and beta-catenin phosphorylation in osteoblasts and aged mouse bones. Phlorhizin 9-18 glycogen synthase kinase 3 beta Mus musculus 45-54 28866105-10 2017 Finally, phlorizin and phloretin antagonized GSK-3beta induction and beta-catenin phosphorylation in osteoblasts and aged mouse bones. Phloretin 23-32 glycogen synthase kinase 3 beta Mus musculus 45-54 28866105-11 2017 Therefore, phlorizin and phloretin were potential therapeutic agents encumbering senile osteoporosis through promoting bone-forming osteoblastogenesis via modulation of GSK-3beta/beta-catenin-dependent signaling. Phlorhizin 11-20 glycogen synthase kinase 3 beta Mus musculus 169-178 28866105-11 2017 Therefore, phlorizin and phloretin were potential therapeutic agents encumbering senile osteoporosis through promoting bone-forming osteoblastogenesis via modulation of GSK-3beta/beta-catenin-dependent signaling. Phloretin 25-34 glycogen synthase kinase 3 beta Mus musculus 169-178 28899728-10 2017 Furthermore, maslinic acid normalized the phosphorylation levels of Akt-GSK-3beta and ERK-CREB in the prefrontal cortex. maslinic acid 13-26 glycogen synthase kinase 3 beta Mus musculus 72-81 28899728-11 2017 Overall, maslinic acid ameliorated the schizophrenia-like symptoms induced by MK-801, and these effects may be partly mediated through Akt-GSK-3beta and ERK-CREB activation. maslinic acid 9-22 glycogen synthase kinase 3 beta Mus musculus 139-148 28650469-13 2017 Therefore our study identifies a compartmentalized PtdIns(3,4,5)P3/AKT/GSK3beta signaling axis at cilia in SHH-dependent medulloblastoma that is regulated by INPP5E to maintain tumor cell cilia, promote SHH signaling and thereby medulloblastoma progression. phosphatidylinositol 3,4,5-triphosphate 51-66 glycogen synthase kinase 3 beta Mus musculus 71-79 28807675-5 2017 Furthermore, using the in vivo PD model of C57BL/6 mice insulted with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that intragastrical administration of SU4312 (0.2 and 1 mg/kg) greatly ameliorated Parkinsonian motor defects, and restored protein levels of MEF2D, phosphorylated-Ser473-Akt and phosphorylated-Ser9-GSK3beta. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 116-120 glycogen synthase kinase 3 beta Mus musculus 331-339 28807675-5 2017 Furthermore, using the in vivo PD model of C57BL/6 mice insulted with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we found that intragastrical administration of SU4312 (0.2 and 1 mg/kg) greatly ameliorated Parkinsonian motor defects, and restored protein levels of MEF2D, phosphorylated-Ser473-Akt and phosphorylated-Ser9-GSK3beta. 3-(4-dimethylaminobenzylidene)-1,3-dihydroindol-2-one 170-176 glycogen synthase kinase 3 beta Mus musculus 331-339 28882840-2 2017 We tested the role of phosphorylation of a GSK-3beta consensus site (S493) located in the proximal portion of the NF-H tail in NF dynamics by transfection of NB2a/d1 cells with NF-H, where S493 was mutated to aspartic acid (S493D) or to alanine (S493A) to mimic constitutive phosphorylation and non-phosphorylation. Aspartic Acid 209-222 glycogen synthase kinase 3 beta Mus musculus 43-52 28882840-2 2017 We tested the role of phosphorylation of a GSK-3beta consensus site (S493) located in the proximal portion of the NF-H tail in NF dynamics by transfection of NB2a/d1 cells with NF-H, where S493 was mutated to aspartic acid (S493D) or to alanine (S493A) to mimic constitutive phosphorylation and non-phosphorylation. Alanine 237-244 glycogen synthase kinase 3 beta Mus musculus 43-52 28720386-0 2017 Cdc42-interacting protein 4 silencing relieves pulmonary fibrosis in STZ-induced diabetic mice via the Wnt/GSK-3beta/beta-catenin pathway. Streptozocin 69-72 glycogen synthase kinase 3 beta Mus musculus 107-116 29160373-1 2017 PURPOSE: To investigate whether the neuroprotective effect of TSA on cerebral ischemia reperfusion injury is mediated by the activation of Akt/GSK-3beta signaling pathway. trichostatin A 62-65 glycogen synthase kinase 3 beta Mus musculus 143-152 29160373-5 2017 RESULTS: TSA significantly increased the expression of p-Akt, p-GSK-3beta proteins and the levels of SOD, Bcl-2, reduced the infarct volume and the levels of MDA, ROS, TNF-alpha, IL-1beta, Bax, Caspase-3, TUNEL and attenuated neurological deficit in mice with transient MCAO, LY294002 weakened such effect of TSA dramatically. trichostatin A 9-12 glycogen synthase kinase 3 beta Mus musculus 64-73 29160373-6 2017 CONCLUSIONS: TSA could significantly decrease the neurological deficit and reduce the cerebral infarct volume, oxidative stress, inflammation, as well as apoptosis during cerebral ischemia reperfusion injury, which was achieved by activation of the Akt/GSK-3beta signaling pathway. trichostatin A 13-16 glycogen synthase kinase 3 beta Mus musculus 253-262 28720386-10 2017 These results suggest that CIP4 silencing can efficiently alleviate STZ-induced PF in mice, perhaps through suppressing Wnt/GSK-3beta/beta-catenin signaling. Streptozocin 68-71 glycogen synthase kinase 3 beta Mus musculus 124-133 28754590-8 2017 Taken together, our findings demonstrated that telmisartan ameliorates hyperglycemia-exacerbated vascular inflammation, at least in part, by inducing GSK3beta-Ser9 phosphorylation, which consequently inhibits IKKbeta expression, NF-kappaB p65-Ser536 phosphorylation, and VCAM-1 expression in a PPARgamma-independent manner. Telmisartan 47-58 glycogen synthase kinase 3 beta Mus musculus 150-163 28754590-0 2017 Telmisartan mitigates hyperglycemia-induced vascular inflammation by increasing GSK3beta-Ser9 phosphorylation in endothelial cells and mouse aortas. Telmisartan 0-11 glycogen synthase kinase 3 beta Mus musculus 80-93 28881139-3 2017 Here, a bone-targeted nanoparticle (NP) delivery system for a beta-catenin agonist, 3-amino-6-(4-((4-methylpiperazin-1-yl)sulfonyl)phenyl)-N-(pyridin-3-yl)pyrazine-2-carboxamide, a glycogen synthase kinase 3 beta (GSK-3beta) inhibitor, was developed to enhance fracture healing. AZD2858 84-177 glycogen synthase kinase 3 beta Mus musculus 181-212 28754590-3 2017 Telmisartan remarkably induced GSK3beta-Ser9 phosphorylation in hyperglycemia-treated endothelial cells that accompanied a decrease in hyperglycemia-induced NF-kappaB p65-Ser536 phosphorylation, vascular cell adhesion molecule-1 (VCAM-1) expression, and THP-1 monocyte adhesion. Telmisartan 0-11 glycogen synthase kinase 3 beta Mus musculus 31-39 28754590-4 2017 Ectopic expression of GSK3beta-S9A, a constitutively active mutant of GSK3beta, significantly restored complete telmisartan-inhibited NF-kappaB p65-Ser536 phosphorylation, VCAM-1 expression, and THP-1 monocyte adhesion. Telmisartan 112-123 glycogen synthase kinase 3 beta Mus musculus 22-30 28754590-4 2017 Ectopic expression of GSK3beta-S9A, a constitutively active mutant of GSK3beta, significantly restored complete telmisartan-inhibited NF-kappaB p65-Ser536 phosphorylation, VCAM-1 expression, and THP-1 monocyte adhesion. Telmisartan 112-123 glycogen synthase kinase 3 beta Mus musculus 70-78 28754590-6 2017 Among the ARB, including losartan and fimasartan, only telmisartan increased GSK3beta-Ser9 phosphorylation, and telmisartan-induced GSK3beta-Ser9 phosphorylation remained unchanged by pretreatment with GW9662, a specific and irreversible peroxisome proliferator-activated receptor gamma (PPARgamma) antagonist. Telmisartan 55-66 glycogen synthase kinase 3 beta Mus musculus 77-90 28754590-6 2017 Among the ARB, including losartan and fimasartan, only telmisartan increased GSK3beta-Ser9 phosphorylation, and telmisartan-induced GSK3beta-Ser9 phosphorylation remained unchanged by pretreatment with GW9662, a specific and irreversible peroxisome proliferator-activated receptor gamma (PPARgamma) antagonist. Telmisartan 112-123 glycogen synthase kinase 3 beta Mus musculus 132-145 28754590-7 2017 Finally, in the aortas of HFD-fed mice, telmisartan treatment significantly attenuated HFD-induced upregulation of NF-kappaB p65-Ser536 phosphorylation, VCAM-1 expression, and IKKbeta expression and downregulation of GSK3beta-Ser9 phosphorylation. Telmisartan 40-51 glycogen synthase kinase 3 beta Mus musculus 217-230 28615299-4 2017 In molecular docking analysis, ormeloxifene showed proficient docking with beta-catenin and GSK3beta. ormeloxifene 31-43 glycogen synthase kinase 3 beta Mus musculus 92-100 28803855-4 2017 A two-week-long pretreatment regime with imipramine (7.5mg/kg/day) or thiamine (200mg/kg/day), which is known to have antidepressant properties, reduced the GSK3beta over-expression and decreased floating behaviour on Day 5. Imipramine 41-51 glycogen synthase kinase 3 beta Mus musculus 157-165 28803855-4 2017 A two-week-long pretreatment regime with imipramine (7.5mg/kg/day) or thiamine (200mg/kg/day), which is known to have antidepressant properties, reduced the GSK3beta over-expression and decreased floating behaviour on Day 5. Thiamine 70-78 glycogen synthase kinase 3 beta Mus musculus 157-165 28881139-3 2017 Here, a bone-targeted nanoparticle (NP) delivery system for a beta-catenin agonist, 3-amino-6-(4-((4-methylpiperazin-1-yl)sulfonyl)phenyl)-N-(pyridin-3-yl)pyrazine-2-carboxamide, a glycogen synthase kinase 3 beta (GSK-3beta) inhibitor, was developed to enhance fracture healing. AZD2858 84-177 glycogen synthase kinase 3 beta Mus musculus 214-223 28734998-12 2017 These results suggest ROS produced by DAB causes tau hyperphosphorylation via GSK-3beta phosphorylation and it might be related to impaired memory deficit. ros 22-25 glycogen synthase kinase 3 beta Mus musculus 78-87 30263674-5 2017 Subsequently, the betaine-stimulated melanocytes showed inhibition of PKA-CREB signaling axis but activation of extracellular-signal-regulated kinase and AKT-GSK3beta signaling pathways. Betaine 18-25 glycogen synthase kinase 3 beta Mus musculus 158-166 29163781-6 2017 SYNJ2BP increased the levels of phosphorylation for AKT and GSK3beta, which could be inhibited by the PI3K inhibitor, LY294002, and the GSK3beta inhibitor, LiCl, and regulated the accumulation of SNAI1 in the nucleus and the expression of the SNAI1 target gene, E-cadherin (EMT marker). 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 118-126 glycogen synthase kinase 3 beta Mus musculus 60-68 29163781-6 2017 SYNJ2BP increased the levels of phosphorylation for AKT and GSK3beta, which could be inhibited by the PI3K inhibitor, LY294002, and the GSK3beta inhibitor, LiCl, and regulated the accumulation of SNAI1 in the nucleus and the expression of the SNAI1 target gene, E-cadherin (EMT marker). Lithium Chloride 156-160 glycogen synthase kinase 3 beta Mus musculus 60-68 29163781-6 2017 SYNJ2BP increased the levels of phosphorylation for AKT and GSK3beta, which could be inhibited by the PI3K inhibitor, LY294002, and the GSK3beta inhibitor, LiCl, and regulated the accumulation of SNAI1 in the nucleus and the expression of the SNAI1 target gene, E-cadherin (EMT marker). Lithium Chloride 156-160 glycogen synthase kinase 3 beta Mus musculus 136-144 28734998-12 2017 These results suggest ROS produced by DAB causes tau hyperphosphorylation via GSK-3beta phosphorylation and it might be related to impaired memory deficit. 1,2-diacetylbenzene 38-41 glycogen synthase kinase 3 beta Mus musculus 78-87 28734031-15 2017 CONCLUSION: Downregulation of DEC1 contributes to MPP+ -induced neurotoxicity by suppressing PI3K/Akt/GSK3beta pathway. mangion-purified polysaccharide (Candida albicans) 50-54 glycogen synthase kinase 3 beta Mus musculus 102-110 28637674-5 2017 H2O2 downregulates GSK-3beta to reduce PRMT4 at protein level. Hydrogen Peroxide 0-4 glycogen synthase kinase 3 beta Mus musculus 19-28 28609678-6 2017 To examine whether GSK3beta activation mediates tau phosphorylation and impairs memory in diabetes, db/db and wild-type mice received intrahippocampal infusions of TDZD-8, a non-ATP competitive thiadiazolidinone inhibitor of GSK3beta. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 164-170 glycogen synthase kinase 3 beta Mus musculus 19-27 28266127-15 2017 In addition, mitochondrial membrane potential ( Psim ) was reduced in ALDH2-/- mice after I/R, which was partly reversed by the GSK-3beta inhibitor (SB216763) or PKC-delta shRNA. SB 216763 149-157 glycogen synthase kinase 3 beta Mus musculus 128-137 28639695-4 2017 We show that GSK-3beta promotes TGF-alpha-induced ADM in 3D cultured primary acinar cells, whereas deletion of GSK-3beta attenuates caerulein-induced ADM formation and PanIN progression in KrasG12D transgenic mice. Ceruletide 132-141 glycogen synthase kinase 3 beta Mus musculus 111-120 28639695-7 2017 Taken together, these results indicate that GSK-3beta participates in early pancreatitis-induced ADM and thus could be a target for the treatment of chronic pancreatitis and the prevention of PDAC progression. pdac 192-196 glycogen synthase kinase 3 beta Mus musculus 44-53 29179438-0 2017 Valproate hampers podocyte acquisition of immune phenotypes via intercepting the GSK3beta facilitated NFkB activation. Valproic Acid 0-9 glycogen synthase kinase 3 beta Mus musculus 81-89 28712706-0 2017 Discovery of novel 2-(4-aryl-2-methylpiperazin-1-yl)-pyrimidin-4-ones as glycogen synthase kinase-3beta inhibitors. 2-(4-aryl-2-methylpiperazin-1-yl)-pyrimidin-4-ones 19-69 glycogen synthase kinase 3 beta Mus musculus 73-103 28712706-2 2017 Transformation of the morpholine moiety into a piperazine moiety resulted in potent GSK-3beta inhibitors. morpholine 22-32 glycogen synthase kinase 3 beta Mus musculus 84-93 28712706-2 2017 Transformation of the morpholine moiety into a piperazine moiety resulted in potent GSK-3beta inhibitors. Piperazine 47-57 glycogen synthase kinase 3 beta Mus musculus 84-93 28712706-3 2017 SAR studies focused on the nitrogen atom of the piperazine moiety revealed that a phenyl group afforded potent inhibitory activity toward GSK-3beta. Nitrogen 27-35 glycogen synthase kinase 3 beta Mus musculus 138-147 28712706-3 2017 SAR studies focused on the nitrogen atom of the piperazine moiety revealed that a phenyl group afforded potent inhibitory activity toward GSK-3beta. Piperazine 48-58 glycogen synthase kinase 3 beta Mus musculus 138-147 28712706-4 2017 Docking studies indicated that the phenyl group on the piperazine nitrogen atom and the methyl group on the piperazine make cation-pi and CH-pi interactions with GSK-3beta respectively. Piperazine 55-65 glycogen synthase kinase 3 beta Mus musculus 162-171 28712706-4 2017 Docking studies indicated that the phenyl group on the piperazine nitrogen atom and the methyl group on the piperazine make cation-pi and CH-pi interactions with GSK-3beta respectively. Nitrogen 66-74 glycogen synthase kinase 3 beta Mus musculus 162-171 28712706-4 2017 Docking studies indicated that the phenyl group on the piperazine nitrogen atom and the methyl group on the piperazine make cation-pi and CH-pi interactions with GSK-3beta respectively. Piperazine 108-118 glycogen synthase kinase 3 beta Mus musculus 162-171 28790387-11 2017 Inhibition of GSK3beta by LiCl reduces its level, but the inhibition of ERK by PD98059 increases it. Lithium Chloride 26-30 glycogen synthase kinase 3 beta Mus musculus 14-22 27723376-0 2017 Ketamine up-regulates a cluster of intronic miRNAs within the serotonin receptor 2C gene by inhibiting glycogen synthase kinase-3. Ketamine 0-8 glycogen synthase kinase 3 beta Mus musculus 103-129 27723376-1 2017 OBJECTIVES: We examined mechanisms that contribute to the rapid antidepressant effect of ketamine in mice that is dependent on glycogen synthase kinase-3 (GSK3) inhibition. Ketamine 89-97 glycogen synthase kinase 3 beta Mus musculus 127-153 27723376-1 2017 OBJECTIVES: We examined mechanisms that contribute to the rapid antidepressant effect of ketamine in mice that is dependent on glycogen synthase kinase-3 (GSK3) inhibition. Ketamine 89-97 glycogen synthase kinase 3 beta Mus musculus 155-159 27723376-2 2017 METHODS: We measured serotonergic (5HT)-2C-receptor (5HTR2C) cluster microRNA (miRNA) levels in mouse hippocampus after administering an antidepressant dose of ketamine (10 mg/kg) in wild-type and GSK3 knockin mice, after GSK3 inhibition with L803-mts, and in learned helpless mice. Ketamine 160-168 glycogen synthase kinase 3 beta Mus musculus 197-201 27723376-2 2017 METHODS: We measured serotonergic (5HT)-2C-receptor (5HTR2C) cluster microRNA (miRNA) levels in mouse hippocampus after administering an antidepressant dose of ketamine (10 mg/kg) in wild-type and GSK3 knockin mice, after GSK3 inhibition with L803-mts, and in learned helpless mice. Ketamine 160-168 glycogen synthase kinase 3 beta Mus musculus 222-226 27723376-9 2017 CONCLUSIONS: These findings identify a new outcome of GSK3 inhibition by ketamine that may contribute to antidepressant effects. Ketamine 73-81 glycogen synthase kinase 3 beta Mus musculus 54-58 28819213-4 2017 Here, we applied the Phos-tag SDS-PAGE technique to the analysis of GSK3beta phosphoisotypes in cells and brains. Sodium Dodecyl Sulfate 30-33 glycogen synthase kinase 3 beta Mus musculus 68-76 28819213-9 2017 These results indicate that the Phos-tag SDS-PAGE method provides a simple and appropriate measurement of active GSK3beta in vivo, and the activity is regulated by the mechanism other than phosphorylation on Ser9. Sodium Dodecyl Sulfate 41-44 glycogen synthase kinase 3 beta Mus musculus 113-121 29179438-4 2017 In contrast, valproate, an anticonvulsant and mood stabilizer, offset GSK3beta overactivity in LPS-injured podocytes and mitigated NFkB activation and podocyte acquisition of immune phenotypes as well as the ensuing cytopathic changes, podocyte cytoskeleton disorganization and dysfunction. Valproic Acid 13-22 glycogen synthase kinase 3 beta Mus musculus 70-78 29179438-5 2017 The protective effect of valproate was strikingly blunted in podocytes expressing the constitutively active GSK3beta, suggesting an essential role of inhibitory phosphorylation of GSK3beta. Valproic Acid 25-34 glycogen synthase kinase 3 beta Mus musculus 108-116 29179438-5 2017 The protective effect of valproate was strikingly blunted in podocytes expressing the constitutively active GSK3beta, suggesting an essential role of inhibitory phosphorylation of GSK3beta. Valproic Acid 25-34 glycogen synthase kinase 3 beta Mus musculus 180-188 29179438-6 2017 In vivo in LPS-injured mice, valproate therapy abolished GSK3beta overactivity in glomeruli and attenuated podocyte injury and albuminuria, concomitant with a lessened NFkB activation and diminished induction of diverse podocytopathic immune molecules in podocytes and glomeruli. Valproic Acid 29-38 glycogen synthase kinase 3 beta Mus musculus 57-65 29179438-7 2017 Taken together, valproate directly protects against podocyte injury and hampers podocyte acquisition of de novo immune phenotypes via intercepting the GSK3beta facilitated NFkB activation. Valproic Acid 16-25 glycogen synthase kinase 3 beta Mus musculus 151-159 29082320-11 2017 Phosphorylation of glycogen synthase kinase-3beta (GSK3beta), a Cdk5 target, was reduced in PFC after repeated THC treatment regardless of THC history, and phosphorylation of dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) at the Cdk5-regulated threonine 75 site was unchanged. Threonine 262-271 glycogen synthase kinase 3 beta Mus musculus 19-49 29082320-11 2017 Phosphorylation of glycogen synthase kinase-3beta (GSK3beta), a Cdk5 target, was reduced in PFC after repeated THC treatment regardless of THC history, and phosphorylation of dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) at the Cdk5-regulated threonine 75 site was unchanged. Threonine 262-271 glycogen synthase kinase 3 beta Mus musculus 51-59 29082320-11 2017 Phosphorylation of glycogen synthase kinase-3beta (GSK3beta), a Cdk5 target, was reduced in PFC after repeated THC treatment regardless of THC history, and phosphorylation of dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) at the Cdk5-regulated threonine 75 site was unchanged. Dronabinol 111-114 glycogen synthase kinase 3 beta Mus musculus 19-49 28597201-0 2017 Methane alleviates carbon tetrachloride induced liver injury in mice: anti-inflammatory action demonstrated by increased PI3K/Akt/GSK-3beta-mediated IL-10 expression. Carbon Tetrachloride 19-39 glycogen synthase kinase 3 beta Mus musculus 130-139 29082320-11 2017 Phosphorylation of glycogen synthase kinase-3beta (GSK3beta), a Cdk5 target, was reduced in PFC after repeated THC treatment regardless of THC history, and phosphorylation of dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) at the Cdk5-regulated threonine 75 site was unchanged. Dronabinol 111-114 glycogen synthase kinase 3 beta Mus musculus 51-59 28597201-0 2017 Methane alleviates carbon tetrachloride induced liver injury in mice: anti-inflammatory action demonstrated by increased PI3K/Akt/GSK-3beta-mediated IL-10 expression. Methane 0-7 glycogen synthase kinase 3 beta Mus musculus 130-139 28498916-7 2017 The glycogen content in the liver was significantly reduced by constitutively active GSK3beta expression. Glycogen 4-12 glycogen synthase kinase 3 beta Mus musculus 85-93 28597201-11 2017 After pre-treatment with wortmannin (0.7 mg/kg), phosphorylation of GSK-3beta and AKT proteins were reduced compared to its solvent control group-DMSO-treated animals. Wortmannin 25-35 glycogen synthase kinase 3 beta Mus musculus 68-77 28597201-11 2017 After pre-treatment with wortmannin (0.7 mg/kg), phosphorylation of GSK-3beta and AKT proteins were reduced compared to its solvent control group-DMSO-treated animals. Dimethyl Sulfoxide 146-150 glycogen synthase kinase 3 beta Mus musculus 68-77 28285192-0 2017 Xanthohumol ameliorates lipopolysaccharide (LPS)-induced acute lung injury via induction of AMPK/GSK3beta-Nrf2 signal axis. xanthohumol 0-11 glycogen synthase kinase 3 beta Mus musculus 97-110 28478325-2 2017 Here, we established that the nicotinamide adenine dinucleotide-dependent deacetylase sirtuin 2 (SIRT2) interacts with protein kinase B, and, via the glycogen synthase kinase 3beta/beta-catenin pathway, modulates the differentiation of DA neurons. Niacinamide 30-42 glycogen synthase kinase 3 beta Mus musculus 150-180 28478325-2 2017 Here, we established that the nicotinamide adenine dinucleotide-dependent deacetylase sirtuin 2 (SIRT2) interacts with protein kinase B, and, via the glycogen synthase kinase 3beta/beta-catenin pathway, modulates the differentiation of DA neurons. Dopamine 236-238 glycogen synthase kinase 3 beta Mus musculus 150-180 28536070-2 2017 Cotinine, the main metabolite of nicotine, reduced working memory deficits, synaptic loss, and amyloid beta peptide aggregation into oligomers and plaques as well as inhibited the cerebral Tau kinase, glycogen synthase 3beta (GSK3beta) in the transgenic (Tg)6799 (5XFAD) mice. Cotinine 0-8 glycogen synthase kinase 3 beta Mus musculus 226-234 28536070-3 2017 In this study, the effect of cotinine on visual recognition memory and cortical Tau phosphorylation at the GSK3beta sites Serine (Ser)-396/Ser-404 and phospho-CREB were investigated in the Tg6799 and non-transgenic (NT) littermate mice. Serine 122-128 glycogen synthase kinase 3 beta Mus musculus 107-115 28536070-3 2017 In this study, the effect of cotinine on visual recognition memory and cortical Tau phosphorylation at the GSK3beta sites Serine (Ser)-396/Ser-404 and phospho-CREB were investigated in the Tg6799 and non-transgenic (NT) littermate mice. Serine 122-125 glycogen synthase kinase 3 beta Mus musculus 107-115 28285192-7 2017 Additionally, Xn evidently decreased t-BHP-stimulated cell apoptosis, ROS generation and GSH depletion but increased various anti-oxidative enzymes expression regulated by Keap1-Nrf2/ARE activation, which may be associated with AMPK and GSK3beta phosphorylation. tert-Butylhydroperoxide 37-42 glycogen synthase kinase 3 beta Mus musculus 237-245 28590916-9 2017 The administration of AR-A014418, a selective GSK-3beta inhibitor, diminished acute stress-induced behavioral and biochemical changes. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 22-32 glycogen synthase kinase 3 beta Mus musculus 46-55 28577307-1 2017 The 2i-media, composed of two small molecule inhibitors (PD0325901 and CHIR99021) against MEK and GSK3-kinases, respectively, is known to establish naive ground state pluripotency in mouse embryonic stem cells (mESCs). 2i-media 4-12 glycogen synthase kinase 3 beta Mus musculus 98-102 28577307-1 2017 The 2i-media, composed of two small molecule inhibitors (PD0325901 and CHIR99021) against MEK and GSK3-kinases, respectively, is known to establish naive ground state pluripotency in mouse embryonic stem cells (mESCs). mirdametinib 57-66 glycogen synthase kinase 3 beta Mus musculus 98-102 28460311-0 2017 The discovery of novel benzothiazinones as highly selective non-ATP competitive glycogen synthase kinase 3beta inhibitors for the treatment of ovarian cancer. benzothiazinones 23-39 glycogen synthase kinase 3 beta Mus musculus 80-110 28460311-3 2017 Here, we reported a series of novel substituted benzothiazinones as non-ATP competitive inhibitors of GSK 3beta. benzothiazinones 48-64 glycogen synthase kinase 3 beta Mus musculus 102-111 28460311-3 2017 Here, we reported a series of novel substituted benzothiazinones as non-ATP competitive inhibitors of GSK 3beta. Adenosine Triphosphate 72-75 glycogen synthase kinase 3 beta Mus musculus 102-111 28408345-0 2017 Icariin protects against glucocorticoid induced osteoporosis, increases the expression of the bone enhancer DEC1 and modulates the PI3K/Akt/GSK3beta/beta-catenin integrated signaling pathway. icariin 0-7 glycogen synthase kinase 3 beta Mus musculus 140-148 28933767-4 2017 Here we show that hemin enhances insulin-induced phosphorylation of insulin receptors, Akt, Gsk3beta, FoxO1 and cytoplasmic translocation of FoxO1 in cultured primary hepatocytes under insulin-resistant conditions. Hemin 18-23 glycogen synthase kinase 3 beta Mus musculus 92-100 28720858-6 2017 GSK-3beta deletion also suppressed the activity-dependent neural activation and calcium/calmodulin-dependent protein kinase II (CaMKII)/CaMKIV-cAMP response element binding protein (CREB) signaling. Cyclic AMP 143-147 glycogen synthase kinase 3 beta Mus musculus 0-9 28414056-6 2017 Furthermore, GA reduced gluconeogenesis through repressing PEPCK and G6Pase, and increased glycogen synthesis through an induction in gene expression of PDase and GSK3beta. Glycyrrhizic Acid 13-15 glycogen synthase kinase 3 beta Mus musculus 163-171 28408345-10 2017 Dexamethasone decreased but icariin increased GSK3beta phosphorylation. icariin 28-35 glycogen synthase kinase 3 beta Mus musculus 46-54 28408345-12 2017 Taken together, it is concluded that DEC1 likely supports the action of icariin against glucocorticoid induced osteoporosis with an involvement of the PI3K/Akt/GSK3beta/beta-catenin integrated signaling pathway. icariin 72-79 glycogen synthase kinase 3 beta Mus musculus 160-168 28506637-5 2017 This reduction was prevented when the mice were treated (200mg/kg/day in drinking water for 20days) with thiamine or benfotiamine, that were recently found to prevent stress-induced behavioral changes and glycogen synthase kinase-3beta (GSK-3beta) upregulation in the CNS. Thiamine 105-113 glycogen synthase kinase 3 beta Mus musculus 205-235 28591721-0 2017 Ginkgolide K attenuates neuronal injury after ischemic stroke by inhibiting mitochondrial fission and GSK-3beta-dependent increases in mitochondrial membrane permeability. ginkgolide K 0-12 glycogen synthase kinase 3 beta Mus musculus 102-111 28591721-3 2017 Co-immunoprecipitation showed that Drp1 binding to GSK-3beta was increased after an oxygen-glucose deprivation/reperfusion (OGD/R) insult in cultured neuroblastoma cells. oxygen-glucose 84-98 glycogen synthase kinase 3 beta Mus musculus 51-60 28591721-6 2017 In addition, GK exposure induced GSK-3beta phosphorylation at Ser9 and enhanced the interaction between adenine nucleotide translocator (ANT) and p-GSK-3beta. Adenine Nucleotides 104-122 glycogen synthase kinase 3 beta Mus musculus 148-157 28952290-0 2017 Study of GSK3b inhibitors SB415286 and SB216763 to improve osteoblastic differentiation on microstructured titanium. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 26-34 glycogen synthase kinase 3 beta Mus musculus 9-14 28952290-0 2017 Study of GSK3b inhibitors SB415286 and SB216763 to improve osteoblastic differentiation on microstructured titanium. Titanium 107-115 glycogen synthase kinase 3 beta Mus musculus 9-14 28952290-2 2017 The present study investigated the effects of GSK3beta-inhibitors SB216763 and SB415286 on osteoblastic differentiation on titanium surfaces with different topography and wettability. SB 216763 66-74 glycogen synthase kinase 3 beta Mus musculus 46-54 28483667-8 2017 The levels of glycogen synthase kinase 3b (GSK3b) was ~3-fold higher suggesting increased glycogen synthesis. Glycogen 14-22 glycogen synthase kinase 3 beta Mus musculus 43-48 28506637-5 2017 This reduction was prevented when the mice were treated (200mg/kg/day in drinking water for 20days) with thiamine or benfotiamine, that were recently found to prevent stress-induced behavioral changes and glycogen synthase kinase-3beta (GSK-3beta) upregulation in the CNS. Thiamine 105-113 glycogen synthase kinase 3 beta Mus musculus 237-246 28506637-5 2017 This reduction was prevented when the mice were treated (200mg/kg/day in drinking water for 20days) with thiamine or benfotiamine, that were recently found to prevent stress-induced behavioral changes and glycogen synthase kinase-3beta (GSK-3beta) upregulation in the CNS. benphothiamine 117-129 glycogen synthase kinase 3 beta Mus musculus 205-235 28506637-5 2017 This reduction was prevented when the mice were treated (200mg/kg/day in drinking water for 20days) with thiamine or benfotiamine, that were recently found to prevent stress-induced behavioral changes and glycogen synthase kinase-3beta (GSK-3beta) upregulation in the CNS. benphothiamine 117-129 glycogen synthase kinase 3 beta Mus musculus 237-246 28456716-6 2017 Moreover, our results showed that the dopamine D1 receptor (DARP D1) pathway and adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) were also activated, which indicates a relationship between GSK3beta and neurogenesis. adenosine 5"-monophosphate 81-107 glycogen synthase kinase 3 beta Mus musculus 206-214 28642577-5 2017 To explore the mechanisms underlying this phenomenon, we showed that chronic alcohol exposure enhanced beta-arrestin 2 (Arrb2) expression and Akt and glycogen synthase kinase-3 (GSK3)beta activation in the kidneys. Alcohols 77-84 glycogen synthase kinase 3 beta Mus musculus 178-182 28642577-8 2017 Taken together, our results suggest that chronic alcohol exposure may potentiate AKI via beta-arrestin 2/Akt/GSK3beta-mediated signaling in the kidney. Alcohols 49-56 glycogen synthase kinase 3 beta Mus musculus 109-117 28456716-6 2017 Moreover, our results showed that the dopamine D1 receptor (DARP D1) pathway and adenosine 5"-monophosphate (AMP)-activated protein kinase (AMPK) were also activated, which indicates a relationship between GSK3beta and neurogenesis. Adenosine Monophosphate 109-112 glycogen synthase kinase 3 beta Mus musculus 206-214 28569794-5 2017 In MES23.5 cells, P7C3 inhibited glycogen synthase kinase-3 beta (GSK3beta) activation induced by MPP+. mangion-purified polysaccharide (Candida albicans) 98-102 glycogen synthase kinase 3 beta Mus musculus 66-74 28617442-0 2017 Titanium particle-induced osteogenic inhibition and bone destruction are mediated by the GSK-3beta/beta-catenin signal pathway. Titanium 0-8 glycogen synthase kinase 3 beta Mus musculus 89-98 28617442-8 2017 In addition, our in vivo results showed that Ti particles induced bone loss via regulating GSK-3beta and beta-catenin signals. Titanium 45-47 glycogen synthase kinase 3 beta Mus musculus 91-100 29228573-8 2017 Next we have found that phosphorylation at Thr533 re-located Pnma5 strongly to spindles & cortex and was required for the phosphorylation of Akt and Gsk3beta, while Src and Erk1/2 phosphorylation was required for the phosphorylation of Pnma5, indicating that phosphorylated Pnma5 is the active form and subsequently activates Akt and Gsk3beta. Adenosine Monophosphate 89-92 glycogen synthase kinase 3 beta Mus musculus 153-161 29228573-8 2017 Next we have found that phosphorylation at Thr533 re-located Pnma5 strongly to spindles & cortex and was required for the phosphorylation of Akt and Gsk3beta, while Src and Erk1/2 phosphorylation was required for the phosphorylation of Pnma5, indicating that phosphorylated Pnma5 is the active form and subsequently activates Akt and Gsk3beta. Adenosine Monophosphate 89-92 glycogen synthase kinase 3 beta Mus musculus 338-346 28617434-5 2017 We found that LISPRO (8-week oral treatment) reduces beta-amyloid plaques and phosphorylation of tau by reducing neuroinflammation and inactivating glycogen synthase kinase 3beta in transgenic Tg2576 mice. Insulin Lispro 14-20 glycogen synthase kinase 3 beta Mus musculus 148-178 27896926-0 2017 (Z)-2-(3-Chlorobenzylidene)-3,4-dihydro-N-(2-methoxyethyl)-3-oxo-2H-benzo[b][1,4]oxazine-6-carboxamide as GSK-3beta inhibitor: Identification by virtual screening and its validation in enzyme- and cell-based assay. (z)-2-(3-chlorobenzylidene)-3,4-dihydro-n-(2-methoxyethyl)-3-oxo-2h-benzo 0-73 glycogen synthase kinase 3 beta Mus musculus 106-115 27896926-6 2017 (Z)-2-(3-chlorobenzylidene)-3,4-dihydro-N-(2-methoxyethyl)-3-oxo-2H-benzo[b][1,4]oxazine-6-carboxamide (F389-0663, 7) was identified as a potent inhibitor of GSK-3beta with an IC50 value of 1.6 mum. (z)-2-(3-chlorobenzylidene)-3,4-dihydro-n-(2-methoxyethyl)-3-oxo-2h-benzo[b 0-75 glycogen synthase kinase 3 beta Mus musculus 158-167 27896926-6 2017 (Z)-2-(3-chlorobenzylidene)-3,4-dihydro-N-(2-methoxyethyl)-3-oxo-2H-benzo[b][1,4]oxazine-6-carboxamide (F389-0663, 7) was identified as a potent inhibitor of GSK-3beta with an IC50 value of 1.6 mum. 1,4]oxazine-6-carboxamide 77-102 glycogen synthase kinase 3 beta Mus musculus 158-167 27966087-8 2017 in combination with a sub-effective dose of AR-A014418 (0.001 mug/mouse, GSK-3beta inhibitor) induced a synergic antidepressant-like effect. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 44-54 glycogen synthase kinase 3 beta Mus musculus 73-82 28111010-9 2017 Blocking GSK3beta phosphorylation inhibited SREBP1 activation and consequently blocked LPA-induced TGFbeta expression in SV40 MES13 cells. lysophosphatidic acid 87-90 glycogen synthase kinase 3 beta Mus musculus 9-17 28111010-10 2017 Phosphorylated GSK3beta and nuclear SREBP1 accumulation were increased in the kidney cortex of db/db mice and ki16425 treatment blocked these pathways. 3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl) benzylsulfanyl) propanoic acid 110-117 glycogen synthase kinase 3 beta Mus musculus 15-23 27966087-12 2017 Our findings provided new evidence that the antidepressant-like effect of inosine in the TST involves the activation of PKA, PI3K/Akt, ERK1/2, and CaMKII and the inhibition of GSK-3beta. Inosine 74-81 glycogen synthase kinase 3 beta Mus musculus 176-185 28558014-0 2017 Correction: Retinoic acid exacerbates chlorpyrifos action in ensuing adipogenic differentiation of C3H10T1/2 cells in a GSK3beta dependent pathway. Tretinoin 12-25 glycogen synthase kinase 3 beta Mus musculus 120-128 28558014-0 2017 Correction: Retinoic acid exacerbates chlorpyrifos action in ensuing adipogenic differentiation of C3H10T1/2 cells in a GSK3beta dependent pathway. Chlorpyrifos 38-50 glycogen synthase kinase 3 beta Mus musculus 120-128 28359080-3 2017 Temozolomide (TMZ) inhibits GSK-3 and activates Fas in tumour protein (TP)53 wild-type (TP53wt) glioma cells. Temozolomide 0-12 glycogen synthase kinase 3 beta Mus musculus 28-33 28518138-5 2017 Importantly, we found betulin-induced activation of Nrf2 is AMPK/AKT/GSK3beta dependent, as pharmacologically inactivating AMPK blocked the activating effect of betulin on AKT, GSK3beta and Nrf2. betulin 22-29 glycogen synthase kinase 3 beta Mus musculus 69-77 28518138-5 2017 Importantly, we found betulin-induced activation of Nrf2 is AMPK/AKT/GSK3beta dependent, as pharmacologically inactivating AMPK blocked the activating effect of betulin on AKT, GSK3beta and Nrf2. betulin 22-29 glycogen synthase kinase 3 beta Mus musculus 177-185 28518138-5 2017 Importantly, we found betulin-induced activation of Nrf2 is AMPK/AKT/GSK3beta dependent, as pharmacologically inactivating AMPK blocked the activating effect of betulin on AKT, GSK3beta and Nrf2. betulin 161-168 glycogen synthase kinase 3 beta Mus musculus 69-77 28518138-5 2017 Importantly, we found betulin-induced activation of Nrf2 is AMPK/AKT/GSK3beta dependent, as pharmacologically inactivating AMPK blocked the activating effect of betulin on AKT, GSK3beta and Nrf2. betulin 161-168 glycogen synthase kinase 3 beta Mus musculus 177-185 28539835-0 2017 The Myosin II Inhibitor, Blebbistatin, Ameliorates FeCl3-induced Arterial Thrombosis via the GSK3beta-NF-kappaB Pathway. blebbistatin 25-37 glycogen synthase kinase 3 beta Mus musculus 93-101 28539835-0 2017 The Myosin II Inhibitor, Blebbistatin, Ameliorates FeCl3-induced Arterial Thrombosis via the GSK3beta-NF-kappaB Pathway. ferric chloride 51-56 glycogen synthase kinase 3 beta Mus musculus 93-101 28539835-8 2017 The present study demonstrates that blebbistatin may impede TF expression partly via the Akt/GSK3beta-NF-kappaB signalling pathways in the endothelium in a FeCl3 model, shedding new insights into the pathogenesis of arterial thrombosis and providing new clues for the development of antithrombotic drugs. blebbistatin 36-48 glycogen synthase kinase 3 beta Mus musculus 93-101 28539835-8 2017 The present study demonstrates that blebbistatin may impede TF expression partly via the Akt/GSK3beta-NF-kappaB signalling pathways in the endothelium in a FeCl3 model, shedding new insights into the pathogenesis of arterial thrombosis and providing new clues for the development of antithrombotic drugs. ferric chloride 156-161 glycogen synthase kinase 3 beta Mus musculus 93-101 28366776-0 2017 Involvement of Akt/GSK3beta/CREB signaling pathway on chronic omethoate induced depressive-like behavior and improvement effects of combined lithium chloride and astaxanthin treatment. dimethoxon 62-71 glycogen synthase kinase 3 beta Mus musculus 19-27 28366776-0 2017 Involvement of Akt/GSK3beta/CREB signaling pathway on chronic omethoate induced depressive-like behavior and improvement effects of combined lithium chloride and astaxanthin treatment. Lithium Chloride 141-157 glycogen synthase kinase 3 beta Mus musculus 19-27 28366776-0 2017 Involvement of Akt/GSK3beta/CREB signaling pathway on chronic omethoate induced depressive-like behavior and improvement effects of combined lithium chloride and astaxanthin treatment. astaxanthine 162-173 glycogen synthase kinase 3 beta Mus musculus 19-27 28366776-5 2017 Moreover, the combined application of AST and LiCl had synergistic therapeutic effects compared to LiCl and AST treatment alone, the expression of p-GSK3beta, p-CREB, p-PI3K and p-Akt after combined LiCl-AST treatment were significantly higher than that with single drug application. Lithium Chloride 46-50 glycogen synthase kinase 3 beta Mus musculus 149-157 28359080-3 2017 Temozolomide (TMZ) inhibits GSK-3 and activates Fas in tumour protein (TP)53 wild-type (TP53wt) glioma cells. Temozolomide 14-17 glycogen synthase kinase 3 beta Mus musculus 28-33 28359080-7 2017 Temozolomide combined with Li treatment inhibited GSK-3 activation, promoted NFAT1 nuclear translocation and upregulated Fas/FasL expression. Temozolomide 0-12 glycogen synthase kinase 3 beta Mus musculus 50-55 28485728-6 2017 The A2AR control of p-tau is further supported by the observations that a KO of A2AR decreased the activity of the tau phosphorylation kinases, glycogen synthase kinase-3beta (GSK-3beta) and protein kinase A (PKA) after TBI, and by that CGS21680 (A2AR agonist) exacerbated okadaic acid-induced tau hyperphosphorylation in cultured primary hippocampal neurons. Okadaic Acid 273-285 glycogen synthase kinase 3 beta Mus musculus 144-174 28415722-2 2017 Recently, it has been reported a new culture condition comprising serum-free medium with ERK and GSK3beta inhibitors (2i) could drive ES cells into a state of pluripotency more like inner cell mass (ICM) in mouse blastocysts called ground state. Einsteinium 134-136 glycogen synthase kinase 3 beta Mus musculus 97-105 28485728-6 2017 The A2AR control of p-tau is further supported by the observations that a KO of A2AR decreased the activity of the tau phosphorylation kinases, glycogen synthase kinase-3beta (GSK-3beta) and protein kinase A (PKA) after TBI, and by that CGS21680 (A2AR agonist) exacerbated okadaic acid-induced tau hyperphosphorylation in cultured primary hippocampal neurons. Okadaic Acid 273-285 glycogen synthase kinase 3 beta Mus musculus 176-185 28485728-7 2017 Lastly, CGS21680-induced neuronal tau hyperphosphorylation and axonal injury were effectively alleviated by individual treatments with ZM241385 (A2AR antagonist), H89 (PKA antagonist) and SB216763 (GSK-3beta antagonist), or by the combined treatment with H89 and SB216763. 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine 8-16 glycogen synthase kinase 3 beta Mus musculus 198-207 28298444-4 2017 Here we show that GSK3beta is degraded by the ubiquitin-proteasome pathway in murine lung epithelial cells through lysine 183 as an acceptor site for K48 polyubiquitination. Lysine 115-121 glycogen synthase kinase 3 beta Mus musculus 18-26 28453729-10 2017 Administration of SB216763, a GSK3beta inhibitor, to knockout neonatal mice decreased myocardial fibrosis and increased angiogenesis in the infarcted area after MI. SB 216763 18-26 glycogen synthase kinase 3 beta Mus musculus 30-38 28186985-4 2017 We further found that miR-12-3p directly targeted Caveolin-1; miR-124-3p inhibited abnormal hyperphosphorylation of Tau by regulating Caveolin-1-PI3K/Akt/GSK3beta pathway in AD. mir-12-3p 22-31 glycogen synthase kinase 3 beta Mus musculus 154-162 28256059-0 2017 GSK-3beta inhibitor TDZD-8 reduces neonatal hypoxic-ischemic brain injury in mice. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 20-26 glycogen synthase kinase 3 beta Mus musculus 0-9 28256059-2 2017 TDZD-8 is a specific GSK-3beta inhibitor. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 0-6 glycogen synthase kinase 3 beta Mus musculus 21-30 28256059-10 2017 TDZD-8 reversed the reduction of phosphorylated Akt and GSK-3beta, and the activation of caspase-3 induced by hypoxia-ischemia. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 0-6 glycogen synthase kinase 3 beta Mus musculus 56-65 27639185-1 2017 Valproic acid (VPA), with inhibition activity mainly toward histone deacetylase (HDAC) and Glycogen Synthase Kinase (GSK)-3, and lithium, with inhibition activity mainly toward GSK-3, are both prescribed in clinical as mood-stabilizers and anticonvulsants for the control of bipolar disorder. Valproic Acid 0-13 glycogen synthase kinase 3 beta Mus musculus 91-123 27639185-1 2017 Valproic acid (VPA), with inhibition activity mainly toward histone deacetylase (HDAC) and Glycogen Synthase Kinase (GSK)-3, and lithium, with inhibition activity mainly toward GSK-3, are both prescribed in clinical as mood-stabilizers and anticonvulsants for the control of bipolar disorder. Valproic Acid 15-18 glycogen synthase kinase 3 beta Mus musculus 91-123 28181071-0 2017 Neurotrophic Effect of Asiatic acid, a Triterpene of Centella asiatica Against Chronic 1-Methyl 4-Phenyl 1, 2, 3, 6-Tetrahydropyridine Hydrochloride/Probenecid Mouse Model of Parkinson"s disease: The Role of MAPK, PI3K-Akt-GSK3beta and mTOR Signalling Pathways. asiatic acid 23-35 glycogen synthase kinase 3 beta Mus musculus 223-231 27825907-8 2017 As for imipramine, both compounds inhibited the upregulation of GSK-3beta induced by predator stress or repeated swimming, and reduced floating scores and the predator stress-induced behavioural changes in anxiety and exploration. Imipramine 7-17 glycogen synthase kinase 3 beta Mus musculus 64-73 28328738-0 2017 Inhibition of hippocampal long-term potentiation by high-fat diets: is it related to an effect of palmitic acid involving glycogen synthase kinase-3? Palmitic Acid 98-111 glycogen synthase kinase 3 beta Mus musculus 122-148 28328738-7 2017 Moreover, tideglusib, an ATP-noncompetitive inhibitor of GSK-3, induced hippocampal LTP and partially reversed the impairment of LTP induced by palmitic acid. tideglusib 10-20 glycogen synthase kinase 3 beta Mus musculus 57-62 28328738-7 2017 Moreover, tideglusib, an ATP-noncompetitive inhibitor of GSK-3, induced hippocampal LTP and partially reversed the impairment of LTP induced by palmitic acid. Palmitic Acid 144-157 glycogen synthase kinase 3 beta Mus musculus 57-62 27825907-0 2017 Thiamine and benfotiamine improve cognition and ameliorate GSK-3beta-associated stress-induced behaviours in mice. Thiamine 0-8 glycogen synthase kinase 3 beta Mus musculus 59-68 27825907-0 2017 Thiamine and benfotiamine improve cognition and ameliorate GSK-3beta-associated stress-induced behaviours in mice. benphothiamine 13-25 glycogen synthase kinase 3 beta Mus musculus 59-68 27825907-2 2017 Indirect evidence suggests that thiamine may contribute to these pathologies by controlling the activities of glycogen synthase kinase (GSK)-3beta. Thiamine 32-40 glycogen synthase kinase 3 beta Mus musculus 110-146 27825907-4 2017 However, hitherto direct evidence for the effects of thiamine on GSK-3beta function has not been reported. Thiamine 53-61 glycogen synthase kinase 3 beta Mus musculus 65-74 27825907-10 2017 Our data indicate that thiamine and benfotiamine have antidepressant/anti-stress effects in naive animals that are associated with reduced GSK-3beta expression and conditioning of adverse memories. Thiamine 23-31 glycogen synthase kinase 3 beta Mus musculus 139-148 27825907-10 2017 Our data indicate that thiamine and benfotiamine have antidepressant/anti-stress effects in naive animals that are associated with reduced GSK-3beta expression and conditioning of adverse memories. benphothiamine 36-48 glycogen synthase kinase 3 beta Mus musculus 139-148 27825907-11 2017 Thus thiamine and benfotiamine may modulate GSK-3beta functions in a manner that is dependent on whether the contextual conditioning is adaptive or maladaptive. Thiamine 5-13 glycogen synthase kinase 3 beta Mus musculus 44-53 27825907-11 2017 Thus thiamine and benfotiamine may modulate GSK-3beta functions in a manner that is dependent on whether the contextual conditioning is adaptive or maladaptive. benphothiamine 18-30 glycogen synthase kinase 3 beta Mus musculus 44-53 28005221-0 2017 Tetramethylpyrazine Analogue CXC195 Protects Against Dopaminergic Neuronal Apoptosis via Activation of PI3K/Akt/GSK3beta Signaling Pathway in 6-OHDA-Induced Parkinson"s Disease Mice. tetramethylpyrazine 0-19 glycogen synthase kinase 3 beta Mus musculus 112-120 28330809-7 2017 Piperine blocked activation of protein kinase B (AKT) and, downstream, glycogen synthase kinase 3beta (GSK3beta). piperine 0-8 glycogen synthase kinase 3 beta Mus musculus 71-101 28330809-7 2017 Piperine blocked activation of protein kinase B (AKT) and, downstream, glycogen synthase kinase 3beta (GSK3beta). piperine 0-8 glycogen synthase kinase 3 beta Mus musculus 103-111 28330809-8 2017 The overexpression of constitutively active AKT or the knockdown of GSK3beta completely abolished the piperine-mediated protection of cardiac fibroblasts. piperine 102-110 glycogen synthase kinase 3 beta Mus musculus 68-76 28330809-11 2017 In conclusion, piperine attenuated cardiac fibrosis via the activation of PPAR-gamma and the resultant inhibition of AKT/GSK3beta. piperine 15-23 glycogen synthase kinase 3 beta Mus musculus 121-129 28244152-6 2017 Immunofluorescence staining in the SCN of mice showed that late-night light exposure significantly increased GSK3 activity (decreased pGSK3beta levels) 30-60 min after the light-pulse. pgsk3beta 134-143 glycogen synthase kinase 3 beta Mus musculus 109-113 28111255-1 2017 Glycogen synthase kinase 3beta (GSK3beta) was originally identified as a regulator for glycogen metabolism and is now an important therapeutic target for a variety of brain disorders including neurodegenerative diseases due to it"s pivotal role in cellular metabolism, proliferation and differentiation. Glycogen 87-95 glycogen synthase kinase 3 beta Mus musculus 0-30 28111255-1 2017 Glycogen synthase kinase 3beta (GSK3beta) was originally identified as a regulator for glycogen metabolism and is now an important therapeutic target for a variety of brain disorders including neurodegenerative diseases due to it"s pivotal role in cellular metabolism, proliferation and differentiation. Glycogen 87-95 glycogen synthase kinase 3 beta Mus musculus 32-40 28111255-3 2017 In the present investigation, we explored the effects of a GSK3beta specific inhibitor, 6-Bromoindirubin-3"-oxime (BIO), on regenerative activities of neuroblasts in the subventricular zone (SVZ) and functional recovery after focal cerebral ischemia. 6-bromoindirubin-3'-oxime 88-113 glycogen synthase kinase 3 beta Mus musculus 59-67 28005221-7 2017 Meanwhile, 6-OHDA also decreased the amount of phosphorylated Akt while increased GSK-3beta activity (the amount of phosphorylated GSK-3beta at Ser9 was decreased) which was prevented by CXC195. Oxidopamine 11-17 glycogen synthase kinase 3 beta Mus musculus 82-91 28005221-7 2017 Meanwhile, 6-OHDA also decreased the amount of phosphorylated Akt while increased GSK-3beta activity (the amount of phosphorylated GSK-3beta at Ser9 was decreased) which was prevented by CXC195. Oxidopamine 11-17 glycogen synthase kinase 3 beta Mus musculus 131-140 28005221-9 2017 Our study firstly demonstrated that CXC195 protected against DA neurodegeneration in 6-OHDA-induced PD model by its anti-apoptotic properties and PI3K/Akt/GSK3beta signaling pathway was involved in it. Oxidopamine 85-91 glycogen synthase kinase 3 beta Mus musculus 155-163 28005221-0 2017 Tetramethylpyrazine Analogue CXC195 Protects Against Dopaminergic Neuronal Apoptosis via Activation of PI3K/Akt/GSK3beta Signaling Pathway in 6-OHDA-Induced Parkinson"s Disease Mice. CXC 195 29-35 glycogen synthase kinase 3 beta Mus musculus 112-120 28005221-0 2017 Tetramethylpyrazine Analogue CXC195 Protects Against Dopaminergic Neuronal Apoptosis via Activation of PI3K/Akt/GSK3beta Signaling Pathway in 6-OHDA-Induced Parkinson"s Disease Mice. Oxidopamine 142-148 glycogen synthase kinase 3 beta Mus musculus 112-120 28482409-3 2017 SB216763 was used to inhibit the activity of GSK3beta and PPARalpha siRNA was used to inhibit the expression of PPARalpha. SB 216763 0-8 glycogen synthase kinase 3 beta Mus musculus 45-53 28107044-8 2017 Results show downregulation in phosphorylation of AKT and PDK1 by quercetin, which was consistent with decreased phosphorylation of downstream survival factors such as BAD, GSK-3beta, mTOR, and IkBalpha. Quercetin 66-75 glycogen synthase kinase 3 beta Mus musculus 173-182 28553339-0 2017 Tibolone modulates neuronal plasticity through regulating Tau, GSK3beta/Akt/PI3K pathway and CDK5 p35/p25 complexes in the hippocampus of aged male mice. tibolone 0-8 glycogen synthase kinase 3 beta Mus musculus 63-71 28553339-2 2017 Also, an age-related decrease in sex steroid hormones may have a negative impact on the formation of neurofibrillary tangles (NFTs); these hormones can regulate Tau phosphorylation and the principal kinase GSK3beta involved in this process. Steroids 37-44 glycogen synthase kinase 3 beta Mus musculus 206-214 28195036-2 2017 In the present investigation, we tested 6-bromoindirubin-3"-oxime (BIO) as a selective glycogen synthase kinase-3beta (GSK-3beta) inhibitor in a mouse model of intracerebral hemorrhage (ICH). 6-bromoindirubin-3'-oxime 40-65 glycogen synthase kinase 3 beta Mus musculus 87-117 28195036-2 2017 In the present investigation, we tested 6-bromoindirubin-3"-oxime (BIO) as a selective glycogen synthase kinase-3beta (GSK-3beta) inhibitor in a mouse model of intracerebral hemorrhage (ICH). 6-bromoindirubin-3'-oxime 40-65 glycogen synthase kinase 3 beta Mus musculus 119-128 27174997-9 2017 Thus, Tregs ameliorated ICH-induced inflammatory injury by modulating microglia/macrophage polarization toward the M2 phenotype through the IL-10/GSK3beta/PTEN axis. tregs 6-11 glycogen synthase kinase 3 beta Mus musculus 146-154 28256546-3 2017 The dual inhibition is synergistic, as increasing intracellular levels of cAMP by cyclic nucleotide PDE inhibition both suppresses the immune response and increases remyelination, and in addition, inhibition of GSK3 limits experimental autoimmune encephalomyelitis in mice. Cyclic AMP 74-78 glycogen synthase kinase 3 beta Mus musculus 211-215 28256546-3 2017 The dual inhibition is synergistic, as increasing intracellular levels of cAMP by cyclic nucleotide PDE inhibition both suppresses the immune response and increases remyelination, and in addition, inhibition of GSK3 limits experimental autoimmune encephalomyelitis in mice. Nucleotides, Cyclic 82-99 glycogen synthase kinase 3 beta Mus musculus 211-215 27126323-0 2017 Lithium-induced neuroprotection in stroke involves increased miR-124 expression, reduced RE1-silencing transcription factor abundance and decreased protein deubiquitination by GSK3beta inhibition-independent pathways. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 176-184 27126323-1 2017 Lithium promotes acute poststroke neuronal survival, which includes mechanisms that are not limited to GSK3beta inhibition. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 103-111 28291828-0 2017 Retinoic acid exacerbates chlorpyrifos action in ensuing adipogenic differentiation of C3H10T1/2 cells in a GSK3beta dependent pathway. Tretinoin 0-13 glycogen synthase kinase 3 beta Mus musculus 108-116 28291828-0 2017 Retinoic acid exacerbates chlorpyrifos action in ensuing adipogenic differentiation of C3H10T1/2 cells in a GSK3beta dependent pathway. Chlorpyrifos 26-38 glycogen synthase kinase 3 beta Mus musculus 108-116 28291828-9 2017 Mechanistically, GSK3beta pathway was found to be a major player, whereby inhibiting it with lithium chloride (LiCl) resulted in complete blockage of lipid accumulation, accompanied by complete down regulation of PLIN1 and ADN gene expression. Lithium Chloride 93-109 glycogen synthase kinase 3 beta Mus musculus 17-25 28291828-9 2017 Mechanistically, GSK3beta pathway was found to be a major player, whereby inhibiting it with lithium chloride (LiCl) resulted in complete blockage of lipid accumulation, accompanied by complete down regulation of PLIN1 and ADN gene expression. Lithium Chloride 111-115 glycogen synthase kinase 3 beta Mus musculus 17-25 28253260-5 2017 Comparatively, lithium, an inhibitor of the Nrf2 suppressor GSK-3, prevented Abeta42 toxicity by mechanisms independent of Nrf2. Lithium 15-22 glycogen synthase kinase 3 beta Mus musculus 60-65 28068511-0 2017 Inhibition of Glycogen Synthase Kinase 3 Accelerated Liver Regeneration after Acetaminophen-Induced Hepatotoxicity in Mice. Acetaminophen 78-91 glycogen synthase kinase 3 beta Mus musculus 14-40 28068511-9 2017 Taken together, our study has revealed a novel role of GSK3 in liver regeneration after APAP overdose and identified GSK3 as a potential therapeutic target to improve liver regeneration after APAP-induced ALF. Acetaminophen 88-92 glycogen synthase kinase 3 beta Mus musculus 55-59 28137967-8 2017 In addition to attenuating the hyperphosphorylation of tau by modulating the activity of Akt/glycogen synthase kinase-3beta and protein phosphatase 2A, Se-Met-induced reduction of tau was also mediated by an autophagy-based pathway. Selenomethionine 152-158 glycogen synthase kinase 3 beta Mus musculus 93-123 27412116-13 2017 The up-regulation of TRPC1 gene expression by ammonium was suppressed by GSK-3beta inhibitors, lithium salt and AR-A014418, suggesting that increase of GSK-3beta activity may play a role in ammonium-related pathologies. Ammonium Compounds 190-198 glycogen synthase kinase 3 beta Mus musculus 152-161 27648737-0 2017 Down-regulation of beta-catenin and the associated migration ability by Taiwanin C in arecoline and 4-NQO-induced oral cancer cells via GSK-3beta activation. Arecoline 86-95 glycogen synthase kinase 3 beta Mus musculus 136-145 27648737-0 2017 Down-regulation of beta-catenin and the associated migration ability by Taiwanin C in arecoline and 4-NQO-induced oral cancer cells via GSK-3beta activation. 4-Nitroquinoline-1-oxide 100-105 glycogen synthase kinase 3 beta Mus musculus 136-145 27412116-0 2017 Ammonium Increases TRPC1 Expression Via Cav-1/PTEN/AKT/GSK3beta Pathway. Ammonium Compounds 0-8 glycogen synthase kinase 3 beta Mus musculus 55-63 28337257-0 2017 Subcutaneous liraglutide ameliorates methylglyoxal-induced Alzheimer-like tau pathology and cognitive impairment by modulating tau hyperphosphorylation and glycogen synthase kinase-3beta. Pyruvaldehyde 37-50 glycogen synthase kinase 3 beta Mus musculus 156-186 27412116-13 2017 The up-regulation of TRPC1 gene expression by ammonium was suppressed by GSK-3beta inhibitors, lithium salt and AR-A014418, suggesting that increase of GSK-3beta activity may play a role in ammonium-related pathologies. Ammonium Compounds 46-54 glycogen synthase kinase 3 beta Mus musculus 73-82 27412116-13 2017 The up-regulation of TRPC1 gene expression by ammonium was suppressed by GSK-3beta inhibitors, lithium salt and AR-A014418, suggesting that increase of GSK-3beta activity may play a role in ammonium-related pathologies. Ammonium Compounds 46-54 glycogen synthase kinase 3 beta Mus musculus 152-161 27412116-13 2017 The up-regulation of TRPC1 gene expression by ammonium was suppressed by GSK-3beta inhibitors, lithium salt and AR-A014418, suggesting that increase of GSK-3beta activity may play a role in ammonium-related pathologies. lithium salt 95-107 glycogen synthase kinase 3 beta Mus musculus 152-161 27412116-13 2017 The up-regulation of TRPC1 gene expression by ammonium was suppressed by GSK-3beta inhibitors, lithium salt and AR-A014418, suggesting that increase of GSK-3beta activity may play a role in ammonium-related pathologies. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 112-122 glycogen synthase kinase 3 beta Mus musculus 152-161 28102395-7 2017 Importantly, sesamol treatment up-regulated brain insulin signaling by stimulating IRS-1/AKT as well as ERK/CREB/BDNF pathways; meanwhile it down-regulated neuronal death signaling GSK3beta and JNK. sesamol 13-20 glycogen synthase kinase 3 beta Mus musculus 181-189 28207769-14 2017 CONCLUSIONS: The DSS-induced intestinal fibrosis was improved by the new PPAR-gamma modulator GED-0507-34 Levo through the modulation of EMT mediators and pro-fibrotic molecules and through GSK-3beta induction. levo 106-110 glycogen synthase kinase 3 beta Mus musculus 190-199 28205608-6 2017 Meanwhile, treatment with HC-067047 attenuated the decrease in the activation of reperfusion injury salvage kinase (RISK) pathway (phosphorylation of Akt, ERK1/2, and GSK-3beta), while the activation of survival activating factor enhancement (SAFE) pathway (phosphorylation of STAT3) remained unchanged. HC-067047 26-35 glycogen synthase kinase 3 beta Mus musculus 167-176 27599525-11 2017 Detailed analysis of the mechanism revealed AKT and mTOR were activated, while ERK, FoxO3a, and GSK3beta were inhibited in the selumetinib -treated cachexia group. AZD 6244 127-138 glycogen synthase kinase 3 beta Mus musculus 96-104 28161398-0 2017 Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3beta Signaling Pathway. 25-hydroxycholesterol 53-74 glycogen synthase kinase 3 beta Mus musculus 79-87 27628899-0 2017 2,5-Dimethylcelecoxib prevents pressure-induced left ventricular remodeling through GSK-3 activation. 2,5-dimethylcelecoxib 0-21 glycogen synthase kinase 3 beta Mus musculus 84-89 27628899-2 2017 We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating GSK-3, resulting in lifespan prolongation in a mouse model of genetic dilated cardiomyopathy. 2,5-dimethylcelecoxib 28-49 glycogen synthase kinase 3 beta Mus musculus 168-173 27628899-2 2017 We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating GSK-3, resulting in lifespan prolongation in a mouse model of genetic dilated cardiomyopathy. dm-celecoxib 51-63 glycogen synthase kinase 3 beta Mus musculus 168-173 27628899-2 2017 We previously reported that 2,5-dimethylcelecoxib (DM-celecoxib), a celecoxib derivative unable to inhibit cyclooxygenase-2, prevented cardiac remodeling by activating GSK-3, resulting in lifespan prolongation in a mouse model of genetic dilated cardiomyopathy. Celecoxib 40-49 glycogen synthase kinase 3 beta Mus musculus 168-173 28146408-0 2017 The Antimalarial Effect of Curcumin Is Mediated by the Inhibition of Glycogen Synthase Kinase-3beta. Curcumin 27-35 glycogen synthase kinase 3 beta Mus musculus 69-99 28146408-2 2017 In silico docking simulation studies suggest that curcumin possesses glycogen synthase kinase-3beta (GSK3beta)-inhibitory properties. Curcumin 50-58 glycogen synthase kinase 3 beta Mus musculus 69-99 28146408-2 2017 In silico docking simulation studies suggest that curcumin possesses glycogen synthase kinase-3beta (GSK3beta)-inhibitory properties. Curcumin 50-58 glycogen synthase kinase 3 beta Mus musculus 101-109 28146408-4 2017 In this study, we aimed to evaluate whether the antimalarial effects of curcumin involve phosphorylation of host GSK3beta. Curcumin 72-80 glycogen synthase kinase 3 beta Mus musculus 113-121 28146408-7 2017 Western analysis revealed a 5.5-fold (therapeutic group) and 1.8-fold (prophylactic group) increase in phosphorylation of Ser 9 GSK3beta and 1.6-fold (therapeutic group) and 1.7-fold (prophylactic group) increase in Ser 473 Akt in liver of curcumin-treated infected animals. Serine 122-125 glycogen synthase kinase 3 beta Mus musculus 128-136 28146408-10 2017 Findings from the present study demonstrate for the first time that the antimalarial action of curcumin involved inhibition of GSK3beta. Curcumin 95-103 glycogen synthase kinase 3 beta Mus musculus 127-135 28196122-9 2017 Utilizing ventilator-induced lung injury or intra-tracheal installation of hydrochloric acid to induce ARDS in mice, we observed increased mRNA and protein expression of ELAVL-1/HuR and GSK3beta. Hydrochloric Acid 75-92 glycogen synthase kinase 3 beta Mus musculus 186-194 27775852-2 2017 We tested if acute cotinine treatment is capable of improving cognition in the mouse model of Fragile X syndrome, Fmr1-/- knockout mice, and if this is related to inhibition by cotinine treatment of glycogen synthase kinase-3beta (GSK3beta), which is abnormally active in Fmr1-/- mice. Cotinine 177-185 glycogen synthase kinase 3 beta Mus musculus 199-229 27775852-3 2017 Acute cotinine treatment increased the inhibitory serine-phosphorylation of GSK3beta and the activating phosphorylation of AKT, which can mediate serine-phosphorylation of GSK3beta, in both wild-type and Fmr1-/- mouse hippocampus. Cotinine 6-14 glycogen synthase kinase 3 beta Mus musculus 76-84 27775852-3 2017 Acute cotinine treatment increased the inhibitory serine-phosphorylation of GSK3beta and the activating phosphorylation of AKT, which can mediate serine-phosphorylation of GSK3beta, in both wild-type and Fmr1-/- mouse hippocampus. Cotinine 6-14 glycogen synthase kinase 3 beta Mus musculus 172-180 27775852-3 2017 Acute cotinine treatment increased the inhibitory serine-phosphorylation of GSK3beta and the activating phosphorylation of AKT, which can mediate serine-phosphorylation of GSK3beta, in both wild-type and Fmr1-/- mouse hippocampus. Serine 50-56 glycogen synthase kinase 3 beta Mus musculus 76-84 27775852-3 2017 Acute cotinine treatment increased the inhibitory serine-phosphorylation of GSK3beta and the activating phosphorylation of AKT, which can mediate serine-phosphorylation of GSK3beta, in both wild-type and Fmr1-/- mouse hippocampus. Serine 50-56 glycogen synthase kinase 3 beta Mus musculus 172-180 27775852-3 2017 Acute cotinine treatment increased the inhibitory serine-phosphorylation of GSK3beta and the activating phosphorylation of AKT, which can mediate serine-phosphorylation of GSK3beta, in both wild-type and Fmr1-/- mouse hippocampus. Serine 146-152 glycogen synthase kinase 3 beta Mus musculus 76-84 27775852-3 2017 Acute cotinine treatment increased the inhibitory serine-phosphorylation of GSK3beta and the activating phosphorylation of AKT, which can mediate serine-phosphorylation of GSK3beta, in both wild-type and Fmr1-/- mouse hippocampus. Serine 146-152 glycogen synthase kinase 3 beta Mus musculus 172-180 27775852-5 2017 However, cotinine failed to restore impaired cognition in GSK3beta knockin mice, in which a serine9-to-alanine9 mutation blocks the inhibitory serine phosphorylation of GSK3beta, causing GSK3beta to be hyperactive. serine9 92-99 glycogen synthase kinase 3 beta Mus musculus 169-177 27775852-5 2017 However, cotinine failed to restore impaired cognition in GSK3beta knockin mice, in which a serine9-to-alanine9 mutation blocks the inhibitory serine phosphorylation of GSK3beta, causing GSK3beta to be hyperactive. serine9 92-99 glycogen synthase kinase 3 beta Mus musculus 169-177 27775852-5 2017 However, cotinine failed to restore impaired cognition in GSK3beta knockin mice, in which a serine9-to-alanine9 mutation blocks the inhibitory serine phosphorylation of GSK3beta, causing GSK3beta to be hyperactive. alanine9 103-111 glycogen synthase kinase 3 beta Mus musculus 169-177 27775852-5 2017 However, cotinine failed to restore impaired cognition in GSK3beta knockin mice, in which a serine9-to-alanine9 mutation blocks the inhibitory serine phosphorylation of GSK3beta, causing GSK3beta to be hyperactive. alanine9 103-111 glycogen synthase kinase 3 beta Mus musculus 169-177 27775852-5 2017 However, cotinine failed to restore impaired cognition in GSK3beta knockin mice, in which a serine9-to-alanine9 mutation blocks the inhibitory serine phosphorylation of GSK3beta, causing GSK3beta to be hyperactive. Serine 92-98 glycogen synthase kinase 3 beta Mus musculus 169-177 27775852-5 2017 However, cotinine failed to restore impaired cognition in GSK3beta knockin mice, in which a serine9-to-alanine9 mutation blocks the inhibitory serine phosphorylation of GSK3beta, causing GSK3beta to be hyperactive. Serine 92-98 glycogen synthase kinase 3 beta Mus musculus 169-177 27775852-6 2017 These results indicate that acute cotinine treatment effectively repairs impairments of these four cognitive tasks in Fmr1-/- mice, and suggest that this cognition-enhancing effect of cotinine is linked to its induction of inhibitory serine-phosphorylation of GSK3. Cotinine 34-42 glycogen synthase kinase 3 beta Mus musculus 260-264 27775852-6 2017 These results indicate that acute cotinine treatment effectively repairs impairments of these four cognitive tasks in Fmr1-/- mice, and suggest that this cognition-enhancing effect of cotinine is linked to its induction of inhibitory serine-phosphorylation of GSK3. Cotinine 184-192 glycogen synthase kinase 3 beta Mus musculus 260-264 27775852-6 2017 These results indicate that acute cotinine treatment effectively repairs impairments of these four cognitive tasks in Fmr1-/- mice, and suggest that this cognition-enhancing effect of cotinine is linked to its induction of inhibitory serine-phosphorylation of GSK3. Serine 234-240 glycogen synthase kinase 3 beta Mus musculus 260-264 27775852-7 2017 Taken together, these results show that nicotinic receptor agonists can act as cognitive enhancers in a mouse model of Fragile X syndrome and highlight the potential role of inhibiting GSK3beta in mediating the beneficial effects of cotinine on memory. Cotinine 233-241 glycogen synthase kinase 3 beta Mus musculus 185-193 27729563-7 2017 In addition, swertisin normalized the MK-801-induced elevation of phosphorylation levels of Akt and GSK-3beta signaling molecules in the prefrontal cortex. Dizocilpine Maleate 38-44 glycogen synthase kinase 3 beta Mus musculus 100-109 27488110-6 2017 Moreover, Abeta1-42 causes increased phosphorylation of p38MAPK and decreased phosphorylation of Ser9-glycogen synthase kinase 3beta (GSK3beta) and cAMP-response element binding protein (CREB) in the hippocampus of mice, which could be significantly reversed by SB203580. SB 203580 262-270 glycogen synthase kinase 3 beta Mus musculus 134-142 27939977-2 2017 Our previous study demonstrated that melatonin rescues hippocampus-dependent spatial memory deficits by arresting hippocampal pathological progression in an animal model of AD, which occurs via the inhibition of GSK3beta and an increase in c-Fos. Melatonin 37-46 glycogen synthase kinase 3 beta Mus musculus 212-220 28078613-7 2017 Those effects were blocked by the specific PI3K inhibitor, LY294002, indicating the involvement of Akt/GSK-3beta pathway in the neuroprotective effect of L-F001. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 59-67 glycogen synthase kinase 3 beta Mus musculus 103-112 28078613-9 2017 Together, our findings suggest that L-F001 prevents 6-OHDA-induced cell death through activating Akt/GSK-3beta and Nrf2/HO-1 signaling pathway and attenuates MPTP-induced dopaminergic neuron toxicity in mice. Oxidopamine 52-58 glycogen synthase kinase 3 beta Mus musculus 101-110 28128361-0 2017 Protective effect of butin against ischemia/reperfusion-induced myocardial injury in diabetic mice: involvement of the AMPK/GSK-3beta/Nrf2 signaling pathway. butin 21-26 glycogen synthase kinase 3 beta Mus musculus 124-133 28128361-13 2017 Our findings indicated that BUT protected against I/R-induced ROS-mediated apoptosis by upregulating the AMPK/Akt/GSK-3beta pathway, which further activated Nrf2-regulated antioxidant enzymes in diabetic cardiomyocytes exposed to I/R. Reactive Oxygen Species 62-65 glycogen synthase kinase 3 beta Mus musculus 114-123 28093944-1 2017 AIM: To evaluate the fracture healing capabilities of a GSK3beta inhibitor, 6-bromoindirubin-3"-oxime, coupled with an aspartic acid octapeptide in a micellar delivery system. 6-bromoindirubin-3'-oxime 76-101 glycogen synthase kinase 3 beta Mus musculus 56-64 28093944-6 2017 CONCLUSION: Accelerated fracture healing in mice was achieved by targeting the GSK3beta inhibitor, 6-bromoindirubin-3"-oxime, to the fracture site. 6-bromoindirubin-3'-oxime 99-124 glycogen synthase kinase 3 beta Mus musculus 79-87 28098243-6 2017 (intraperitoneal) administration of VA (30 mg/kg, for 3 weeks) after Abeta1-42-injection enhanced glutathione levels (GSH) and abrogated ROS generation accompanied by an induction of the endogenous nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) via the activation of Akt and glycogen synthase kinase 3beta (GSK-3beta) in the brain mice. Vanillic Acid 36-38 glycogen synthase kinase 3 beta Mus musculus 307-337 27542584-0 2017 Up-regulation of insulin-like growth factor 2 by ketamine requires glycogen synthase kinase-3 inhibition. Ketamine 49-57 glycogen synthase kinase 3 beta Mus musculus 67-93 28003464-6 2017 We also found that Nat1-null mES cells possess a transcriptional profile similar, although not identical, to the ground state, which is established in wild-type mES cells when treated with inhibitors of the ERK and glycogen synthase kinase 3 (GSK3) signaling pathways. 2-(N-morpholino)ethanesulfonic acid 29-32 glycogen synthase kinase 3 beta Mus musculus 215-241 28003464-6 2017 We also found that Nat1-null mES cells possess a transcriptional profile similar, although not identical, to the ground state, which is established in wild-type mES cells when treated with inhibitors of the ERK and glycogen synthase kinase 3 (GSK3) signaling pathways. 2-(N-morpholino)ethanesulfonic acid 29-32 glycogen synthase kinase 3 beta Mus musculus 243-247 27894919-0 2017 Resveratrol attenuates MPP+-induced mitochondrial dysfunction and cell apoptosis via AKT/GSK-3beta pathway in SN4741 cells. Resveratrol 0-11 glycogen synthase kinase 3 beta Mus musculus 89-98 27894919-0 2017 Resveratrol attenuates MPP+-induced mitochondrial dysfunction and cell apoptosis via AKT/GSK-3beta pathway in SN4741 cells. mangion-purified polysaccharide (Candida albicans) 23-27 glycogen synthase kinase 3 beta Mus musculus 89-98 27894919-7 2017 Taken together, these results suggest that Res attenuates MPP+- induced mitochondrial dysfunction and cell apoptosis, and these protections may be achieved through AKT/GSK-3beta pathway. mangion-purified polysaccharide (Candida albicans) 58-62 glycogen synthase kinase 3 beta Mus musculus 168-177 27614023-8 2017 Overexpression of SHP-1 reversed RSG-induced GSK3beta activation, thus rescuing the inhibitory effect of RSG on osteoblast differentiation and mineralization. Rosiglitazone 33-36 glycogen synthase kinase 3 beta Mus musculus 45-53 27614023-10 2017 Downregulation of SHP-1 may contribute to RSG-induced inhibition of mouse calvaria osteoblast differentiation by activating GSK3beta-dependent pathway. Rosiglitazone 42-45 glycogen synthase kinase 3 beta Mus musculus 124-132 27542584-1 2017 An antidepressant dose of the rapidly-acting ketamine inhibits glycogen synthase kinase-3 (GSK3) in mouse hippocampus, and this inhibition is required for the antidepressant effect of ketamine in learned helplessness depression-like behavior. Ketamine 45-53 glycogen synthase kinase 3 beta Mus musculus 63-89 27542584-1 2017 An antidepressant dose of the rapidly-acting ketamine inhibits glycogen synthase kinase-3 (GSK3) in mouse hippocampus, and this inhibition is required for the antidepressant effect of ketamine in learned helplessness depression-like behavior. Ketamine 45-53 glycogen synthase kinase 3 beta Mus musculus 91-95 27542584-1 2017 An antidepressant dose of the rapidly-acting ketamine inhibits glycogen synthase kinase-3 (GSK3) in mouse hippocampus, and this inhibition is required for the antidepressant effect of ketamine in learned helplessness depression-like behavior. Ketamine 184-192 glycogen synthase kinase 3 beta Mus musculus 63-89 27542584-1 2017 An antidepressant dose of the rapidly-acting ketamine inhibits glycogen synthase kinase-3 (GSK3) in mouse hippocampus, and this inhibition is required for the antidepressant effect of ketamine in learned helplessness depression-like behavior. Ketamine 184-192 glycogen synthase kinase 3 beta Mus musculus 91-95 27542584-2 2017 Here we report that treatment with an antidepressant dose of ketamine (10mg/kg) increased expression of insulin-like growth factor 2 (IGF2) in mouse hippocampus, an effect that required ketamine-induced inhibition of GSK3. Ketamine 61-69 glycogen synthase kinase 3 beta Mus musculus 217-221 27542584-2 2017 Here we report that treatment with an antidepressant dose of ketamine (10mg/kg) increased expression of insulin-like growth factor 2 (IGF2) in mouse hippocampus, an effect that required ketamine-induced inhibition of GSK3. Ketamine 186-194 glycogen synthase kinase 3 beta Mus musculus 217-221 27542584-3 2017 Ketamine also inhibited hippocampal GSK3 and increased expression of hippocampal IGF2 in mice when administered after the induction of learned helplessness. Ketamine 0-8 glycogen synthase kinase 3 beta Mus musculus 36-40 28056291-7 2017 And 16 weeks treatment with testosterone decreased phosphorylation of GSK3beta and InsR in C57BL/6 adipose tissues (P<0.05), in-creased phosphorylation of NF-kappaBp65.Testosteroneenhanced the expression of CD206, and decreased the expression of CD16/32. Testosterone 28-40 glycogen synthase kinase 3 beta Mus musculus 70-78 27840407-6 2017 Further analyses showed that ARDD (10 mumol/L) significantly increased the phosphorylation of ERK1/2 and the downstream GSK-3beta, subsequently induced beta-catenin expression and up-regulated the gene expression of the Wnt ligands Fzd1 and Wnt3a in neuronal cells. ardd 29-33 glycogen synthase kinase 3 beta Mus musculus 120-129 27668540-2 2016 In this study, we examined the possible protective mechanism and associated signaling pathways of small-molecule glycogen synthase kinase-3 (GSK-3) inhibitor, SB216763, in bupivacaine-injured mouse DRG neurons in vitro. SB 216763 159-167 glycogen synthase kinase 3 beta Mus musculus 113-139 29132216-8 2017 Taken together, our data suggest that curcumin may play an important role in AD via reducing Caveolin-1, inactivating GSK-3[Formula: see text] and inhibiting the abnormal excessive phosphorylation of Tau, which will provide a new theory for AD treatment with curcumin. Curcumin 38-46 glycogen synthase kinase 3 beta Mus musculus 118-123 27778132-9 2017 In addition to this, inhibition of apoptosis by EGCG was also confirmed with expression of proteins Akt, PTEN and GSK3beta. epigallocatechin gallate 48-52 glycogen synthase kinase 3 beta Mus musculus 114-122 27778132-10 2017 MRPE cells with EGCG upregulates phosphorylation of Akt at ser473 and phospho ser380 of PTEN, but phosphorylation at ser9 of GSK3beta was inhibited. epigallocatechin gallate 16-20 glycogen synthase kinase 3 beta Mus musculus 125-133 29141245-0 2017 Roscovitine, a CDK5 Inhibitor, Alleviates Sevoflurane-Induced Cognitive Dysfunction via Regulation Tau/GSK3beta and ERK/PPARgamma/CREB Signaling. Roscovitine 0-11 glycogen synthase kinase 3 beta Mus musculus 103-111 29141245-0 2017 Roscovitine, a CDK5 Inhibitor, Alleviates Sevoflurane-Induced Cognitive Dysfunction via Regulation Tau/GSK3beta and ERK/PPARgamma/CREB Signaling. Sevoflurane 42-53 glycogen synthase kinase 3 beta Mus musculus 103-111 29141245-10 2017 CONCLUSIONS: Inhibiting CDK5 with roscovitine has neuroprotective effects against neuronal injury and cognitive dysfunction caused by sevoflurane anesthesia that are exerted via modulation of Tau/GSK3beta and ERK/PPARgamma/CREB signaling. Roscovitine 34-45 glycogen synthase kinase 3 beta Mus musculus 196-204 28869464-3 2017 Oxygen deprivation (OD) resulted in tau dephosphorylation at several AD-related residues and activation of GSK3beta and phosphatase PP2A. Oxygen 0-6 glycogen synthase kinase 3 beta Mus musculus 107-115 27751939-6 2016 Inhibition of GSK-3beta activity by SB 216763, a potent and selective GSK-3 inhibitor, prominently ameliorated the detrimental effects in C57BL/6J mice with TP administration, which was associated with a correction of GSK-3beta overactivity. SB 216763 36-45 glycogen synthase kinase 3 beta Mus musculus 14-23 27751939-6 2016 Inhibition of GSK-3beta activity by SB 216763, a potent and selective GSK-3 inhibitor, prominently ameliorated the detrimental effects in C57BL/6J mice with TP administration, which was associated with a correction of GSK-3beta overactivity. SB 216763 36-45 glycogen synthase kinase 3 beta Mus musculus 14-19 27751939-6 2016 Inhibition of GSK-3beta activity by SB 216763, a potent and selective GSK-3 inhibitor, prominently ameliorated the detrimental effects in C57BL/6J mice with TP administration, which was associated with a correction of GSK-3beta overactivity. SB 216763 36-45 glycogen synthase kinase 3 beta Mus musculus 218-227 27751939-6 2016 Inhibition of GSK-3beta activity by SB 216763, a potent and selective GSK-3 inhibitor, prominently ameliorated the detrimental effects in C57BL/6J mice with TP administration, which was associated with a correction of GSK-3beta overactivity. triptolide 157-159 glycogen synthase kinase 3 beta Mus musculus 14-23 27751939-6 2016 Inhibition of GSK-3beta activity by SB 216763, a potent and selective GSK-3 inhibitor, prominently ameliorated the detrimental effects in C57BL/6J mice with TP administration, which was associated with a correction of GSK-3beta overactivity. triptolide 157-159 glycogen synthase kinase 3 beta Mus musculus 14-19 27751939-6 2016 Inhibition of GSK-3beta activity by SB 216763, a potent and selective GSK-3 inhibitor, prominently ameliorated the detrimental effects in C57BL/6J mice with TP administration, which was associated with a correction of GSK-3beta overactivity. triptolide 157-159 glycogen synthase kinase 3 beta Mus musculus 218-227 27390215-0 2016 Antinociceptive and Anti-Inflammatory Effects of Ketamine and the Relationship to Its Antidepressant Action and GSK3 Inhibition. Ketamine 49-57 glycogen synthase kinase 3 beta Mus musculus 112-116 28848172-6 2017 Paricalcitol treatment resulted in the up-regulation of VDR and down-regulation of GSK-3beta and beta-catenin, indicating that VDR had a regulatory effect on the Wnt signaling pathway. paricalcitol 0-12 glycogen synthase kinase 3 beta Mus musculus 83-92 26738851-6 2017 Administration of the nonspecific GSK-3beta inhibitor lithium in animals with active MMP-9 and animals lacking MMP-9 revealed that GSK-3beta and MMP-9 act in concert to control dendritic spine morphology. Lithium 54-61 glycogen synthase kinase 3 beta Mus musculus 34-43 26738851-6 2017 Administration of the nonspecific GSK-3beta inhibitor lithium in animals with active MMP-9 and animals lacking MMP-9 revealed that GSK-3beta and MMP-9 act in concert to control dendritic spine morphology. Lithium 54-61 glycogen synthase kinase 3 beta Mus musculus 131-140 28078012-1 2016 Glycogen synthase kinase 3beta (GSK3beta) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or anti-inflammatory agents. Lithium Chloride 85-101 glycogen synthase kinase 3 beta Mus musculus 0-30 28078012-1 2016 Glycogen synthase kinase 3beta (GSK3beta) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or anti-inflammatory agents. Lithium Chloride 85-101 glycogen synthase kinase 3 beta Mus musculus 32-40 28078012-7 2016 Taken together, our results provide the first evidence that the GSK3beta could be considered as an important drug in inducing early myelin debris clearance and regulating the expression of myelin genes, which open new approaches in the clinical treatment of nerve injuries by utilizing GSK3beta inhibitors such as lithium. Lithium 314-321 glycogen synthase kinase 3 beta Mus musculus 64-72 28078012-7 2016 Taken together, our results provide the first evidence that the GSK3beta could be considered as an important drug in inducing early myelin debris clearance and regulating the expression of myelin genes, which open new approaches in the clinical treatment of nerve injuries by utilizing GSK3beta inhibitors such as lithium. Lithium 314-321 glycogen synthase kinase 3 beta Mus musculus 286-294 27668540-2 2016 In this study, we examined the possible protective mechanism and associated signaling pathways of small-molecule glycogen synthase kinase-3 (GSK-3) inhibitor, SB216763, in bupivacaine-injured mouse DRG neurons in vitro. SB 216763 159-167 glycogen synthase kinase 3 beta Mus musculus 141-146 27668540-2 2016 In this study, we examined the possible protective mechanism and associated signaling pathways of small-molecule glycogen synthase kinase-3 (GSK-3) inhibitor, SB216763, in bupivacaine-injured mouse DRG neurons in vitro. Bupivacaine 172-183 glycogen synthase kinase 3 beta Mus musculus 113-139 27668540-2 2016 In this study, we examined the possible protective mechanism and associated signaling pathways of small-molecule glycogen synthase kinase-3 (GSK-3) inhibitor, SB216763, in bupivacaine-injured mouse DRG neurons in vitro. Bupivacaine 172-183 glycogen synthase kinase 3 beta Mus musculus 141-146 27668540-12 2016 CONCLUSIONS: GSK-3 inhibitor SB216763, through PKC, is effective in protecting anesthetics-induced neurotoxicity in DRG. SB 216763 29-37 glycogen synthase kinase 3 beta Mus musculus 13-18 27857162-6 2016 Inhibition of GSK3beta is likely a key mechanism mediating the therapeutic activity of Tanshinone IIA, because sodium nitroprusside, a GSK3beta activator, largely offset its renoprotective effect. Nitroprusside 111-131 glycogen synthase kinase 3 beta Mus musculus 14-22 27018151-0 2016 Perfluorooctane sulfonate (PFOS) impairs the proliferation of C17.2 neural stem cells via the downregulation of GSK-3beta/beta-catenin signaling. perfluorooctane sulfonic acid 0-25 glycogen synthase kinase 3 beta Mus musculus 112-121 27018151-0 2016 Perfluorooctane sulfonate (PFOS) impairs the proliferation of C17.2 neural stem cells via the downregulation of GSK-3beta/beta-catenin signaling. perfluorooctane sulfonic acid 27-31 glycogen synthase kinase 3 beta Mus musculus 112-121 27018151-4 2016 Additionally, we found that PFOS decreased Ser9 phosphorylation of glycogen synthase kinase-3beta (pSer9-GSK-3beta), leading to the activation of GSK-3beta and resultant downregulation of cellular beta-catenin. perfluorooctane sulfonic acid 28-32 glycogen synthase kinase 3 beta Mus musculus 67-97 27018151-4 2016 Additionally, we found that PFOS decreased Ser9 phosphorylation of glycogen synthase kinase-3beta (pSer9-GSK-3beta), leading to the activation of GSK-3beta and resultant downregulation of cellular beta-catenin. perfluorooctane sulfonic acid 28-32 glycogen synthase kinase 3 beta Mus musculus 105-114 27018151-4 2016 Additionally, we found that PFOS decreased Ser9 phosphorylation of glycogen synthase kinase-3beta (pSer9-GSK-3beta), leading to the activation of GSK-3beta and resultant downregulation of cellular beta-catenin. perfluorooctane sulfonic acid 28-32 glycogen synthase kinase 3 beta Mus musculus 146-155 27018151-5 2016 Furthermore, blockage of GSK-3beta with lithium chloride significantly attenuated both the PFOS-induced downregulation of GSK-3beta/beta-catenin and the proliferative impairment of C17.2 cells. Lithium Chloride 40-56 glycogen synthase kinase 3 beta Mus musculus 25-34 27018151-5 2016 Furthermore, blockage of GSK-3beta with lithium chloride significantly attenuated both the PFOS-induced downregulation of GSK-3beta/beta-catenin and the proliferative impairment of C17.2 cells. Lithium Chloride 40-56 glycogen synthase kinase 3 beta Mus musculus 122-131 27018151-5 2016 Furthermore, blockage of GSK-3beta with lithium chloride significantly attenuated both the PFOS-induced downregulation of GSK-3beta/beta-catenin and the proliferative impairment of C17.2 cells. perfluorooctane sulfonic acid 91-95 glycogen synthase kinase 3 beta Mus musculus 25-34 27018151-5 2016 Furthermore, blockage of GSK-3beta with lithium chloride significantly attenuated both the PFOS-induced downregulation of GSK-3beta/beta-catenin and the proliferative impairment of C17.2 cells. perfluorooctane sulfonic acid 91-95 glycogen synthase kinase 3 beta Mus musculus 122-131 27018151-7 2016 In conclusion, the present study demonstrated that PFOS decreased the proliferation of C17.2 cells via the negative modulation of the GSK-3beta/beta-catenin pathway. perfluorooctane sulfonic acid 51-55 glycogen synthase kinase 3 beta Mus musculus 134-143 27649883-10 2016 Mechanism study showed that l-theanine inhibited the activation of glycogen synthase kinase-3beta (GSK-3beta) which contributed to the hyperphosphorylation of tau and Cd-induced cytotoxicity. theanine 28-38 glycogen synthase kinase 3 beta Mus musculus 67-97 27649883-10 2016 Mechanism study showed that l-theanine inhibited the activation of glycogen synthase kinase-3beta (GSK-3beta) which contributed to the hyperphosphorylation of tau and Cd-induced cytotoxicity. theanine 28-38 glycogen synthase kinase 3 beta Mus musculus 99-108 27649883-10 2016 Mechanism study showed that l-theanine inhibited the activation of glycogen synthase kinase-3beta (GSK-3beta) which contributed to the hyperphosphorylation of tau and Cd-induced cytotoxicity. Cadmium 167-169 glycogen synthase kinase 3 beta Mus musculus 67-97 27649883-10 2016 Mechanism study showed that l-theanine inhibited the activation of glycogen synthase kinase-3beta (GSK-3beta) which contributed to the hyperphosphorylation of tau and Cd-induced cytotoxicity. Cadmium 167-169 glycogen synthase kinase 3 beta Mus musculus 99-108 27713171-6 2016 Furthermore, sulfuretin treatment increased mRNA expression of Wnt ligands, phosphorylation of GSK3, and nuclear beta-catenin protein expression. sulfuretin 13-23 glycogen synthase kinase 3 beta Mus musculus 95-99 27738106-4 2016 We report here that liver BVRA protects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing serine 9 phosphorylation, which inhibits its activity. Serine 135-141 glycogen synthase kinase 3 beta Mus musculus 80-110 27738106-4 2016 We report here that liver BVRA protects against hepatic steatosis by inhibiting glycogen synthase kinase 3beta (GSK3beta) by enhancing serine 9 phosphorylation, which inhibits its activity. Serine 135-141 glycogen synthase kinase 3 beta Mus musculus 112-120 27738106-5 2016 We show that GSK3beta phosphorylates serine 73 (Ser(P)73) of the peroxisome proliferator-activated receptor alpha (PPARalpha), which in turn increased ubiquitination and protein turnover, as well as decreased activity. Serine 37-43 glycogen synthase kinase 3 beta Mus musculus 13-21 27738106-5 2016 We show that GSK3beta phosphorylates serine 73 (Ser(P)73) of the peroxisome proliferator-activated receptor alpha (PPARalpha), which in turn increased ubiquitination and protein turnover, as well as decreased activity. Serine 48-51 glycogen synthase kinase 3 beta Mus musculus 13-21 27780915-6 2016 Expression of the active form of GSK- 3beta (tyrosine 216-phosphorylated) was higher in osteosarcoma than osteoblast cells. Tyrosine 45-53 glycogen synthase kinase 3 beta Mus musculus 33-43 27190311-0 2016 A cAMP and CREB-mediated feed-forward mechanism regulates GSK3beta in polycystic kidney disease. Cyclic AMP 2-6 glycogen synthase kinase 3 beta Mus musculus 58-66 27190311-4 2016 In mouse models of PKD, increases in renal GSK3beta corresponded with increases in renal cAMP levels and disease progression. Cyclic AMP 89-93 glycogen synthase kinase 3 beta Mus musculus 43-51 27190311-5 2016 In vivo and in vitro studies revealed that GSK3beta is a cAMP-responsive gene, and elevated cAMP levels, as seen in PKD, can increase GSK3beta expression. Cyclic AMP 57-61 glycogen synthase kinase 3 beta Mus musculus 43-51 27190311-5 2016 In vivo and in vitro studies revealed that GSK3beta is a cAMP-responsive gene, and elevated cAMP levels, as seen in PKD, can increase GSK3beta expression. Cyclic AMP 57-61 glycogen synthase kinase 3 beta Mus musculus 134-142 27190311-5 2016 In vivo and in vitro studies revealed that GSK3beta is a cAMP-responsive gene, and elevated cAMP levels, as seen in PKD, can increase GSK3beta expression. Cyclic AMP 92-96 glycogen synthase kinase 3 beta Mus musculus 134-142 27190311-6 2016 In normal mice, vasopressin signaling induced by water deprivation increased GSK3beta expression, which decreased following rehydration. Water 49-54 glycogen synthase kinase 3 beta Mus musculus 77-85 27190311-8 2016 CREB was found to bind to GSK3beta promoter and essential for cAMP-mediated regulation of GSK3beta. Cyclic AMP 62-66 glycogen synthase kinase 3 beta Mus musculus 26-34 27190311-8 2016 CREB was found to bind to GSK3beta promoter and essential for cAMP-mediated regulation of GSK3beta. Cyclic AMP 62-66 glycogen synthase kinase 3 beta Mus musculus 90-98 27190311-9 2016 Importantly, this regulation was demonstrated to be part of a feed-forward loop in which cAMP through CREB regulates GSK3beta expression, and GSK3beta in turn positively regulates cAMP generation. Cyclic AMP 89-93 glycogen synthase kinase 3 beta Mus musculus 117-125 27190311-9 2016 Importantly, this regulation was demonstrated to be part of a feed-forward loop in which cAMP through CREB regulates GSK3beta expression, and GSK3beta in turn positively regulates cAMP generation. Cyclic AMP 180-184 glycogen synthase kinase 3 beta Mus musculus 117-125 27190311-9 2016 Importantly, this regulation was demonstrated to be part of a feed-forward loop in which cAMP through CREB regulates GSK3beta expression, and GSK3beta in turn positively regulates cAMP generation. Cyclic AMP 180-184 glycogen synthase kinase 3 beta Mus musculus 142-150 27965573-7 2016 In addition to that, long-term treatment of 7,8-DHF dramatically ameliorated cognitive decline in ApoE-KO mice, accompanied by the activation in phosphorylated protein kinase B (Akt)/glycogen synthase kinase-3beta (GSK-3beta) pathway and down-regulated expression of tau S396 and PHF-tau (phosphorylated tau at ser396 and ser404 epitope). 6,7-dihydroxyflavone 44-51 glycogen synthase kinase 3 beta Mus musculus 183-213 27965573-7 2016 In addition to that, long-term treatment of 7,8-DHF dramatically ameliorated cognitive decline in ApoE-KO mice, accompanied by the activation in phosphorylated protein kinase B (Akt)/glycogen synthase kinase-3beta (GSK-3beta) pathway and down-regulated expression of tau S396 and PHF-tau (phosphorylated tau at ser396 and ser404 epitope). 6,7-dihydroxyflavone 44-51 glycogen synthase kinase 3 beta Mus musculus 215-224 27857162-6 2016 Inhibition of GSK3beta is likely a key mechanism mediating the therapeutic activity of Tanshinone IIA, because sodium nitroprusside, a GSK3beta activator, largely offset its renoprotective effect. Nitroprusside 111-131 glycogen synthase kinase 3 beta Mus musculus 135-143 27851811-0 2016 Atorvastatin Alleviates Experimental Diabetic Cardiomyopathy by Regulating the GSK-3beta-PP2Ac-NF-kappaB Signaling Axis. Atorvastatin 0-12 glycogen synthase kinase 3 beta Mus musculus 79-88 27851811-10 2016 In mice with type 1 diabetes mellitus, treatment with ATOR, at 10 mg-kg-1-d-1, significantly suppressed GSK-3beta activation, IKK/IkBalpha phosphorylation, NF-kB nuclear translocation and caspase-3 activation, while also activating PP2Ac. Atorvastatin 54-58 glycogen synthase kinase 3 beta Mus musculus 104-113 27748847-0 2016 Glycogen synthase kinase-3beta is required for epithelial-mesenchymal transition and barrier dysfunction in mouse podocytes under high glucose conditions. Glucose 135-142 glycogen synthase kinase 3 beta Mus musculus 0-30 30108748-0 2017 Synthesis of substituted 2H-benzo[e]indazole-9-carboxylate as a potent antihyperglycemic agent that may act through IRS-1, Akt and GSK-3beta pathways. 2h-benzo[e]indazole-9-carboxylate 25-58 glycogen synthase kinase 3 beta Mus musculus 131-140 30108748-7 2017 The mechanistic studies revealed that the 2H-benzo[e]indazole 5e significantly stimulated insulin-induced signaling at the level of IRS-1, Akt and GSK-3beta in L6 skeletal muscle cells, possibly by inhibiting protein tyrosine phosphatase-1B. 2h-benzo[e]indazole 5e 42-64 glycogen synthase kinase 3 beta Mus musculus 147-156 27568038-0 2016 20-HETE attenuates the response of glucose-stimulated insulin secretion through the AKT/GSK-3beta/Glut2 pathway. Glucose 35-42 glycogen synthase kinase 3 beta Mus musculus 88-97 27568038-7 2016 TWS119, a GSK-3beta selective inhibitor, blocked the 20-HETE-mediated reduction in Glut2 expression. TWS 119 0-6 glycogen synthase kinase 3 beta Mus musculus 10-19 28009972-13 2016 Cyclopamine and the overexpression of Sufu inhibited the phosphorylation of GSK-3beta and restrained the migration of fibroblasts. cyclopamine 0-11 glycogen synthase kinase 3 beta Mus musculus 76-85 28009972-15 2016 Our findings suggest that cyclopamine and Sufu-overexpression may effectively inhibit the endogenous as well as the TGF-beta1-induced activation of fibroblasts through subsequent activation of GSK-3beta. cyclopamine 26-37 glycogen synthase kinase 3 beta Mus musculus 193-202 27468164-0 2016 Involvement of PI3K/Akt/GSK-3beta and mTOR in the antidepressant-like effect of atorvastatin in mice. Atorvastatin 80-92 glycogen synthase kinase 3 beta Mus musculus 24-33 27468164-4 2016 The present study investigated the participation of the PI3K/Akt/GSK-3beta/mTOR signaling pathway in the antidepressant-like effect of an acute atorvastatin treatment in mice. Atorvastatin 144-156 glycogen synthase kinase 3 beta Mus musculus 65-74 27468164-7 2016 The participation of GSK-3beta in the antidepressant-like effect of atorvastatin was demonstrated by co-administration of a sub-effective dose of atorvastatin (0.01 mg/kg, p.o.) Atorvastatin 68-80 glycogen synthase kinase 3 beta Mus musculus 21-30 27468164-7 2016 The participation of GSK-3beta in the antidepressant-like effect of atorvastatin was demonstrated by co-administration of a sub-effective dose of atorvastatin (0.01 mg/kg, p.o.) Atorvastatin 146-158 glycogen synthase kinase 3 beta Mus musculus 21-30 27468164-12 2016 These behavioral findings were supported by neurochemical observations, as atorvastatin treatment increased the immunocontent of the phosphorylated isoforms of Akt, GSK-3beta and mTOR in the hippocampus of mice. Atorvastatin 75-87 glycogen synthase kinase 3 beta Mus musculus 165-174 27468164-13 2016 Taken together, our results suggest an involvement of the PI3K/Akt/GSK-3beta/mTOR signaling pathway in the antidepressant-like effect of atorvastatin in mice. Atorvastatin 137-149 glycogen synthase kinase 3 beta Mus musculus 67-76 27748847-4 2016 The present study aimed to determine the function of glycogen synthase kinase (GSK)-3beta in EMT and barrier dysfunction of mouse podocytes exposed to high glucose (HG) conditions. Glucose 156-163 glycogen synthase kinase 3 beta Mus musculus 53-89 27748847-11 2016 HG also induced barrier dysfunction and increased the expression level of total GSK-3beta, Try216-phosphorylated-GSK-3beta and the GSK-3beta activity in podocytes. try216 91-97 glycogen synthase kinase 3 beta Mus musculus 113-122 27748847-11 2016 HG also induced barrier dysfunction and increased the expression level of total GSK-3beta, Try216-phosphorylated-GSK-3beta and the GSK-3beta activity in podocytes. try216 91-97 glycogen synthase kinase 3 beta Mus musculus 113-122 27894404-12 2016 These results suggest that STZ induces neurite outgrowth via activation of PI3K-Akt signaling pathway and GSK3beta inhibition. Streptozocin 27-30 glycogen synthase kinase 3 beta Mus musculus 106-114 27333945-9 2016 iCS generated from adult skin fibroblasts by somatic reprogramming and a cocktail of Gsk3beta inhibitor-6-Bromoindirubin-3"-oxime and Oncostatin M may represent a novel source for cell therapy in MI. 6-bromoindirubin-3'-oxime 104-129 glycogen synthase kinase 3 beta Mus musculus 85-93 27809235-9 2016 Consistent with this result, we also observed that genistein alleviated activity of c-Jun N-terminal kinase and glycogen synthase kinase 3beta, which are involved in tau hyperphosphorylation. Genistein 51-60 glycogen synthase kinase 3 beta Mus musculus 112-142 27894404-0 2016 Streptozotocin induces neurite outgrowth via PI3K-Akt and glycogen synthase kinase 3beta in Neuro2a cells. Streptozocin 0-14 glycogen synthase kinase 3 beta Mus musculus 58-88 27894404-10 2016 Glycogen synthase kinase 3beta (GSK3beta), which has been reported to be inactivated by Akt, was also transiently phosphorylated at Ser9 by STZ (5 mM) administration. Streptozocin 140-143 glycogen synthase kinase 3 beta Mus musculus 0-30 27894404-10 2016 Glycogen synthase kinase 3beta (GSK3beta), which has been reported to be inactivated by Akt, was also transiently phosphorylated at Ser9 by STZ (5 mM) administration. Streptozocin 140-143 glycogen synthase kinase 3 beta Mus musculus 32-40 27609227-5 2016 SalA also intensively limited cortical infarction and promoted the expression of neurogenesis protein near the peri-infarct cortex and subgranular zone of the hippocampal dentate gyrus by compromising the activation of GSK3beta and p25/Cdk5, which in turn upregulated beta-catenin, doublecortin (DCX), and Bcl-2, most possibly through the activation of PI3K/Akt signaling via the upregulation of brain-derived neurotrophic factor. salvianolic acid A 0-4 glycogen synthase kinase 3 beta Mus musculus 219-227 27725131-2 2016 In the present study, oral administration of diosmin reduced cerebral Abeta oligomer levels, tau-hyperphosphorylation and cognitive impairment in the 3xTg-AD mouse model through glycogen synthase kinase-3 (GSK-3) and transient receptor potential canonical 6-related mechanisms. Diosmin 45-52 glycogen synthase kinase 3 beta Mus musculus 178-204 27725131-2 2016 In the present study, oral administration of diosmin reduced cerebral Abeta oligomer levels, tau-hyperphosphorylation and cognitive impairment in the 3xTg-AD mouse model through glycogen synthase kinase-3 (GSK-3) and transient receptor potential canonical 6-related mechanisms. Diosmin 45-52 glycogen synthase kinase 3 beta Mus musculus 206-211 27725131-3 2016 Diosmetin, one major bioactive metabolite of diosmin, increased inhibitory GSK-3beta phosphorylation, while selectively reducing gamma-secretase activity, Abeta generation, tau hyperphosphorylation and pro-inflammatory activation of microglia in vitro, without altering Notch processing. diosmetin 0-9 glycogen synthase kinase 3 beta Mus musculus 75-84 27725131-3 2016 Diosmetin, one major bioactive metabolite of diosmin, increased inhibitory GSK-3beta phosphorylation, while selectively reducing gamma-secretase activity, Abeta generation, tau hyperphosphorylation and pro-inflammatory activation of microglia in vitro, without altering Notch processing. Diosmin 45-52 glycogen synthase kinase 3 beta Mus musculus 75-84 27784989-0 2016 Moringin activates Wnt canonical pathway by inhibiting GSK3beta in a mouse model of experimental autoimmune encephalomyelitis. moringin 0-8 glycogen synthase kinase 3 beta Mus musculus 55-63 27784989-6 2016 Moringin pretreatment normalizes the aberrant Wnt-beta-catenin pathway, resulting in GSK3beta inhibition and beta-catenin upregulation, which regulates T-cell activation (CD4 and FoxP3), suppresses the main inflammatory mediators (IL-1beta, IL-6, and COX2), through activation of PPARgamma. moringin 0-8 glycogen synthase kinase 3 beta Mus musculus 85-93 26956696-8 2016 In co-treatment Zn with PI3K/Akt/GSK-3beta signaling pathway, inhibitor LY294002 prevented HG/hypoxic-induced HIF-1alpha increase and EMT changes, suggesting that Zn may mediate HG/hypoxic-induced EMT through PI3K/Akt/GSK-3beta pathway. Zinc 16-18 glycogen synthase kinase 3 beta Mus musculus 33-42 26956696-8 2016 In co-treatment Zn with PI3K/Akt/GSK-3beta signaling pathway, inhibitor LY294002 prevented HG/hypoxic-induced HIF-1alpha increase and EMT changes, suggesting that Zn may mediate HG/hypoxic-induced EMT through PI3K/Akt/GSK-3beta pathway. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 72-80 glycogen synthase kinase 3 beta Mus musculus 33-42 26956696-8 2016 In co-treatment Zn with PI3K/Akt/GSK-3beta signaling pathway, inhibitor LY294002 prevented HG/hypoxic-induced HIF-1alpha increase and EMT changes, suggesting that Zn may mediate HG/hypoxic-induced EMT through PI3K/Akt/GSK-3beta pathway. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 72-80 glycogen synthase kinase 3 beta Mus musculus 218-227 26956696-8 2016 In co-treatment Zn with PI3K/Akt/GSK-3beta signaling pathway, inhibitor LY294002 prevented HG/hypoxic-induced HIF-1alpha increase and EMT changes, suggesting that Zn may mediate HG/hypoxic-induced EMT through PI3K/Akt/GSK-3beta pathway. Zinc 163-165 glycogen synthase kinase 3 beta Mus musculus 33-42 26956696-8 2016 In co-treatment Zn with PI3K/Akt/GSK-3beta signaling pathway, inhibitor LY294002 prevented HG/hypoxic-induced HIF-1alpha increase and EMT changes, suggesting that Zn may mediate HG/hypoxic-induced EMT through PI3K/Akt/GSK-3beta pathway. Zinc 163-165 glycogen synthase kinase 3 beta Mus musculus 218-227 26956696-9 2016 Therefore, we concluded that Zn had an important anti-fibrosis role under HG/hypoxic conditions, and a novel mechanism contributing to Zn protection on renal tubular epithelial cells from HG/hypoxia-induced EMT through activation of PI3K/Akt/GSK-3beta signaling pathway, which subsequently leads to the downregulation of the expression of HIF-1alpha. Zinc 29-31 glycogen synthase kinase 3 beta Mus musculus 242-251 27723793-5 2016 Using inhibitors of cell signaling we have shown that Src family kinases, p38 MAPK, ERK1/2 and GSK3beta are required for the transition between mES and EPL cells. 2-(N-morpholino)ethanesulfonic acid 144-147 glycogen synthase kinase 3 beta Mus musculus 95-103 27723793-6 2016 ERK1/2, c-Src and GSK3beta are likely to be enforcing a receptive, primed state in mES cells, while Src family kinases and p38 MAPK are involved in the establishment of EPL cells. 2-(N-morpholino)ethanesulfonic acid 83-86 glycogen synthase kinase 3 beta Mus musculus 18-26 27716735-8 2016 GLA also attenuated microvascular thrombosis (P<0.05) and increased the phosphorylation of pro-survival kinase AKT (P<0.05) and GSK-3beta (P<0.05) in the myocardium upon reperfusion injury. glaucocalyxin A 0-3 glycogen synthase kinase 3 beta Mus musculus 134-143 27378458-0 2016 Tideglusib, a chemical inhibitor of GSK3beta, attenuates hypoxic-ischemic brain injury in neonatal mice. tideglusib 0-10 glycogen synthase kinase 3 beta Mus musculus 36-44 27378458-3 2016 Tideglusib is a GSK-3beta inhibitor which has neuroprotective effects against neurodegenerative diseases in clinical trials. tideglusib 0-10 glycogen synthase kinase 3 beta Mus musculus 16-25 27609227-6 2016 We conclude that SalA blocks inflammatory responses by impairing NF-kappaB signaling, thereby limiting inflammation/nitrosative stress and preserving the integrity of the BBB; SalA also concomitantly promotes neurogenesis-related protein expression by compromising GSK3beta/Cdk5 activity to enhance the expression levels of beta-catenin/DCX and Bcl-2 for neuroprotection. salvianolic acid A 17-21 glycogen synthase kinase 3 beta Mus musculus 265-273 27588407-4 2016 Activation of beta-catenin pathway by GSK3 inhibitors suppresses CFTR mutation/knockdown-induced NF-kappaB/COX-2/PGE2 pathway in DeltaF508 mouse intestine and CFTR-knockdown cells. Dinoprostone 113-117 glycogen synthase kinase 3 beta Mus musculus 38-42 27291828-9 2016 Western blot analysis revealed that ABT-239 or donepezil systemic treatments increased GSK-3beta phosphorylation in cortical and hippocampal homogenates of normal, but not of histamine-depleted mice. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 36-39 glycogen synthase kinase 3 beta Mus musculus 87-96 27291828-9 2016 Western blot analysis revealed that ABT-239 or donepezil systemic treatments increased GSK-3beta phosphorylation in cortical and hippocampal homogenates of normal, but not of histamine-depleted mice. Donepezil 47-56 glycogen synthase kinase 3 beta Mus musculus 87-96 27291828-10 2016 Furthermore, administration of the PI3K inhibitor LY294002 that blocks GSK-3beta phosphorylation, prevented the procognitive effects of both drugs in normal mice. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 50-58 glycogen synthase kinase 3 beta Mus musculus 71-80 27291828-11 2016 Our results indicate that both donepezil and ABT-239 require the integrity of the brain histaminergic system to exert their procognitive effects and strongly suggest that impairments of PI3K/AKT/GSK-3beta intracellular pathway activation is responsible for the inefficacy of both drugs in histamine-deficient animals. Donepezil 31-40 glycogen synthase kinase 3 beta Mus musculus 195-204 27291828-11 2016 Our results indicate that both donepezil and ABT-239 require the integrity of the brain histaminergic system to exert their procognitive effects and strongly suggest that impairments of PI3K/AKT/GSK-3beta intracellular pathway activation is responsible for the inefficacy of both drugs in histamine-deficient animals. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid 45-48 glycogen synthase kinase 3 beta Mus musculus 195-204 27291828-11 2016 Our results indicate that both donepezil and ABT-239 require the integrity of the brain histaminergic system to exert their procognitive effects and strongly suggest that impairments of PI3K/AKT/GSK-3beta intracellular pathway activation is responsible for the inefficacy of both drugs in histamine-deficient animals. Histamine 88-97 glycogen synthase kinase 3 beta Mus musculus 195-204 27689994-4 2016 The administration of Se-Met effectively decreased the production and deposition of Abeta by inhibiting beta-site amyloid precursor protein cleaving enzyme 1 (BACE1)-regulated amyloid precursor protein (APP) processing and reduced the level of total tau and phosphorylated tau, which depended on depressing the activity and expression of glycogen synthase kinase-3beta (GSK-3beta) and cyclin-dependent kinase 5 (CDK5). Selenomethionine 22-28 glycogen synthase kinase 3 beta Mus musculus 338-368 27689994-4 2016 The administration of Se-Met effectively decreased the production and deposition of Abeta by inhibiting beta-site amyloid precursor protein cleaving enzyme 1 (BACE1)-regulated amyloid precursor protein (APP) processing and reduced the level of total tau and phosphorylated tau, which depended on depressing the activity and expression of glycogen synthase kinase-3beta (GSK-3beta) and cyclin-dependent kinase 5 (CDK5). Selenomethionine 22-28 glycogen synthase kinase 3 beta Mus musculus 370-379 27649495-0 2016 Renoprotective Effects of Atorvastatin in Diabetic Mice: Downregulation of RhoA and Upregulation of Akt/GSK3. Atorvastatin 26-38 glycogen synthase kinase 3 beta Mus musculus 104-108 27649495-10 2016 Atorvastatin also upregulated Akt/GSK3beta phosphorylation in the renal cortex of db/db mice. Atorvastatin 0-12 glycogen synthase kinase 3 beta Mus musculus 34-42 27649495-11 2016 Our findings suggest that atorvastatin attenuates diabetes-associated renal injury by reducing ROS generation, RhoA activity and normalizing Akt/GSK3beta signaling pathways. Atorvastatin 26-38 glycogen synthase kinase 3 beta Mus musculus 145-153 27475717-9 2016 In addition, ERK and GSK3beta-dependent C/EBPbeta phosphorylation was attenuated by andrographolide. andrographolide 84-99 glycogen synthase kinase 3 beta Mus musculus 21-29 27453433-0 2016 Inhibition of GSK-3 reduces prostaglandin E2 production by decreasing the expression levels of COX-2 and mPGES-1 in monocyte/macrophage lineage cells. Dinoprostone 28-44 glycogen synthase kinase 3 beta Mus musculus 14-19 27453433-3 2016 In the present study, therefore, we examined whether inhibition of GSK-3 can reduce inflammatory PGE2 production in vitro and in vivo. Dinoprostone 97-101 glycogen synthase kinase 3 beta Mus musculus 67-72 27453433-5 2016 GSK-3 inhibitors LiCl and SB216763 strongly suppressed their protein levels through inhibition of mRNA expressions. SB 216763 26-34 glycogen synthase kinase 3 beta Mus musculus 0-5 27453433-8 2016 Pharmacological and genetic inhibitions of GSK-3 also strongly suppressed PGE2 production in cultured peritoneal macrophages and in inflammatory air pouches made under the skin of living mice. Dinoprostone 74-78 glycogen synthase kinase 3 beta Mus musculus 43-48 27453433-9 2016 These results suggested that GSK-3 plays a key role in PGE2 production by increasing COX-2 and mPGES-1 probably through Egr-1-mediated transcription and GSK-3 inhibitors may be potential as novel anti-inflammatory drugs. Dinoprostone 55-59 glycogen synthase kinase 3 beta Mus musculus 29-34 27453433-9 2016 These results suggested that GSK-3 plays a key role in PGE2 production by increasing COX-2 and mPGES-1 probably through Egr-1-mediated transcription and GSK-3 inhibitors may be potential as novel anti-inflammatory drugs. Dinoprostone 55-59 glycogen synthase kinase 3 beta Mus musculus 153-158 27667108-5 2016 Results: In in vivo experiment, the expression levels of ER stress markers, glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP), were upregulated during the progression of D-GalN/LPS-induced ALF, indicating activation of severe ER stress and increased activity of GSK3beta. Galactosamine 218-224 glycogen synthase kinase 3 beta Mus musculus 310-318 27507058-7 2016 The effects of myricetin were associated with a modulation the GSK-3beta and Wnt/beta-catenin pathways. myricetin 15-24 glycogen synthase kinase 3 beta Mus musculus 63-72 27667108-8 2016 The in vitro experiment of tunicamycin-induced hepatocyte apoptosis showed that inhibition of GSK3beta activity increased the cell survival rate. Tunicamycin 27-38 glycogen synthase kinase 3 beta Mus musculus 94-102 27667108-9 2016 Conclusion: In ALF induced by D-GalN/LPS, severe ER stress may accelerate the development and progress of ALF by upregulating the activity of GSK3beta. Galactosamine 30-36 glycogen synthase kinase 3 beta Mus musculus 142-150 27374489-0 2016 Dihydromyricetin protects neurons in an MPTP-induced model of Parkinson"s disease by suppressing glycogen synthase kinase-3 beta activity. dihydromyricetin 0-16 glycogen synthase kinase 3 beta Mus musculus 97-128 27374489-0 2016 Dihydromyricetin protects neurons in an MPTP-induced model of Parkinson"s disease by suppressing glycogen synthase kinase-3 beta activity. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 40-44 glycogen synthase kinase 3 beta Mus musculus 97-128 27374489-11 2016 In addition, DHM increased glycogen synthase kinase-3 beta phosphorylation in a dose- and time-dependent manner, which may be associated with DHM-induced dopaminergic neuronal protection. dihydromyricetin 13-16 glycogen synthase kinase 3 beta Mus musculus 27-58 27374489-11 2016 In addition, DHM increased glycogen synthase kinase-3 beta phosphorylation in a dose- and time-dependent manner, which may be associated with DHM-induced dopaminergic neuronal protection. dihydromyricetin 142-145 glycogen synthase kinase 3 beta Mus musculus 27-58 27206526-9 2016 In MC3T3-E1 cells, BzATP increased inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta), a process that was blocked by A 438079 and diminished by inhibition of protein kinase C. Thus, P2X7 signaling may potentiate the canonical Wnt pathway through GSK3beta inhibition. BzATP 19-24 glycogen synthase kinase 3 beta Mus musculus 65-95 27321043-0 2016 Xanthatin anti-tumor cytotoxicity is mediated via glycogen synthase kinase-3beta and beta-catenin. xanthatin 0-9 glycogen synthase kinase 3 beta Mus musculus 50-80 27321043-4 2016 Genetic inactivation of GSK-3beta, but not the related isoform GSK-3alpha, compromised xanthatin cytotoxicity while inactivation of beta-catenin enhanced xanthatin-mediated cell death. xanthatin 87-96 glycogen synthase kinase 3 beta Mus musculus 24-33 27355132-12 2016 In addition, RIPostC increased the phosphorylation of TOPK, PTEN, Akt, GSK3beta and the nuclear translocation of Nrf2 and decreased the nuclear translocation of NF-kappaB. ripostc 13-20 glycogen synthase kinase 3 beta Mus musculus 71-79 27687706-0 2016 Ketamine-induced inhibition of glycogen synthase kinase-3 contributes to the augmentation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor signaling. Ketamine 0-8 glycogen synthase kinase 3 beta Mus musculus 31-57 27687706-0 2016 Ketamine-induced inhibition of glycogen synthase kinase-3 contributes to the augmentation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor signaling. alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic 93-144 glycogen synthase kinase 3 beta Mus musculus 31-57 27687706-3 2016 METHODS: In this study, we tested if the inhibitory effect of ketamine on glycogen synthase kinase-3 (GSK3) affected hippocampal cell-surface AMPA receptors using immunoblotting of membrane and synaptosomal extracts from wild-type and GSK3 knockin mice. Ketamine 62-70 glycogen synthase kinase 3 beta Mus musculus 74-100 27687706-3 2016 METHODS: In this study, we tested if the inhibitory effect of ketamine on glycogen synthase kinase-3 (GSK3) affected hippocampal cell-surface AMPA receptors using immunoblotting of membrane and synaptosomal extracts from wild-type and GSK3 knockin mice. Ketamine 62-70 glycogen synthase kinase 3 beta Mus musculus 102-106 27687706-3 2016 METHODS: In this study, we tested if the inhibitory effect of ketamine on glycogen synthase kinase-3 (GSK3) affected hippocampal cell-surface AMPA receptors using immunoblotting of membrane and synaptosomal extracts from wild-type and GSK3 knockin mice. Ketamine 62-70 glycogen synthase kinase 3 beta Mus musculus 235-239 27687706-5 2016 This effect of ketamine was abrogated in GSK3 knockin mice expressing mutant GSK3 that cannot be inhibited by ketamine, demonstrating that ketamine-induced inhibition of GSK3 is necessary for up-regulation of cell surface AMPA GluA1 subunits. Ketamine 15-23 glycogen synthase kinase 3 beta Mus musculus 41-45 27687706-5 2016 This effect of ketamine was abrogated in GSK3 knockin mice expressing mutant GSK3 that cannot be inhibited by ketamine, demonstrating that ketamine-induced inhibition of GSK3 is necessary for up-regulation of cell surface AMPA GluA1 subunits. Ketamine 15-23 glycogen synthase kinase 3 beta Mus musculus 77-81 27687706-5 2016 This effect of ketamine was abrogated in GSK3 knockin mice expressing mutant GSK3 that cannot be inhibited by ketamine, demonstrating that ketamine-induced inhibition of GSK3 is necessary for up-regulation of cell surface AMPA GluA1 subunits. Ketamine 15-23 glycogen synthase kinase 3 beta Mus musculus 77-81 27687706-5 2016 This effect of ketamine was abrogated in GSK3 knockin mice expressing mutant GSK3 that cannot be inhibited by ketamine, demonstrating that ketamine-induced inhibition of GSK3 is necessary for up-regulation of cell surface AMPA GluA1 subunits. Ketamine 110-118 glycogen synthase kinase 3 beta Mus musculus 41-45 27687706-5 2016 This effect of ketamine was abrogated in GSK3 knockin mice expressing mutant GSK3 that cannot be inhibited by ketamine, demonstrating that ketamine-induced inhibition of GSK3 is necessary for up-regulation of cell surface AMPA GluA1 subunits. Ketamine 110-118 glycogen synthase kinase 3 beta Mus musculus 41-45 27687706-7 2016 Ketamine treatment decreased the hippocampal membrane level of phosphorylated PSD-95 on Thr-19, the target of GSK3 that promotes AMPA receptor internalization. Ketamine 0-8 glycogen synthase kinase 3 beta Mus musculus 110-114 27687706-7 2016 Ketamine treatment decreased the hippocampal membrane level of phosphorylated PSD-95 on Thr-19, the target of GSK3 that promotes AMPA receptor internalization. Threonine 88-91 glycogen synthase kinase 3 beta Mus musculus 110-114 27687706-8 2016 CONCLUSIONS: These results demonstrate that ketamine-induced inhibition of GSK3 causes reduced phosphorylation of PSD-95, diminishing the internalization of AMPA GluA1 subunits to allow for augmented signaling through AMPA receptors following ketamine treatment. Ketamine 44-52 glycogen synthase kinase 3 beta Mus musculus 75-79 27687706-8 2016 CONCLUSIONS: These results demonstrate that ketamine-induced inhibition of GSK3 causes reduced phosphorylation of PSD-95, diminishing the internalization of AMPA GluA1 subunits to allow for augmented signaling through AMPA receptors following ketamine treatment. Ketamine 243-251 glycogen synthase kinase 3 beta Mus musculus 75-79 26328540-4 2016 Inhibition of protein tyrosine phosphatase 1B (PTP1B), alternatively, caused an enhancement in the tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1), allowing activation of Akt through a pathway along an IRS-1/phosphatidylinositol 3 kinase (PI3K)/3-phosphoinositide-dependent protein kinase-1 (PDK1)/Akt axis, to phosphorylate and inactivate GSK-3beta. Tyrosine 22-30 glycogen synthase kinase 3 beta Mus musculus 357-366 27206526-9 2016 In MC3T3-E1 cells, BzATP increased inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta), a process that was blocked by A 438079 and diminished by inhibition of protein kinase C. Thus, P2X7 signaling may potentiate the canonical Wnt pathway through GSK3beta inhibition. BzATP 19-24 glycogen synthase kinase 3 beta Mus musculus 97-105 27206526-9 2016 In MC3T3-E1 cells, BzATP increased inhibitory phosphorylation of glycogen synthase kinase 3beta (GSK3beta), a process that was blocked by A 438079 and diminished by inhibition of protein kinase C. Thus, P2X7 signaling may potentiate the canonical Wnt pathway through GSK3beta inhibition. BzATP 19-24 glycogen synthase kinase 3 beta Mus musculus 267-275 27497480-11 2016 Supplementations of vitamin B6/B12/folate+choline could significantly ameliorate the hypoxia-induced memory deficits, observably decreased Hcy concentrations in serum, and markedly attenuated tau hyperphosphorylation at multiple AD-related sites through upregulating inhibitory Ser9-phosphorylated GSK-3beta. Vitamin B 6 20-30 glycogen synthase kinase 3 beta Mus musculus 298-307 27566245-4 2016 Therefore, we hypothesized that Ex-4 would stabilize the blood-brain barrier (BBB) and suppress neuroinflammation through PI3K-Akt-induced inhibition of glycogen synthase kinase-3beta (GSK-3beta) after warfarin-associated HT post-cerebral ischemia. Warfarin 202-210 glycogen synthase kinase 3 beta Mus musculus 185-194 27566245-15 2016 The PI3K/Akt-GSK-3beta signaling pathway appeared to contribute to the protection afforded by Ex-4 in the warfarin-associated HT model. Warfarin 106-114 glycogen synthase kinase 3 beta Mus musculus 13-22 27558652-5 2016 At the molecular level, wedelolactone directly inhibited GSK3beta activity and enhanced the phosphorylation of GSK3beta, thereafter stimulated the nuclear translocation of beta-catenin and runx2. wedelolactone 24-37 glycogen synthase kinase 3 beta Mus musculus 57-65 27558652-5 2016 At the molecular level, wedelolactone directly inhibited GSK3beta activity and enhanced the phosphorylation of GSK3beta, thereafter stimulated the nuclear translocation of beta-catenin and runx2. wedelolactone 24-37 glycogen synthase kinase 3 beta Mus musculus 111-119 27558652-11 2016 Together, these data demonstrated that wedelolactone facilitated osteoblastogenesis through Wnt/GSK3beta/beta-catenin signaling pathway and suppressed RANKL-induced osteoclastogenesis through NF-kappaB/c-fos/NFATc1 pathway. wedelolactone 39-52 glycogen synthase kinase 3 beta Mus musculus 96-104 27497480-11 2016 Supplementations of vitamin B6/B12/folate+choline could significantly ameliorate the hypoxia-induced memory deficits, observably decreased Hcy concentrations in serum, and markedly attenuated tau hyperphosphorylation at multiple AD-related sites through upregulating inhibitory Ser9-phosphorylated GSK-3beta. Folic Acid 35-41 glycogen synthase kinase 3 beta Mus musculus 298-307 27497480-11 2016 Supplementations of vitamin B6/B12/folate+choline could significantly ameliorate the hypoxia-induced memory deficits, observably decreased Hcy concentrations in serum, and markedly attenuated tau hyperphosphorylation at multiple AD-related sites through upregulating inhibitory Ser9-phosphorylated GSK-3beta. Choline 42-49 glycogen synthase kinase 3 beta Mus musculus 298-307 27138790-0 2016 Diallyl Disulfide (DADS), a Constituent of Garlic, Inactivates NF-kappaB and Prevents Colitis-Induced Colorectal Cancer by Inhibiting GSK-3beta. diallyl disulfide 0-17 glycogen synthase kinase 3 beta Mus musculus 134-143 27102048-6 2016 RESULTS: Corticosterone (CORT) exposure increased abdominal fat mass and induced expression of lipid synthase acetyl-CoA carboxylase and ATP-citrate lyase with activation of GSK3beta phosphorylation in abdominal adipose tissue of C57BL/6J mice. Corticosterone 9-23 glycogen synthase kinase 3 beta Mus musculus 174-182 27102048-6 2016 RESULTS: Corticosterone (CORT) exposure increased abdominal fat mass and induced expression of lipid synthase acetyl-CoA carboxylase and ATP-citrate lyase with activation of GSK3beta phosphorylation in abdominal adipose tissue of C57BL/6J mice. Corticosterone 25-29 glycogen synthase kinase 3 beta Mus musculus 174-182 27102048-8 2016 In addition, mifepristone treatment reversed the production of H6pdh and attenuated CORT-mediated production of 11ss-HSD1 and lipogenic gene expression with reduction of pSer(9) GSK3beta, thereby leading to improvement of phenotype of adiposity within adipose tissue in mice treated with excess GCs. Mifepristone 13-25 glycogen synthase kinase 3 beta Mus musculus 178-186 27102048-9 2016 Suppression of pSer(9) GSK3beta by mifepristone was accompanied by activation of pThr(308) Akt and blockade of CORT-induced adipogenic transcriptor C/EBPalpha and PPARgamma. Mifepristone 35-47 glycogen synthase kinase 3 beta Mus musculus 23-31 26647425-4 2016 SB216763, a highly selective small molecule inhibitor of GSK3, exerted a protective effect that depended on the potentiated Nrf2 antioxidant response, marked by increased Nrf2 expression and nuclear accumulation and augmented production of the Nrf2 target heme oxygenase-1. SB 216763 0-8 glycogen synthase kinase 3 beta Mus musculus 57-61 26647425-5 2016 Ectopic expression of the kinase-dead mutant of GSK3beta in cultured podocytes reinforced the doxorubicin-induced Nrf2 activation and prevented podocyte injury. Doxorubicin 94-105 glycogen synthase kinase 3 beta Mus musculus 48-56 26647425-6 2016 Conversely, a constitutively active GSK3beta mutant blunted the doxorubicin-induced Nrf2 response and exacerbated podocyte injury, which could be abolished by treatment with SB216763. Doxorubicin 64-75 glycogen synthase kinase 3 beta Mus musculus 36-44 26647425-6 2016 Conversely, a constitutively active GSK3beta mutant blunted the doxorubicin-induced Nrf2 response and exacerbated podocyte injury, which could be abolished by treatment with SB216763. SB 216763 174-182 glycogen synthase kinase 3 beta Mus musculus 36-44 27288435-10 2016 Apoptosis and activation of GSK-3beta (proapoptotic kinase) were significantly lower in the infarct region of hKO-MI group. hko-mi 110-116 glycogen synthase kinase 3 beta Mus musculus 28-37 27053301-6 2016 On the other hand, immunoreactivities and protein levels of Wnt-3, beta-catenin and serine-9-glycogen synthase kinase-3beta (p-GSK-3beta), which are related with morphogenesis, were significantly increased in the granule cell layer of the DG only in the 2 mg/kg TsI-treated-group. tanshinone 262-265 glycogen synthase kinase 3 beta Mus musculus 127-136 27688851-4 2016 We have previously shown that the GSK3 inhibitor, lithium chloride (LiCl), was able to suppress parasitaemia development in a rodent model of malarial infection. Lithium Chloride 50-66 glycogen synthase kinase 3 beta Mus musculus 34-38 27688851-4 2016 We have previously shown that the GSK3 inhibitor, lithium chloride (LiCl), was able to suppress parasitaemia development in a rodent model of malarial infection. Lithium Chloride 68-72 glycogen synthase kinase 3 beta Mus musculus 34-38 27688851-9 2016 Western analysis revealed increased phosphorylation of serine (Ser 9) GSK3beta (by 6.79 to 6.83-fold) in liver samples from infected mice treated with H11809 or FH025 compared to samples from non-infected or non-treated infected mice. Serine 55-61 glycogen synthase kinase 3 beta Mus musculus 70-78 27688851-9 2016 Western analysis revealed increased phosphorylation of serine (Ser 9) GSK3beta (by 6.79 to 6.83-fold) in liver samples from infected mice treated with H11809 or FH025 compared to samples from non-infected or non-treated infected mice. Serine 63-66 glycogen synthase kinase 3 beta Mus musculus 70-78 27688851-11 2016 DBP administration also resulted in increased phosphorylation of Ser 9 GSK3beta compared to controls. Serine 65-68 glycogen synthase kinase 3 beta Mus musculus 71-79 27405597-0 2016 Methane limit LPS-induced NF-kappaB/MAPKs signal in macrophages and suppress immune response in mice by enhancing PI3K/AKT/GSK-3beta-mediated IL-10 expression. Methane 0-7 glycogen synthase kinase 3 beta Mus musculus 123-132 27138790-0 2016 Diallyl Disulfide (DADS), a Constituent of Garlic, Inactivates NF-kappaB and Prevents Colitis-Induced Colorectal Cancer by Inhibiting GSK-3beta. diallyl disulfide 19-23 glycogen synthase kinase 3 beta Mus musculus 134-143 27138790-9 2016 Inhibition of GSK-3beta and loss of nuclear NF-kappaB activity were also observed in vivo in AOM/DSS-treated mice fed a diet supplemented with 85 ppm DADS. dss 97-100 glycogen synthase kinase 3 beta Mus musculus 14-23 27138790-9 2016 Inhibition of GSK-3beta and loss of nuclear NF-kappaB activity were also observed in vivo in AOM/DSS-treated mice fed a diet supplemented with 85 ppm DADS. diallyl disulfide 150-154 glycogen synthase kinase 3 beta Mus musculus 14-23 26984787-6 2016 As Fap1 substrates include Fas and glycogen synthase kinase-3beta (Gsk3beta), increased Fap1 activity in CML is anticipated to induce Fas resistance and stabilization of beta-catenin protein. ammonium ferrous sulfate 134-137 glycogen synthase kinase 3 beta Mus musculus 35-65 25943184-7 2016 These results indicate that the antidepressant-like effect of creatine in the TST depends on the activation of Akt, Nrf2/HO-1, GPx, and mTOR, and GSK3 inhibition. Creatine 62-70 glycogen synthase kinase 3 beta Mus musculus 146-150 26984787-6 2016 As Fap1 substrates include Fas and glycogen synthase kinase-3beta (Gsk3beta), increased Fap1 activity in CML is anticipated to induce Fas resistance and stabilization of beta-catenin protein. ammonium ferrous sulfate 134-137 glycogen synthase kinase 3 beta Mus musculus 67-75 27126914-0 2016 Synthesis and preliminary characterization of radioiodinated benzofuran-3-yl-(indol-3-yl)maleimide derivatives as potential SPECT imaging probes for the detection of glycogen synthase kinase-3beta (GSK-3beta) in the brain. SCHEMBL3254216 61-98 glycogen synthase kinase 3 beta Mus musculus 166-196 27126914-6 2016 These preliminary results suggest that the further optimization of radioiodinated benzofuran-3-yl-(indol-3-yl)maleimide derivatives may facilitate the development of clinically useful SPECT imaging probes for the in vivo detection of GSK-3beta. SCHEMBL3254216 82-119 glycogen synthase kinase 3 beta Mus musculus 234-243 27126914-0 2016 Synthesis and preliminary characterization of radioiodinated benzofuran-3-yl-(indol-3-yl)maleimide derivatives as potential SPECT imaging probes for the detection of glycogen synthase kinase-3beta (GSK-3beta) in the brain. SCHEMBL3254216 61-98 glycogen synthase kinase 3 beta Mus musculus 198-207 27074656-6 2016 In particular, isoflurane increases glycogen synthase kinase-3beta (GSK3beta) phosphorylation at the inhibitory Ser(9) residue and regulates the phosphorylation of multiple proteins downstream and upstream of this promiscuous kinase that regulate diverse biological functions. Isoflurane 15-25 glycogen synthase kinase 3 beta Mus musculus 36-66 27074656-8 2016 We further demonstrate that diverse anesthetics (sevoflurane, urethane, ketamine) produce essentially similar phosphorylation changes on GSK3beta, p44/p42-MAPK, and MAP2 as observed with isoflurane. Urethane 62-70 glycogen synthase kinase 3 beta Mus musculus 137-145 27074656-6 2016 In particular, isoflurane increases glycogen synthase kinase-3beta (GSK3beta) phosphorylation at the inhibitory Ser(9) residue and regulates the phosphorylation of multiple proteins downstream and upstream of this promiscuous kinase that regulate diverse biological functions. Isoflurane 15-25 glycogen synthase kinase 3 beta Mus musculus 68-76 27074656-8 2016 We further demonstrate that diverse anesthetics (sevoflurane, urethane, ketamine) produce essentially similar phosphorylation changes on GSK3beta, p44/p42-MAPK, and MAP2 as observed with isoflurane. Ketamine 72-80 glycogen synthase kinase 3 beta Mus musculus 137-145 27074656-6 2016 In particular, isoflurane increases glycogen synthase kinase-3beta (GSK3beta) phosphorylation at the inhibitory Ser(9) residue and regulates the phosphorylation of multiple proteins downstream and upstream of this promiscuous kinase that regulate diverse biological functions. Serine 112-115 glycogen synthase kinase 3 beta Mus musculus 36-66 27074656-8 2016 We further demonstrate that diverse anesthetics (sevoflurane, urethane, ketamine) produce essentially similar phosphorylation changes on GSK3beta, p44/p42-MAPK, and MAP2 as observed with isoflurane. Isoflurane 187-197 glycogen synthase kinase 3 beta Mus musculus 137-145 27074656-6 2016 In particular, isoflurane increases glycogen synthase kinase-3beta (GSK3beta) phosphorylation at the inhibitory Ser(9) residue and regulates the phosphorylation of multiple proteins downstream and upstream of this promiscuous kinase that regulate diverse biological functions. Serine 112-115 glycogen synthase kinase 3 beta Mus musculus 68-76 27074656-8 2016 We further demonstrate that diverse anesthetics (sevoflurane, urethane, ketamine) produce essentially similar phosphorylation changes on GSK3beta, p44/p42-MAPK, and MAP2 as observed with isoflurane. Sevoflurane 49-60 glycogen synthase kinase 3 beta Mus musculus 137-145 27000529-6 2016 Sakuranetin was also found to inhibit the phosphorylation of AKT at threonine 308 and serine 473 and leads to activation of GSK3beta via decreased phosphorylation at serine 9. sakuranetin 0-11 glycogen synthase kinase 3 beta Mus musculus 124-132 27284979-3 2016 The mechanisms underpinning GSK3 regulation in this context are not completely understood, with some evidence suggesting this occurs through inhibitory N-terminal serine phosphorylation in a similar way to GSK3 inactivation in insulin signaling. Serine 163-169 glycogen synthase kinase 3 beta Mus musculus 28-32 27061850-12 2016 These results indicate that the antidepressant-like effect of agmatine in the TST may be dependent on the activation of AMPA and TrkB receptors, PI3K and mTOR signaling as well as inhibition of GSK-3beta, and increase in synaptic proteins. Agmatine 62-70 glycogen synthase kinase 3 beta Mus musculus 194-203 27287266-13 2016 In the seipin-KO mice, the level of glycogen synthase kinase-3beta (GSK3beta) phosphorylation at Tyr216 was elevated, while at Ser9, it was reduced compared to the WT mice, which were corrected by the rosi treatment but were unaffected by the Abeta25-35 injection. Rosiglitazone 201-205 glycogen synthase kinase 3 beta Mus musculus 68-76 27083516-5 2016 Inhibition of Gsk3b using lithium chloride in Runx2-overexpressing osteoporotic female mice rescued the Wnt/beta-catenin signaling in vivo and completely restored trabecular bone volume by increasing bone formation and decreasing bone resorption. Lithium Chloride 26-42 glycogen synthase kinase 3 beta Mus musculus 14-19 27000529-6 2016 Sakuranetin was also found to inhibit the phosphorylation of AKT at threonine 308 and serine 473 and leads to activation of GSK3beta via decreased phosphorylation at serine 9. Serine 166-172 glycogen synthase kinase 3 beta Mus musculus 124-132 27188603-19 2016 The protein level of GSK3beta in the model, BL, BM, BH, PD98059 and BP groups were increased gradually, while the protein level of p-GSK3beta and p-Bad were decreased gradually. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 56-63 glycogen synthase kinase 3 beta Mus musculus 21-29 26883430-8 2016 In addition, atorvastatin treatment also increased phosphorylation of AKT, inhibited GSK3beta activity by increasing phosphorylation of GSK3beta (Ser9) and decreasing the beta-site APP cleaving enzyme 1 (BACE1) expression. Atorvastatin 13-25 glycogen synthase kinase 3 beta Mus musculus 85-93 26883430-8 2016 In addition, atorvastatin treatment also increased phosphorylation of AKT, inhibited GSK3beta activity by increasing phosphorylation of GSK3beta (Ser9) and decreasing the beta-site APP cleaving enzyme 1 (BACE1) expression. Atorvastatin 13-25 glycogen synthase kinase 3 beta Mus musculus 136-144 26883430-9 2016 These results indicated that the memory ameliorating effect of atorvastatin may be, in part, by regulation the AKT/GSK3beta signaling which may contribute to down-regulation of Abeta1-42 and tau hyperphosphorylation. Atorvastatin 63-75 glycogen synthase kinase 3 beta Mus musculus 115-123 27188603-19 2016 The protein level of GSK3beta in the model, BL, BM, BH, PD98059 and BP groups were increased gradually, while the protein level of p-GSK3beta and p-Bad were decreased gradually. Benzo(a)pyrene 68-70 glycogen synthase kinase 3 beta Mus musculus 21-29 27188603-21 2016 Bufalin may suppress the growth of xenogragts in nude mice by down-regulating the level of ERK and RSK2 phosphorylation, inhibit the proliferation of xenogragts via inactivating GSK3beta and promote apoptosis through down-regulation of p-Bad. bufalin 0-7 glycogen synthase kinase 3 beta Mus musculus 178-186 27140617-10 2016 Treatment with GSK3 inhibitor lithium significantly decreased the serum adiponectin concentration of gsk3(KI) mice and abrogated the difference in C/EBPalpha activity between the genotypes. Lithium 30-37 glycogen synthase kinase 3 beta Mus musculus 15-19 27140617-10 2016 Treatment with GSK3 inhibitor lithium significantly decreased the serum adiponectin concentration of gsk3(KI) mice and abrogated the difference in C/EBPalpha activity between the genotypes. Lithium 30-37 glycogen synthase kinase 3 beta Mus musculus 101-109 27140617-8 2016 Compared with gsk3(WT) mice, gsk3(KI) mice were protected against the development of metabolic syndrome as evident from a markedly lower weight gain, lower total body and liver fat accumulation, better glucose tolerance, stronger hepatic insulin-dependent PKB/Akt phosphorylation, lower serum insulin, cholesterol, and triglyceride levels, as well as higher energy expenditure. Glucose 202-209 glycogen synthase kinase 3 beta Mus musculus 29-37 27050373-9 2016 Further studies showed that AZD1080, a GSK-3beta inhibitor, could also inhibit EC cell proliferation, migration and invasion, while induced cell apoptosis through modulating relevant genes downstream of GSK-3beta signaling. 2-hydroxy-3-(5-((morpholin-4-yl)methyl)pyridin-2-yl)-1H-indole-5-carbonitrile 28-35 glycogen synthase kinase 3 beta Mus musculus 39-48 27140617-8 2016 Compared with gsk3(WT) mice, gsk3(KI) mice were protected against the development of metabolic syndrome as evident from a markedly lower weight gain, lower total body and liver fat accumulation, better glucose tolerance, stronger hepatic insulin-dependent PKB/Akt phosphorylation, lower serum insulin, cholesterol, and triglyceride levels, as well as higher energy expenditure. Cholesterol 302-313 glycogen synthase kinase 3 beta Mus musculus 29-37 27140617-8 2016 Compared with gsk3(WT) mice, gsk3(KI) mice were protected against the development of metabolic syndrome as evident from a markedly lower weight gain, lower total body and liver fat accumulation, better glucose tolerance, stronger hepatic insulin-dependent PKB/Akt phosphorylation, lower serum insulin, cholesterol, and triglyceride levels, as well as higher energy expenditure. Triglycerides 319-331 glycogen synthase kinase 3 beta Mus musculus 29-37 26952045-9 2016 GSK-3beta inhibition by SB216763 mimicked in Kcne2+/+ mice the cardioprotective effects of Kcne2 deletion, but did not further enhance them in Kcne2-/-mice, suggesting that GSK-3beta inactivation was a primary cardioprotective mechanism arising from Kcne2 deletion. SB 216763 24-32 glycogen synthase kinase 3 beta Mus musculus 0-9 26909848-3 2016 In addition, we assessed the effect of PD149163 on glycogen synthase kinase-3 (GSK-3) activity, a downstream molecular target of antipsychotics and mood stabilizers, using phospho-specific antibodies. PD149163 39-47 glycogen synthase kinase 3 beta Mus musculus 51-77 26909848-3 2016 In addition, we assessed the effect of PD149163 on glycogen synthase kinase-3 (GSK-3) activity, a downstream molecular target of antipsychotics and mood stabilizers, using phospho-specific antibodies. PD149163 39-47 glycogen synthase kinase 3 beta Mus musculus 79-84 26909848-6 2016 Interestingly, PD149163 increased the inhibitory serine phosphorylation on both GSK-3alpha and GSK-3beta in a dose- and time-dependent manner in the nucleus accumbens and medial prefrontal cortex of the mice. PD149163 15-23 glycogen synthase kinase 3 beta Mus musculus 95-104 26909848-6 2016 Interestingly, PD149163 increased the inhibitory serine phosphorylation on both GSK-3alpha and GSK-3beta in a dose- and time-dependent manner in the nucleus accumbens and medial prefrontal cortex of the mice. Serine 49-55 glycogen synthase kinase 3 beta Mus musculus 95-104 26909848-7 2016 Moreover, PD149163 inhibited GSK-3 activity in the nucleus accumbens and medial prefrontal cortex in the presence of amphetamine. PD149163 10-18 glycogen synthase kinase 3 beta Mus musculus 29-34 26909848-7 2016 Moreover, PD149163 inhibited GSK-3 activity in the nucleus accumbens and medial prefrontal cortex in the presence of amphetamine. Amphetamine 117-128 glycogen synthase kinase 3 beta Mus musculus 29-34 26909848-8 2016 Thus, like most current antipsychotics and mood stabilizers, PD149163 inhibited GSK-3 activity in cortico-striatal circuitry. PD149163 61-69 glycogen synthase kinase 3 beta Mus musculus 80-85 27050373-9 2016 Further studies showed that AZD1080, a GSK-3beta inhibitor, could also inhibit EC cell proliferation, migration and invasion, while induced cell apoptosis through modulating relevant genes downstream of GSK-3beta signaling. 2-hydroxy-3-(5-((morpholin-4-yl)methyl)pyridin-2-yl)-1H-indole-5-carbonitrile 28-35 glycogen synthase kinase 3 beta Mus musculus 203-212 27050373-13 2016 GSK-3beta inhibitor AZD1080 may be an effective drug for treating endometrial carcinoma. 2-hydroxy-3-(5-((morpholin-4-yl)methyl)pyridin-2-yl)-1H-indole-5-carbonitrile 20-27 glycogen synthase kinase 3 beta Mus musculus 0-9 26026611-0 2016 Cadmium-induced cell death of basal forebrain cholinergic neurons mediated by muscarinic M1 receptor blockade, increase in GSK-3beta enzyme, beta-amyloid and tau protein levels. Cadmium 0-7 glycogen synthase kinase 3 beta Mus musculus 123-132 26950856-5 2016 These effects were abrogated by BAY 60-2770 as well as cyclosporin A and SB-216763, which prevented mPTP opening and inhibited glycogen synthase kinase-3beta (GSK-3beta), respectively. 4-(((4-carboxybutyl) (2- (5-fluoro-2-((4'-(trifluoromethyl) biphenyl-4-yl)methoxy)phenyl)ethyl) amino)methyl)benzoic acid 32-43 glycogen synthase kinase 3 beta Mus musculus 127-157 26950856-5 2016 These effects were abrogated by BAY 60-2770 as well as cyclosporin A and SB-216763, which prevented mPTP opening and inhibited glycogen synthase kinase-3beta (GSK-3beta), respectively. 4-(((4-carboxybutyl) (2- (5-fluoro-2-((4'-(trifluoromethyl) biphenyl-4-yl)methoxy)phenyl)ethyl) amino)methyl)benzoic acid 32-43 glycogen synthase kinase 3 beta Mus musculus 159-168 26950856-5 2016 These effects were abrogated by BAY 60-2770 as well as cyclosporin A and SB-216763, which prevented mPTP opening and inhibited glycogen synthase kinase-3beta (GSK-3beta), respectively. Cyclosporine 55-68 glycogen synthase kinase 3 beta Mus musculus 127-157 26950856-5 2016 These effects were abrogated by BAY 60-2770 as well as cyclosporin A and SB-216763, which prevented mPTP opening and inhibited glycogen synthase kinase-3beta (GSK-3beta), respectively. Cyclosporine 55-68 glycogen synthase kinase 3 beta Mus musculus 159-168 26950856-5 2016 These effects were abrogated by BAY 60-2770 as well as cyclosporin A and SB-216763, which prevented mPTP opening and inhibited glycogen synthase kinase-3beta (GSK-3beta), respectively. SB 216763 73-82 glycogen synthase kinase 3 beta Mus musculus 127-157 26950856-5 2016 These effects were abrogated by BAY 60-2770 as well as cyclosporin A and SB-216763, which prevented mPTP opening and inhibited glycogen synthase kinase-3beta (GSK-3beta), respectively. SB 216763 73-82 glycogen synthase kinase 3 beta Mus musculus 159-168 26950856-6 2016 Western blots of WT and HO-1(-/-) enterocytes indicated that GSK-3beta phosphorylation on Ser(9) (inhibitory site) was reduced by half following I/R alone (increased GSK-3beta activity) and increased by one-third (reduced GSK-3beta activity) following BAY 60-2770. Serine 90-93 glycogen synthase kinase 3 beta Mus musculus 61-70 26452072-11 2016 Our results suggest that CS increases lung EC permeability, thereby enhancing susceptibility to ALI, likely through oxidative stress-induced Akt inactivation and subsequent GSK-3beta activation. Cesium 25-27 glycogen synthase kinase 3 beta Mus musculus 173-182 26452072-12 2016 Activated GSK-3beta may activate HDAC6 via phosphorylation of serine-22, leading to alpha-tubulin deacetylation and microtubule disassembly. Serine 62-68 glycogen synthase kinase 3 beta Mus musculus 10-19 26026611-5 2016 Moreover, cadmium has been described to activate GSK-3beta, induce Abeta protein production and tau filament formation, which have been related to a selective loss of basal forebrain cholinergic neurons and development of AD. Cadmium 10-17 glycogen synthase kinase 3 beta Mus musculus 49-58 26026611-7 2016 For this purpose, we evaluated, in SN56 cholinergic mourine septal cell line from basal forebrain region, the cadmium toxic effects on neuronal viability through muscarinic M1 receptor, AChE splice variants, GSK-3beta enzyme, Abeta and tau proteins. Cadmium 110-117 glycogen synthase kinase 3 beta Mus musculus 208-217 26026611-8 2016 This study proves that cadmium induces cell death on cholinergic neurons through blockade of M1 receptor, overexpression of AChE-S and GSK-3beta, down-regulation of AChE-R and increase in Abeta and total and phosphorylated tau protein levels. Cadmium 23-30 glycogen synthase kinase 3 beta Mus musculus 135-144 26854125-6 2016 SOMCL-668 also rapidly promoted the phosphorylation of GSK3beta (Ser-9) in an allosteric manner in vitro. 3-methylphenyl-2,3,4,5-tetrahydro-1H-benzo(d)azepin-7-ol 0-9 glycogen synthase kinase 3 beta Mus musculus 55-63 26686692-11 2016 MbetaCD and Cav-1 siRNA knockdown increased OM-induced AMPK, Akt, GSK3beta, and CREB phosphorylation, which were reversed by Ara-A, a specific AMPK inhibitor. methyl-beta-cyclodextrin 0-7 glycogen synthase kinase 3 beta Mus musculus 66-74 26686692-11 2016 MbetaCD and Cav-1 siRNA knockdown increased OM-induced AMPK, Akt, GSK3beta, and CREB phosphorylation, which were reversed by Ara-A, a specific AMPK inhibitor. Vidarabine 125-130 glycogen synthase kinase 3 beta Mus musculus 66-74 26854125-6 2016 SOMCL-668 also rapidly promoted the phosphorylation of GSK3beta (Ser-9) in an allosteric manner in vitro. Serine 65-68 glycogen synthase kinase 3 beta Mus musculus 55-63 26876299-5 2016 Podocyte-specific somatic ablation of GSK3beta in adult mice attenuated proteinuria and ameliorated podocyte injury and glomerular damage in experimental adriamycin (ADR) nephropathy. Doxorubicin 154-164 glycogen synthase kinase 3 beta Mus musculus 38-46 26702935-13 2016 CONCLUSION: Naringin prevented intestinal tumorigenesis likely through a collection of activities including anti-proliferation, induction of apoptosis, modulation of GSK-3beta and APC/beta-catenin pathways and anti-inflammation. naringin 12-20 glycogen synthase kinase 3 beta Mus musculus 166-175 27050422-0 2016 Quercetin Protects against Okadaic Acid-Induced Injury via MAPK and PI3K/Akt/GSK3beta Signaling Pathways in HT22 Hippocampal Neurons. Quercetin 0-9 glycogen synthase kinase 3 beta Mus musculus 77-85 27279698-5 2016 In addition, brain-derived neurotrophic factor proteins wee elevated and Akt/GSK-3/cAMP response element-binding protein signaling was activated in the combination group. Cyclic AMP 83-87 glycogen synthase kinase 3 beta Mus musculus 77-82 26968952-5 2016 The suppression of beta-catenin was seen with CoQ0 administration accompanied by a decrease in the expression of Wnt/beta-catenin transcriptional target c-myc, cyclin D1, and survivin through GSK3beta-independent pathway. ubiquinone-O 46-50 glycogen synthase kinase 3 beta Mus musculus 192-200 27092510-3 2016 When a dye-tethered and prephosphorylated (primed) peptide substrate for GSK3 was employed, a distinct mobility shift in the fluorescent bands on the agarose was observed by GSK3-induced phosphorylation of the primed peptides. Sepharose 150-157 glycogen synthase kinase 3 beta Mus musculus 73-77 27092510-3 2016 When a dye-tethered and prephosphorylated (primed) peptide substrate for GSK3 was employed, a distinct mobility shift in the fluorescent bands on the agarose was observed by GSK3-induced phosphorylation of the primed peptides. Sepharose 150-157 glycogen synthase kinase 3 beta Mus musculus 174-178 26976650-4 2016 METHODS AND RESULTS: We generated tamoxifen-inducible cardiac myocyte-specific mice lacking both GSK-3 isoforms (double knockout). Tamoxifen 34-43 glycogen synthase kinase 3 beta Mus musculus 97-102 27050422-0 2016 Quercetin Protects against Okadaic Acid-Induced Injury via MAPK and PI3K/Akt/GSK3beta Signaling Pathways in HT22 Hippocampal Neurons. Okadaic Acid 27-39 glycogen synthase kinase 3 beta Mus musculus 77-85 27053198-3 2016 Here, we unraveled the molecular mechanism underlying this phenomenon, which led to a novel pharmacological approach for the promotion of functional recovery after nerve injury.In vitroandin vivoanalysis of GSK3 single knock-in mice revealed the unexpected contribution of GSK3alpha in addition to GSK3beta, as both GSK3(S/A) knock-ins improved axon regeneration. vitroandin 180-190 glycogen synthase kinase 3 beta Mus musculus 207-211 27050422-9 2016 Moreover, pre-treatment with quercetin not only inhibited OA-induced apoptosis via the reduction of Bax, and up-regulation of cleaved caspase 3, but also via the inhibition of PI3K/Akt/GSK3beta, MAPKs and activation of NF-kappaB p65. Quercetin 29-38 glycogen synthase kinase 3 beta Mus musculus 185-193 26778780-9 2016 Administration of AR-A01, a selective GSK-3beta inhibitor, or diethyldithiocarbamic acid (DDTC), a selective NF-kB inhibitor, diminished acute stress-induced behavioral and biochemical changes. ar-a01 18-24 glycogen synthase kinase 3 beta Mus musculus 38-47 26996481-10 2016 The GSK-3beta activity increased, and expression of beta-catenin decreased significantly in the hippocampus of the CIH-exposed mice. cih 115-118 glycogen synthase kinase 3 beta Mus musculus 4-13 26996481-12 2016 Meanwhile, LiCl decreased the activity of GSK-3beta and increased the expression of beta-catenin and partially reversed the spatial memory deficits in MWM and the apoptosis caused by CIH. Lithium Chloride 11-15 glycogen synthase kinase 3 beta Mus musculus 42-51 26923231-0 2016 Bisphenol A disrupts glucose transport and neurophysiological role of IR/IRS/AKT/GSK3beta axis in the brain of male mice. bisphenol A 0-11 glycogen synthase kinase 3 beta Mus musculus 81-89 26923231-6 2016 Meanwhile, hyperactivation of IR/IRS/AKT/GSK3beta axis was detected in the brain of BPA treated mice. bisphenol A 84-87 glycogen synthase kinase 3 beta Mus musculus 41-49 26750157-6 2016 Furthermore, Norgestrel initiated a bFGF-dependent inactivation of glycogen synthase kinase 3beta (GSK3beta) through phosphorylation at serine 9. Norgestrel 13-23 glycogen synthase kinase 3 beta Mus musculus 67-97 26849944-8 2016 Moreover, FF-induced amelioration of diabetic renal damage, including the stimulation of PI3K/Akt/GSK-3beta/Fyn pathway and the enhancement of Nrf2 function were abolished in FGF21-null mice, confirming the critical role of FGF21 in FF-induced renal protection. Fenofibrate 10-12 glycogen synthase kinase 3 beta Mus musculus 98-107 26750157-6 2016 Furthermore, Norgestrel initiated a bFGF-dependent inactivation of glycogen synthase kinase 3beta (GSK3beta) through phosphorylation at serine 9. Norgestrel 13-23 glycogen synthase kinase 3 beta Mus musculus 99-107 26750157-6 2016 Furthermore, Norgestrel initiated a bFGF-dependent inactivation of glycogen synthase kinase 3beta (GSK3beta) through phosphorylation at serine 9. Serine 136-142 glycogen synthase kinase 3 beta Mus musculus 67-97 26750157-6 2016 Furthermore, Norgestrel initiated a bFGF-dependent inactivation of glycogen synthase kinase 3beta (GSK3beta) through phosphorylation at serine 9. Serine 136-142 glycogen synthase kinase 3 beta Mus musculus 99-107 26750157-8 2016 Specific inhibition of both the PKA and GSK3beta pathways prevented Norgestrel-mediated neuroprotection of stressed photoreceptor cells in vitro. Norgestrel 68-78 glycogen synthase kinase 3 beta Mus musculus 40-48 26750157-10 2016 Therefore, these results indicate that the protective efficacy of Norgestrel is, at least in part, due to the bFGF-mediated activation of the PKA pathway, with subsequent inactivation of GSK3beta. Norgestrel 66-76 glycogen synthase kinase 3 beta Mus musculus 187-195 26882203-7 2016 Moreover, melatonin prevented the cisplatin-induced activating phosphorylation of AKT, GSK3beta, and FOXO3a, all of which trigger follicle activation. Melatonin 10-19 glycogen synthase kinase 3 beta Mus musculus 87-95 26882203-7 2016 Moreover, melatonin prevented the cisplatin-induced activating phosphorylation of AKT, GSK3beta, and FOXO3a, all of which trigger follicle activation. Cisplatin 34-43 glycogen synthase kinase 3 beta Mus musculus 87-95 27003207-7 2016 This protective effect correlates with the inability of Abeta to activate GSK3beta, is mimicked by GSK3beta inhibition with SB126763 (in slices obtained from sedentary mice), and is abolished by the inhibition of PI3K with LY294002 (in slices obtained from mice that exercised). sb126763 124-132 glycogen synthase kinase 3 beta Mus musculus 99-107 26650187-4 2016 In mice with polymicrobial abdominal sepsis or more severe sepsis induced by the combination of hemorrhage and intraabdominal infection, administration of the AMPK activator metformin or the GSK3beta inhibitor SB216763 reduced the severity of acute lung injury (ALI). SB 216763 210-218 glycogen synthase kinase 3 beta Mus musculus 191-199 26773468-6 2016 Interestingly, inhibition of GSK3-mediated MAP1B phosphorylation in map1b-cDNA-transfected fibroblasts protects both tyrosinated and acetylated MTs from nocodazole-induced depolymerization, while detyrosinated MTs are less abundant in the presence of MAP1B. tyrosinated 117-128 glycogen synthase kinase 3 beta Mus musculus 29-33 26773468-6 2016 Interestingly, inhibition of GSK3-mediated MAP1B phosphorylation in map1b-cDNA-transfected fibroblasts protects both tyrosinated and acetylated MTs from nocodazole-induced depolymerization, while detyrosinated MTs are less abundant in the presence of MAP1B. Nocodazole 153-163 glycogen synthase kinase 3 beta Mus musculus 29-33 27003207-7 2016 This protective effect correlates with the inability of Abeta to activate GSK3beta, is mimicked by GSK3beta inhibition with SB126763 (in slices obtained from sedentary mice), and is abolished by the inhibition of PI3K with LY294002 (in slices obtained from mice that exercised). 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 223-231 glycogen synthase kinase 3 beta Mus musculus 99-107 26762765-1 2016 In this study, we show that reduction of glucose concentration increases TR4 expression in 3T3-L1 cells via stimulation of the GSK-3beta-CREB pathway. Glucose 41-48 glycogen synthase kinase 3 beta Mus musculus 127-136 26762765-3 2016 In addition, CREB enhanced murine TR4 promoter activity via direct binding to a cAMP response element located in the promoter, and this CREB effect was further strengthened by GSK-3beta. Cyclic AMP 80-84 glycogen synthase kinase 3 beta Mus musculus 176-185 26772151-7 2016 Administration of the antidepressant fluoxetine or the GSK3 inhibitor TDZD-8 reduced the stress-induced increases of most hippocampal cytokines and chemokines. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 70-76 glycogen synthase kinase 3 beta Mus musculus 55-59 26789651-6 2016 Synapse-related molecule synaptophysin was enhanced, and CRMP-2, AMPA receptor, and GSK-3beta were declined in spinal cord of Fasudil-treated mice. fasudil 126-133 glycogen synthase kinase 3 beta Mus musculus 84-93 26749572-3 2016 These deficits are all evident in GSK3alpha/beta knockin mice, in which serine-to-alanine mutations block the inhibitory serine phosphorylation regulation of both GSK3 isoforms, leaving GSK3 hyperactive. Serine 72-78 glycogen synthase kinase 3 beta Mus musculus 34-38 26749572-3 2016 These deficits are all evident in GSK3alpha/beta knockin mice, in which serine-to-alanine mutations block the inhibitory serine phosphorylation regulation of both GSK3 isoforms, leaving GSK3 hyperactive. Serine 72-78 glycogen synthase kinase 3 beta Mus musculus 163-167 26749572-3 2016 These deficits are all evident in GSK3alpha/beta knockin mice, in which serine-to-alanine mutations block the inhibitory serine phosphorylation regulation of both GSK3 isoforms, leaving GSK3 hyperactive. Alanine 82-89 glycogen synthase kinase 3 beta Mus musculus 34-38 26749572-3 2016 These deficits are all evident in GSK3alpha/beta knockin mice, in which serine-to-alanine mutations block the inhibitory serine phosphorylation regulation of both GSK3 isoforms, leaving GSK3 hyperactive. Alanine 82-89 glycogen synthase kinase 3 beta Mus musculus 163-167 26749572-3 2016 These deficits are all evident in GSK3alpha/beta knockin mice, in which serine-to-alanine mutations block the inhibitory serine phosphorylation regulation of both GSK3 isoforms, leaving GSK3 hyperactive. Serine 121-127 glycogen synthase kinase 3 beta Mus musculus 34-38 26749572-3 2016 These deficits are all evident in GSK3alpha/beta knockin mice, in which serine-to-alanine mutations block the inhibitory serine phosphorylation regulation of both GSK3 isoforms, leaving GSK3 hyperactive. Serine 121-127 glycogen synthase kinase 3 beta Mus musculus 163-167 26350746-0 2016 Caffeine inhibits adipogenesis through modulation of mitotic clonal expansion and the AKT/GSK3 pathway in 3T3-L1 adipocytes. Caffeine 0-8 glycogen synthase kinase 3 beta Mus musculus 90-94 26927057-6 2016 Moreover, DNJ increased the phosphorylation of phosphatidylinositol 3 kinase (PI3K) on p85, protein kinase B (PKB) on Ser473, glycogen synthase kinase 3beta (GSK-3beta) on Ser9, and inhibited phosphorylation of glycogen synthase (GS) on Ser645 in liver tissue of db/db mice. 1-Deoxynojirimycin 10-13 glycogen synthase kinase 3 beta Mus musculus 126-156 26927057-6 2016 Moreover, DNJ increased the phosphorylation of phosphatidylinositol 3 kinase (PI3K) on p85, protein kinase B (PKB) on Ser473, glycogen synthase kinase 3beta (GSK-3beta) on Ser9, and inhibited phosphorylation of glycogen synthase (GS) on Ser645 in liver tissue of db/db mice. 1-Deoxynojirimycin 10-13 glycogen synthase kinase 3 beta Mus musculus 158-167 26927057-7 2016 These results demonstrate that DNJ can increase hepatic insulin sensitivity via strengthening of the insulin-stimulated PKB/GSK-3beta signal pathway and by modulating glucose metabolic enzymes in db/db mice. 1-Deoxynojirimycin 31-34 glycogen synthase kinase 3 beta Mus musculus 124-133 26890140-6 2016 In vitro, Ang2 aggravated high glucose-induced astrocyte apoptosis via GSK-3beta activation. Glucose 31-38 glycogen synthase kinase 3 beta Mus musculus 71-80 26891291-7 2016 miR-9-5p, miR-675-5p, and miR-138-5p targeted glycogen synthase kinase 3 beta (GSK3beta), ATPase Aminophospholipid Transporter Class I Type 8A Member 2 (ATP8A2), and Eukaryotic Translation Initiation Factor 4E Binding Protein 1 (EIF4EBP1), respectively. mir-9-5p 0-8 glycogen synthase kinase 3 beta Mus musculus 46-77 26891291-7 2016 miR-9-5p, miR-675-5p, and miR-138-5p targeted glycogen synthase kinase 3 beta (GSK3beta), ATPase Aminophospholipid Transporter Class I Type 8A Member 2 (ATP8A2), and Eukaryotic Translation Initiation Factor 4E Binding Protein 1 (EIF4EBP1), respectively. mir-9-5p 0-8 glycogen synthase kinase 3 beta Mus musculus 79-87 26751161-4 2016 Here, we present a class of isonicotinamides that are potent, highly kinase-selective GSK-3 inhibitors, the members of which demonstrated oral activity in a triple-transgenic mouse model of AD. isonicotinamide 28-44 glycogen synthase kinase 3 beta Mus musculus 86-91 26872261-6 2016 Western blot analyses of extracts of ex vivo-perfused murine hearts also revealed that rhCCN2 evoked concentration-dependent increase of cardiac phospho-GSK3beta (serine-9) contents. Serine 163-169 glycogen synthase kinase 3 beta Mus musculus 153-161 26872261-8 2016 Mechanistically, this postconditioning effect of rhCCN2 appeared to be mediated by activation of the reperfusion injury salvage kinase pathway as demonstrated by sensitivity to PI3 kinase inhibition and increased CCN2-induced phosphorylation of GSK3beta (Ser-9). Serine 255-258 glycogen synthase kinase 3 beta Mus musculus 245-253 26350746-6 2016 Our data show that caffeine is an anti-adipogenic bioactive compound involved in the modulation of mitotic clonal expansion during adipocyte differentiation through the AKT/GSK3 pathway. Caffeine 19-27 glycogen synthase kinase 3 beta Mus musculus 173-177 26637370-0 2016 2-Deoxy-Glucose Downregulates Endothelial AKT and ERK via Interference with N-Linked Glycosylation, Induction of Endoplasmic Reticulum Stress, and GSK3beta Activation. Deoxyglucose 0-15 glycogen synthase kinase 3 beta Mus musculus 147-155 26320084-4 2016 AIMS: We investigated whether delivery of the GSK3beta inhibitor, lithium chloride (LiCl), during the recovery period from acute DSS-induced colitis in mice promoted colonic regeneration and ameliorated disease symptoms. Lithium Chloride 66-82 glycogen synthase kinase 3 beta Mus musculus 46-54 26320084-4 2016 AIMS: We investigated whether delivery of the GSK3beta inhibitor, lithium chloride (LiCl), during the recovery period from acute DSS-induced colitis in mice promoted colonic regeneration and ameliorated disease symptoms. Lithium Chloride 84-88 glycogen synthase kinase 3 beta Mus musculus 46-54 26320084-4 2016 AIMS: We investigated whether delivery of the GSK3beta inhibitor, lithium chloride (LiCl), during the recovery period from acute DSS-induced colitis in mice promoted colonic regeneration and ameliorated disease symptoms. dss 129-132 glycogen synthase kinase 3 beta Mus musculus 46-54 26527066-8 2016 Propranolol treatment decreased serum FGF23 and loss of renal calcium and phosphate and increased serum phosphate concentration in gsk3(KI) mice. Propranolol 0-11 glycogen synthase kinase 3 beta Mus musculus 131-135 26690975-6 2016 Meanwhile, Hepatic glycogen synthesis was promoted by Ib-FUC via activation of the PI3K/PKB/GSK-3beta signaling and regulation of glucose metabolism-related enzymatic activities. Glycogen 19-27 glycogen synthase kinase 3 beta Mus musculus 92-101 26637370-4 2016 Downregulation of these critical survival pathways is shown to be due to 2-DG"s interference with N-linked glycosylation, leading to alterations in VEGFR2 (and downstream signaling) as well as induction of endoplasmic reticulum (ER) stress, GSK3beta activation, and apoptosis. Deoxyglucose 73-77 glycogen synthase kinase 3 beta Mus musculus 241-249 26637370-4 2016 Downregulation of these critical survival pathways is shown to be due to 2-DG"s interference with N-linked glycosylation, leading to alterations in VEGFR2 (and downstream signaling) as well as induction of endoplasmic reticulum (ER) stress, GSK3beta activation, and apoptosis. Nitrogen 98-99 glycogen synthase kinase 3 beta Mus musculus 241-249 26785133-13 2016 Thus, inhibition of GSK-3beta activity by insulin alone or together with LiCl raised the expression of genes and some proteins central to the metabolic activity of mitochondria resulting in higher ATP synthesis and accelerated myogenesis. Adenosine Triphosphate 197-200 glycogen synthase kinase 3 beta Mus musculus 20-29 26384655-5 2016 Mice were subjected to HI at postnatal day (PND) 9 and treated with a selective GSK3beta inhibitor, SB216763. SB 216763 100-108 glycogen synthase kinase 3 beta Mus musculus 80-88 26384655-7 2016 Our results show that HI reduced phosphorylation of GSK3beta, thus promoting its kinase activity. hi 22-24 glycogen synthase kinase 3 beta Mus musculus 52-60 26384655-8 2016 The GSK3beta inhibitor reduced caspase-3 activation and neuronal cell death elicited by HI and reverted the effects of HI on gene expression of the anti-oxidant enzyme sod2 and mitochondrial factor pgc1alpha. hi 88-90 glycogen synthase kinase 3 beta Mus musculus 4-12 26384655-8 2016 The GSK3beta inhibitor reduced caspase-3 activation and neuronal cell death elicited by HI and reverted the effects of HI on gene expression of the anti-oxidant enzyme sod2 and mitochondrial factor pgc1alpha. hi 119-121 glycogen synthase kinase 3 beta Mus musculus 4-12 26384655-10 2016 Further, GSK3beta inhibition reduced HI-induced gene expression of pro-inflammatory cytokines tnfalpha and Il-6, while promoted the anti-inflammatory factor Il-10. hi 37-39 glycogen synthase kinase 3 beta Mus musculus 9-17 26822034-4 2016 Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs. Serine 49-52 glycogen synthase kinase 3 beta Mus musculus 37-45 26822034-4 2016 Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs. Serine 49-52 glycogen synthase kinase 3 beta Mus musculus 239-247 26822034-4 2016 Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs. dsbs 131-135 glycogen synthase kinase 3 beta Mus musculus 37-45 26822034-4 2016 Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs. dsbs 131-135 glycogen synthase kinase 3 beta Mus musculus 239-247 26822034-4 2016 Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs. dsbs 289-293 glycogen synthase kinase 3 beta Mus musculus 37-45 26822034-4 2016 Here we show that phosphorylation of GSK3beta on Ser(389) by p38 MAPK (mitogen-activated protein kinase) is induced selectively by DSBs through ATM (ataxia telangiectasia mutated) as a unique mechanism to attenuate the activity of nuclear GSK3beta and promote survival of cells undergoing DSBs. dsbs 289-293 glycogen synthase kinase 3 beta Mus musculus 239-247 26822034-5 2016 Inability to inactivate GSK3beta through Ser(389) phosphorylation in Ser(389)Ala knockin mice causes a decrease in the fitness of cells undergoing V(D)J recombination and CSR. Serine 41-44 glycogen synthase kinase 3 beta Mus musculus 24-32 26822034-6 2016 Preselection-Tcrbeta repertoire is impaired and antigen-specific IgG antibody responses following immunization are blunted in Ser(389)GSK3beta knockin mice. Serine 126-129 glycogen synthase kinase 3 beta Mus musculus 134-142 26290374-8 2016 Inhibition of protein phosphatase 2A (PP2A) with okadaic acid reproduced the effects of D2R downregulation on Akt, GSK3beta, and cyclin D1. Okadaic Acid 49-61 glycogen synthase kinase 3 beta Mus musculus 115-123 26822034-0 2016 Inactivation of nuclear GSK3beta by Ser(389) phosphorylation promotes lymphocyte fitness during DNA double-strand break response. Serine 36-39 glycogen synthase kinase 3 beta Mus musculus 24-32 26085056-8 2016 The high expression of GSK-3beta and low expression of IGF1R in the hippocampus of pups may contribute to the neurotoxicity associated with maternal Pb exposure. Lead 149-151 glycogen synthase kinase 3 beta Mus musculus 23-32 26582204-8 2016 On the molecular level, GSKIP deficiency resulted in decreased phosphorylation of GSK3beta at Ser-9 starting early in development (embryonic day 10.5), leading to enhanced GSK3beta activity. Serine 94-97 glycogen synthase kinase 3 beta Mus musculus 82-90 26454089-4 2016 We conclude that rotenone-induced insulin resistance involves a p38MAPK-dependent mechanism for the inhibition of the proximal end of insulin signaling (IRS1), and a p38MAPK-independent mechanism for the inhibition of the distal end (AKT and GSK3beta). Rotenone 17-25 glycogen synthase kinase 3 beta Mus musculus 242-250 27161213-1 2016 AIM: Glycogen synthase kinase 3 (GSK3) regulates urine concentration by mediating the vasopressin-induced aquaporin 2 expression and water permeability, although it is unknown whether GSK3 also mediates the accumulation of the urea transporter A1 (UT-A1). Water 133-138 glycogen synthase kinase 3 beta Mus musculus 5-31 27057548-0 2016 Isoflurane Is More Deleterious to Developing Brain Than Desflurane: The Role of the Akt/GSK3beta Signaling Pathway. Isoflurane 0-10 glycogen synthase kinase 3 beta Mus musculus 88-96 27057548-5 2016 The phosphorylation levels of Akt/GSK3beta and learning and memory were examined after intervention with lithium. Lithium 105-112 glycogen synthase kinase 3 beta Mus musculus 34-42 27057548-7 2016 Accompanied by behavioral change, only isoflurane decreased p-Akt (ser473) and p-GSK3beta (ser9) expressions, which led to GSK3beta overactivation. Isoflurane 39-49 glycogen synthase kinase 3 beta Mus musculus 81-89 27057548-7 2016 Accompanied by behavioral change, only isoflurane decreased p-Akt (ser473) and p-GSK3beta (ser9) expressions, which led to GSK3beta overactivation. Isoflurane 39-49 glycogen synthase kinase 3 beta Mus musculus 123-131 27057548-8 2016 Lithium prevented GSK3beta overactivation and alleviated isoflurane-induced cognitive deficits. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 18-26 27057548-9 2016 These results suggest that isoflurane is more likely to induce developmental neurotoxicity than desflurane in context of multiple exposures and that the Akt/GSK3beta signaling pathway partly participates in this process. Isoflurane 27-37 glycogen synthase kinase 3 beta Mus musculus 157-165 26484916-7 2016 Activity of PP2A negatively correlated to the level of phosphorylated GSK-3beta in kainic acid-induced excitotoxic mouse brain. Kainic Acid 83-94 glycogen synthase kinase 3 beta Mus musculus 70-79 27294151-0 2016 Nanoparticle Delivered Human Biliverdin Reductase-Based Peptide Increases Glucose Uptake by Activating IRK/Akt/GSK3 Axis: The Peptide Is Effective in the Cell and Wild-Type and Diabetic Ob/Ob Mice. Glucose 74-81 glycogen synthase kinase 3 beta Mus musculus 111-115 25577170-9 2016 Atorvastatin treatment increased the expression levels of p85alphaPI3K, phosphorylated Akt, phosphorylated glycogen synthase kinase-3beta, phosphorylated ERK, and Bcl-2, which are proteins related to survival. Atorvastatin 0-12 glycogen synthase kinase 3 beta Mus musculus 107-137 26850346-0 2016 Baicalin attenuates high fat diet-induced insulin resistance and ectopic fat storage in skeletal muscle, through modulating the protein kinase B/Glycogen synthase kinase 3 beta pathway. baicalin 0-8 glycogen synthase kinase 3 beta Mus musculus 145-176 27478647-4 2016 Unexpectedly, floating behaviour and brain glycogen synthase kinase-3 beta (GSK-3beta) mRNA levels, a factor of synaptic plasticity as well as a marker of distress and depression, were increased during the additional swimming session that was prevented by imipramine. Imipramine 256-266 glycogen synthase kinase 3 beta Mus musculus 43-74 27478647-4 2016 Unexpectedly, floating behaviour and brain glycogen synthase kinase-3 beta (GSK-3beta) mRNA levels, a factor of synaptic plasticity as well as a marker of distress and depression, were increased during the additional swimming session that was prevented by imipramine. Imipramine 256-266 glycogen synthase kinase 3 beta Mus musculus 76-85 27161213-1 2016 AIM: Glycogen synthase kinase 3 (GSK3) regulates urine concentration by mediating the vasopressin-induced aquaporin 2 expression and water permeability, although it is unknown whether GSK3 also mediates the accumulation of the urea transporter A1 (UT-A1). Water 133-138 glycogen synthase kinase 3 beta Mus musculus 33-37 27738547-0 2016 Neuroprotective Effects of Salidroside in the MPTP Mouse Model of Parkinson"s Disease: Involvement of the PI3K/Akt/GSK3beta Pathway. rhodioloside 27-38 glycogen synthase kinase 3 beta Mus musculus 115-123 27143997-9 2016 Moreover, LY294002 and GDC-0449 pretreatment both induced phosphorylated GSK-3beta downregulation and significantly promoted apoptosis induced by TMT. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 10-18 glycogen synthase kinase 3 beta Mus musculus 73-82 27143997-9 2016 Moreover, LY294002 and GDC-0449 pretreatment both induced phosphorylated GSK-3beta downregulation and significantly promoted apoptosis induced by TMT. HhAntag691 23-31 glycogen synthase kinase 3 beta Mus musculus 73-82 27738547-2 2016 Our in vitro experiments suggested that salidroside (Sal) could protect against 1-methyl-4-phenylpyridine-induced cell apoptosis in part by regulating the PI3K/Akt/GSK3beta pathway. rhodioloside 40-51 glycogen synthase kinase 3 beta Mus musculus 164-172 27738547-2 2016 Our in vitro experiments suggested that salidroside (Sal) could protect against 1-methyl-4-phenylpyridine-induced cell apoptosis in part by regulating the PI3K/Akt/GSK3beta pathway. rhodioloside 53-56 glycogen synthase kinase 3 beta Mus musculus 164-172 27738547-2 2016 Our in vitro experiments suggested that salidroside (Sal) could protect against 1-methyl-4-phenylpyridine-induced cell apoptosis in part by regulating the PI3K/Akt/GSK3beta pathway. 1-Methyl-4-phenylpyridinium 80-105 glycogen synthase kinase 3 beta Mus musculus 164-172 27738547-7 2016 Furthermore, Sal could increase the phosphorylation level of Akt and GSK3beta, upregulate the ratio of Bcl-2/Bax, and inhibit the activation of caspase-3, caspase-6, and caspase-9. rhodioloside 13-16 glycogen synthase kinase 3 beta Mus musculus 69-77 27738547-8 2016 These results show that Sal prevents the loss of dopaminergic neurons and the PI3K/Akt/GSK3beta pathway signaling pathway may have mediated the protection of Sal against MPTP, suggesting that Sal may be a potential candidate in neuroprotective treatment for PD. rhodioloside 158-161 glycogen synthase kinase 3 beta Mus musculus 87-95 27738547-8 2016 These results show that Sal prevents the loss of dopaminergic neurons and the PI3K/Akt/GSK3beta pathway signaling pathway may have mediated the protection of Sal against MPTP, suggesting that Sal may be a potential candidate in neuroprotective treatment for PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 170-174 glycogen synthase kinase 3 beta Mus musculus 87-95 27738547-8 2016 These results show that Sal prevents the loss of dopaminergic neurons and the PI3K/Akt/GSK3beta pathway signaling pathway may have mediated the protection of Sal against MPTP, suggesting that Sal may be a potential candidate in neuroprotective treatment for PD. rhodioloside 158-161 glycogen synthase kinase 3 beta Mus musculus 87-95 26498061-11 2015 In addition, we found that 6-gingerol induced phosphorylations of glycogen synthase kinase-3beta(GSK-3beta), and promoted the nuclear accumulation of beta-catenin. gingerol 27-37 glycogen synthase kinase 3 beta Mus musculus 66-96 26498061-11 2015 In addition, we found that 6-gingerol induced phosphorylations of glycogen synthase kinase-3beta(GSK-3beta), and promoted the nuclear accumulation of beta-catenin. gingerol 27-37 glycogen synthase kinase 3 beta Mus musculus 97-106 26545981-3 2015 Here, we demonstrate that abnormal and exacerbated hippocampal activity induced by MES triggers specific and temporally distinct patterns of phosphorylation of extracellular signal-related kinase (ERK), mammalian target of rapamycin complex (mTORC) and Akt/glycogen synthase kinase-3 (Akt/GSK-3) pathways in the mouse hippocampus. 2-(N-morpholino)ethanesulfonic acid 83-86 glycogen synthase kinase 3 beta Mus musculus 289-294 26108692-0 2015 Lithium chloride antileukemic activity in acute promyelocytic leukemia is GSK-3 and MEK/ERK dependent. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 74-79 26069270-4 2015 Glycogen synthase kinase 3beta activity was interfered with glycogen synthase kinase 3beta inhibitor lithium chloride or transduced with replication defective adenovirus vector expressing catalytically inactive glycogen synthase kinase 3beta (GSK3beta-KM). Lithium Chloride 101-117 glycogen synthase kinase 3 beta Mus musculus 0-30 26335930-8 2015 AML12 cells treated by Wnt3a or the glycogen synthase kinase 3beta inhibitor LiCl exposed to H-R demonstrated decreased reactive oxygen species and reduced apoptosis compared to controls. Lithium Chloride 77-81 glycogen synthase kinase 3 beta Mus musculus 36-66 26335930-8 2015 AML12 cells treated by Wnt3a or the glycogen synthase kinase 3beta inhibitor LiCl exposed to H-R demonstrated decreased reactive oxygen species and reduced apoptosis compared to controls. h-r 93-96 glycogen synthase kinase 3 beta Mus musculus 36-66 26524968-12 2015 Iso inhibited AKT phosphorylation and led to activation of GSK3beta. isosakuranetin 0-3 glycogen synthase kinase 3 beta Mus musculus 59-67 26626190-10 2015 Aspirin efficiently reversed the upregulation of beta-catenin and P-Akt expression and the TAC- or ANG II-induced downregulation of GSK-3beta. Aspirin 0-7 glycogen synthase kinase 3 beta Mus musculus 132-141 26456500-9 2015 LY294002 (an inhibitor of GSK3beta phosphorylation) and LiCl (an inhibitor of GSK3beta activity) diminished and potentiated increase of IL-10 levels by DGA, respectively. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 0-8 glycogen synthase kinase 3 beta Mus musculus 26-34 26456500-9 2015 LY294002 (an inhibitor of GSK3beta phosphorylation) and LiCl (an inhibitor of GSK3beta activity) diminished and potentiated increase of IL-10 levels by DGA, respectively. Lithium Chloride 56-60 glycogen synthase kinase 3 beta Mus musculus 78-86 26335930-8 2015 AML12 cells treated by Wnt3a or the glycogen synthase kinase 3beta inhibitor LiCl exposed to H-R demonstrated decreased reactive oxygen species and reduced apoptosis compared to controls. Reactive Oxygen Species 120-143 glycogen synthase kinase 3 beta Mus musculus 36-66 26441085-6 2015 Additionally, Reelin treatment led to increased phosphorylation of AKT, GSK3beta, and JNK, which were all effectively blocked by the PI3K inhibitor, LY294002. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 149-157 glycogen synthase kinase 3 beta Mus musculus 72-80 26714922-3 2015 To explore the role of GSK-3beta in maturation and function of DCs, we added SB216763, a selective inhibitor of GSK-3beta, in the cell culture of immature DCs (iDCs), and examined CD40 and CD86 expressions in the cells by flow cytometry and the expression of IL-6, IL-12 and IL-10 mRNA by real-time PCR; the changes of the immunogenicity of the cells was evaluated by mixed lymphocyte reaction. SB 216763 77-85 glycogen synthase kinase 3 beta Mus musculus 112-121 26446842-0 2015 Regulation of Chlamydomonas flagella and ependymal cell motile cilia by ceramide-mediated translocation of GSK3. Ceramides 72-80 glycogen synthase kinase 3 beta Mus musculus 107-111 26446842-2 2015 We characterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids phytoceramide and ceramide that is critical for ciliogenesis in Chlamydomonas and murine ependymal cells, respectively. Sphingolipids 90-103 glycogen synthase kinase 3 beta Mus musculus 49-75 26446842-2 2015 We characterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids phytoceramide and ceramide that is critical for ciliogenesis in Chlamydomonas and murine ependymal cells, respectively. Sphingolipids 90-103 glycogen synthase kinase 3 beta Mus musculus 77-81 26446842-2 2015 We characterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids phytoceramide and ceramide that is critical for ciliogenesis in Chlamydomonas and murine ependymal cells, respectively. phytoceramide 104-117 glycogen synthase kinase 3 beta Mus musculus 49-75 26446842-2 2015 We characterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids phytoceramide and ceramide that is critical for ciliogenesis in Chlamydomonas and murine ependymal cells, respectively. phytoceramide 104-117 glycogen synthase kinase 3 beta Mus musculus 77-81 26446842-2 2015 We characterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids phytoceramide and ceramide that is critical for ciliogenesis in Chlamydomonas and murine ependymal cells, respectively. Ceramides 109-117 glycogen synthase kinase 3 beta Mus musculus 49-75 26446842-2 2015 We characterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids phytoceramide and ceramide that is critical for ciliogenesis in Chlamydomonas and murine ependymal cells, respectively. Ceramides 109-117 glycogen synthase kinase 3 beta Mus musculus 77-81 26446842-5 2015 Immunocytochemistry showed that (phyto)ceramide was colocalized with phospho-Tyr-216-GSK3 (pYGSK3) at the base and tip of Chlamydomonas flagella and motile cilia in ependymal cells. (phyto)ceramide 32-47 glycogen synthase kinase 3 beta Mus musculus 85-89 26446842-5 2015 Immunocytochemistry showed that (phyto)ceramide was colocalized with phospho-Tyr-216-GSK3 (pYGSK3) at the base and tip of Chlamydomonas flagella and motile cilia in ependymal cells. Tyrosine 77-80 glycogen synthase kinase 3 beta Mus musculus 85-89 26446842-7 2015 Ceramide depletion, by myriocin or neutral sphingomyelinase deficiency (fro/fro mouse), led to GSK3 dephosphorylation and defective flagella and cilia. Ceramides 0-8 glycogen synthase kinase 3 beta Mus musculus 95-99 26486317-0 2015 Hit Optimization of 5-Substituted-N-(piperidin-4-ylmethyl)-1H-indazole-3-carboxamides: Potent Glycogen Synthase Kinase-3 (GSK-3) Inhibitors with in Vivo Activity in Model of Mood Disorders. 5-substituted-n-(piperidin-4-ylmethyl)-1h-indazole-3-carboxamides 20-85 glycogen synthase kinase 3 beta Mus musculus 94-120 26486317-0 2015 Hit Optimization of 5-Substituted-N-(piperidin-4-ylmethyl)-1H-indazole-3-carboxamides: Potent Glycogen Synthase Kinase-3 (GSK-3) Inhibitors with in Vivo Activity in Model of Mood Disorders. 5-substituted-n-(piperidin-4-ylmethyl)-1h-indazole-3-carboxamides 20-85 glycogen synthase kinase 3 beta Mus musculus 122-127 26486317-3 2015 A series of novel GSK-3beta inhibitors having the common N-[(1-alkylpiperidin-4-yl)methyl]-1H-indazole-3-carboxamide scaffold were prepared taking advantage of an X-ray cocrystal structure of compound 5 with GSK-3beta. n-[(1-alkylpiperidin-4-yl)methyl]-1h-indazole-3-carboxamide 57-116 glycogen synthase kinase 3 beta Mus musculus 18-27 26486317-4 2015 We probed different substitutions at the indazole 5-position and at the piperidine-nitrogen to obtain potent ATP-competitive GSK-3beta inhibitors with good cell activity. Indazoles 41-49 glycogen synthase kinase 3 beta Mus musculus 125-134 26486317-4 2015 We probed different substitutions at the indazole 5-position and at the piperidine-nitrogen to obtain potent ATP-competitive GSK-3beta inhibitors with good cell activity. piperidine 72-82 glycogen synthase kinase 3 beta Mus musculus 125-134 26486317-4 2015 We probed different substitutions at the indazole 5-position and at the piperidine-nitrogen to obtain potent ATP-competitive GSK-3beta inhibitors with good cell activity. Nitrogen 83-91 glycogen synthase kinase 3 beta Mus musculus 125-134 26486317-4 2015 We probed different substitutions at the indazole 5-position and at the piperidine-nitrogen to obtain potent ATP-competitive GSK-3beta inhibitors with good cell activity. Adenosine Triphosphate 109-112 glycogen synthase kinase 3 beta Mus musculus 125-134 26567873-4 2015 By employing the doxycycline-activated Cre-loxP site specific gene targeting system, GSK3beta was successfully knocked out (KO) selectively in podocytes in adult mice, resulting in a phenotype no different from control littermates. Doxycycline 17-28 glycogen synthase kinase 3 beta Mus musculus 85-93 26486317-7 2015 Compound 14i was selected for further in vitro/in vivo pharmacological evaluation, in order to elucidate the use of ATP-competitive GSK-3beta inhibitors as new tools in the development of new treatments for mood disorders. Adenosine Triphosphate 116-119 glycogen synthase kinase 3 beta Mus musculus 132-141 26385876-0 2015 Valproic Acid Modifies Synaptic Structure and Accelerates Neurite Outgrowth Via the Glycogen Synthase Kinase-3beta Signaling Pathway in an Alzheimer"s Disease Model. Valproic Acid 0-13 glycogen synthase kinase 3 beta Mus musculus 84-114 26398893-0 2015 A novel adamantyl benzylbenzamide derivative, AP736, inhibits melanogenesis in B16F10 mouse melanoma cells via glycogen synthase kinase 3beta phosphorylation. adamantyl benzylbenzamide 8-33 glycogen synthase kinase 3 beta Mus musculus 111-141 26275858-3 2015 The aim of this study was to determine whether lithium chloride (LiCl), a selective inhibitor of glycogen synthetase kinase 3 beta (GSK-3beta), mitigates wear debris-induced osteolysis in a murine calvarial model of osteolysis. Lithium Chloride 47-63 glycogen synthase kinase 3 beta Mus musculus 132-141 26275858-3 2015 The aim of this study was to determine whether lithium chloride (LiCl), a selective inhibitor of glycogen synthetase kinase 3 beta (GSK-3beta), mitigates wear debris-induced osteolysis in a murine calvarial model of osteolysis. Lithium Chloride 65-69 glycogen synthase kinase 3 beta Mus musculus 132-141 26275858-4 2015 GSK-3beta is activated by titanium (Ti) particles, and implantation of Ti particles on the calvarial surface in C57BL/6 mice resulted in osteolysis caused by an increase in the number of osteoclasts and a decrease in the number of osteoblasts. Titanium 26-34 glycogen synthase kinase 3 beta Mus musculus 0-9 26275858-6 2015 The LiCl treatment significantly inhibited GSK-3beta activity and increased beta-catenin and axin-2 expression in a dose-dependent manner, dramatically mitigating the Ti particle-induced suppression of osteoblast numbers and the expression of bone formation markers. Lithium Chloride 4-8 glycogen synthase kinase 3 beta Mus musculus 43-52 26275858-9 2015 This suggests that selective inhibitors of GSK-3beta such as LiCl may help prevent and treat wear debris-induced osteolysis. Lithium Chloride 61-65 glycogen synthase kinase 3 beta Mus musculus 43-52 26320675-8 2015 The activation of SREBP-2 by AOS is mediated by phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3beta pathways. D-(+)-ALLOSE 29-32 glycogen synthase kinase 3 beta Mus musculus 82-112 26171616-0 2015 3,4-Dihydro-1,3,5-triazin-2(1H)-ones as the First Dual BACE-1/GSK-3beta Fragment Hits against Alzheimer"s Disease. 3,4-dihydro-1,3,5-triazin-2(1h)-ones 0-36 glycogen synthase kinase 3 beta Mus musculus 62-71 26105003-12 2015 In addition, DT3 treatment decreased phosphorylation of GSK-3, P38, and CREB in murine PDAC.Inhibition of PKG could be a potential therapeutic strategy for PDAC treatment which should be carefully validated in future pre-clinical studies. dt3 13-16 glycogen synthase kinase 3 beta Mus musculus 56-61 26413814-9 2015 VPA inhibited the activities of histone deacetylase (HDAC) and glycogen synthase kinase-3beta (GSK3beta), the latter of which is only inhibited in normal cells. Valproic Acid 0-3 glycogen synthase kinase 3 beta Mus musculus 63-93 26413814-9 2015 VPA inhibited the activities of histone deacetylase (HDAC) and glycogen synthase kinase-3beta (GSK3beta), the latter of which is only inhibited in normal cells. Valproic Acid 0-3 glycogen synthase kinase 3 beta Mus musculus 95-103 26519157-5 2015 MK-I-81 also alleviated MGO mediated diminished distal insulin signaling by increasing protein kinase B and glycogen synthase kinase 3-beta phosphorylation. mk-i-81 0-7 glycogen synthase kinase 3 beta Mus musculus 108-139 26519157-5 2015 MK-I-81 also alleviated MGO mediated diminished distal insulin signaling by increasing protein kinase B and glycogen synthase kinase 3-beta phosphorylation. Pyruvaldehyde 24-27 glycogen synthase kinase 3 beta Mus musculus 108-139 26171616-4 2015 In this respect, we report herein on the first class of BACE-1/GSK-3beta dual inhibitors based on a 3,4-dihydro-1,3,5-triazin-2(1H)-one skeleton, whose hit compound 1 showed interesting properties in a preliminary investigation. 3,4-dihydro-1,3,5-triazin-2 100-127 glycogen synthase kinase 3 beta Mus musculus 63-72 26171616-4 2015 In this respect, we report herein on the first class of BACE-1/GSK-3beta dual inhibitors based on a 3,4-dihydro-1,3,5-triazin-2(1H)-one skeleton, whose hit compound 1 showed interesting properties in a preliminary investigation. Hydrogen 128-130 glycogen synthase kinase 3 beta Mus musculus 63-72 25939427-8 2015 Moreover, naringin significantly enhanced insulin signaling pathway as indicated by a 34.5% increase in the expression levels of IRS-1, a 47.8% decrease in the p-IRS-1, a 1.43-fold increase in the p-Akt, and a 1.89-fold increase in the p-GSK-3beta in the hippocampus of the HFDN mice versus HFD mice. naringin 10-18 glycogen synthase kinase 3 beta Mus musculus 238-247 26473849-10 2015 In addition, PCP led to the down-regulation of phospho-p38, phospho-PKA, phospho-CREB, phospho-GSK3beta, MITF, and TRP-1 compared with alpha-MSH-stimulated B16F10 cells. pcp 13-16 glycogen synthase kinase 3 beta Mus musculus 95-103 26172083-0 2015 Maslinic acid promotes synaptogenesis and axon growth via Akt/GSK-3beta activation in cerebral ischemia model. maslinic acid 0-13 glycogen synthase kinase 3 beta Mus musculus 62-71 26172083-8 2015 Two Akt inhibitors, LY294002 and MK2206, were used to verify the involvement of Akt/GSK-3beta pathway in maslinic acid-mediated neuroprotection. maslinic acid 105-118 glycogen synthase kinase 3 beta Mus musculus 84-93 26172083-10 2015 In addition, maslinic acid treatment was shown to enhance Akt activity and promote GSK-3beta phorsphorylation in stoke mice. maslinic acid 13-26 glycogen synthase kinase 3 beta Mus musculus 83-92 26172083-12 2015 These findings suggested that maslinic acid promotes synaptogenesis and axonal regeneration by regulating Akt/GSK-3beta signaling pathway, which may, in turn, provide neuroprotection. maslinic acid 30-43 glycogen synthase kinase 3 beta Mus musculus 110-119 26116229-0 2015 Rosiglitazone inhibition of calvaria-derived osteoblast differentiation is through both of PPARgamma and GPR40 and GSK3beta-dependent pathway. Rosiglitazone 0-13 glycogen synthase kinase 3 beta Mus musculus 115-123 26208882-7 2015 Furthermore, we found that the down-regulation of Ndrg2 in Ndrg2-deficient mice and imipramine treatment improved mood behavior with enhanced phosphorylation of GSK3beta through activation of PI3K/AKT signaling, suggesting that the expression level of NDRG2 has a causal influence on mood-related phenotypes. Imipramine 84-94 glycogen synthase kinase 3 beta Mus musculus 161-169 26143616-6 2015 We found that treatment with the GSK3beta inhibitor SB216763 restored neuronal precursor survival, dendritic maturation, connectivity and hippocampus-dependent learning and memory in the Cdkl5 -/Y mouse. SB 216763 52-60 glycogen synthase kinase 3 beta Mus musculus 33-41 26116229-8 2015 RSG-induced GSK3beta activation was mediated through both PPARgamma and GPR40. Rosiglitazone 0-3 glycogen synthase kinase 3 beta Mus musculus 12-20 26116229-9 2015 These results suggest that both PPARgamma and GRP40 are required for RSG-induced inhibition of mouse calvaria osteoblast differentiation, which is mediated through GSK3beta-dependent pathway. Rosiglitazone 69-72 glycogen synthase kinase 3 beta Mus musculus 164-172 26197224-0 2015 Neuroprotective effect of astaxanthin against glutamate-induced cytotoxicity in HT22 cells: Involvement of the Akt/GSK-3beta pathway. astaxanthine 26-37 glycogen synthase kinase 3 beta Mus musculus 115-124 26197224-10 2015 Furthermore, treatment with ATX restored the p-Akt and p-GSK-3beta (Ser9) as well as HO-1 expression reduced by glutamate. astaxanthine 28-31 glycogen synthase kinase 3 beta Mus musculus 57-66 26197224-11 2015 This protective effect was partially blocked by the inhibitors lithium chloride treatment in HT22, indicating the involvement of Akt/GSK-3beta inactivation during the neuroprotective effect of ATX. Lithium Chloride 63-79 glycogen synthase kinase 3 beta Mus musculus 133-142 26356837-7 2015 Inhibition of MEK1/2/ERK1/2 (1 muM U0126) and PI-3K/Akt (10 muM LY294002) signaling showed that the MEK1/2/ERK1/2 pathway via GSK-3beta exclusively was responsible for cardioprotection as an addition of U0126 prevented estrogen-induced GSK-3beta increased phosphorylation, resistance to mitochondrial Ca2+-overload, functional recovery and protection against infarction. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 64-72 glycogen synthase kinase 3 beta Mus musculus 126-135 26356837-7 2015 Inhibition of MEK1/2/ERK1/2 (1 muM U0126) and PI-3K/Akt (10 muM LY294002) signaling showed that the MEK1/2/ERK1/2 pathway via GSK-3beta exclusively was responsible for cardioprotection as an addition of U0126 prevented estrogen-induced GSK-3beta increased phosphorylation, resistance to mitochondrial Ca2+-overload, functional recovery and protection against infarction. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 64-72 glycogen synthase kinase 3 beta Mus musculus 236-245 26197224-11 2015 This protective effect was partially blocked by the inhibitors lithium chloride treatment in HT22, indicating the involvement of Akt/GSK-3beta inactivation during the neuroprotective effect of ATX. astaxanthine 193-196 glycogen synthase kinase 3 beta Mus musculus 133-142 26356837-7 2015 Inhibition of MEK1/2/ERK1/2 (1 muM U0126) and PI-3K/Akt (10 muM LY294002) signaling showed that the MEK1/2/ERK1/2 pathway via GSK-3beta exclusively was responsible for cardioprotection as an addition of U0126 prevented estrogen-induced GSK-3beta increased phosphorylation, resistance to mitochondrial Ca2+-overload, functional recovery and protection against infarction. U 0126 203-208 glycogen synthase kinase 3 beta Mus musculus 126-135 26197224-12 2015 Our results provide the first evidence that ATX can protect glutamate-induced cytotoxicity in HT22 via attenuating caspase activation and mitochondrial dysfunction and modulating the Akt/GSK-3beta signaling, indicating ATX may be useful for the treatment of neurodegenerative disorders such as AD. astaxanthine 44-47 glycogen synthase kinase 3 beta Mus musculus 187-196 26197224-12 2015 Our results provide the first evidence that ATX can protect glutamate-induced cytotoxicity in HT22 via attenuating caspase activation and mitochondrial dysfunction and modulating the Akt/GSK-3beta signaling, indicating ATX may be useful for the treatment of neurodegenerative disorders such as AD. Glutamic Acid 60-69 glycogen synthase kinase 3 beta Mus musculus 187-196 26082469-2 2015 Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase in the crossroad of many signaling pathways that is highly pleiotropic as it phosphorylates more than hundred substrates including structural, metabolic, and signaling proteins. Serine 40-46 glycogen synthase kinase 3 beta Mus musculus 0-26 26082469-2 2015 Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase in the crossroad of many signaling pathways that is highly pleiotropic as it phosphorylates more than hundred substrates including structural, metabolic, and signaling proteins. Serine 40-46 glycogen synthase kinase 3 beta Mus musculus 28-33 26527331-7 2015 RESULTS: In the Tg-TE group that was subjected to treadmill exercise for 12 weeks, abnormal mTOR phosphorylation of PI3K/AKT proteins was improved via increased phosphorylation and its activity was inhibited by increased GSK-3beta phosphorylation compared with those in the Tg-CON group, which was used as the control group. Thioguanine 16-18 glycogen synthase kinase 3 beta Mus musculus 221-230 26235895-5 2015 Treatment with BIO, a GSK3s inhibitor, significantly increased disease remission by enhancing renal progenitor sensitivity to the differentiation effect of endogenous retinoic acid. Tretinoin 167-180 glycogen synthase kinase 3 beta Mus musculus 22-26 26100021-4 2015 Moreover, the use of two selective small-molecule GSK-3 inhibitors (CHIR99021 and BIO-acetoxime) or ES cells reconstituted with the catalytically inactive versions of GSK-3 isoforms showed that GSK-3 activity is required for optimal induction of antiviral innate immunity. acetoxime 86-95 glycogen synthase kinase 3 beta Mus musculus 50-55 26100021-4 2015 Moreover, the use of two selective small-molecule GSK-3 inhibitors (CHIR99021 and BIO-acetoxime) or ES cells reconstituted with the catalytically inactive versions of GSK-3 isoforms showed that GSK-3 activity is required for optimal induction of antiviral innate immunity. acetoxime 86-95 glycogen synthase kinase 3 beta Mus musculus 167-172 26100021-4 2015 Moreover, the use of two selective small-molecule GSK-3 inhibitors (CHIR99021 and BIO-acetoxime) or ES cells reconstituted with the catalytically inactive versions of GSK-3 isoforms showed that GSK-3 activity is required for optimal induction of antiviral innate immunity. acetoxime 86-95 glycogen synthase kinase 3 beta Mus musculus 167-172 26100021-4 2015 Moreover, the use of two selective small-molecule GSK-3 inhibitors (CHIR99021 and BIO-acetoxime) or ES cells reconstituted with the catalytically inactive versions of GSK-3 isoforms showed that GSK-3 activity is required for optimal induction of antiviral innate immunity. Einsteinium 100-102 glycogen synthase kinase 3 beta Mus musculus 167-172 26100021-4 2015 Moreover, the use of two selective small-molecule GSK-3 inhibitors (CHIR99021 and BIO-acetoxime) or ES cells reconstituted with the catalytically inactive versions of GSK-3 isoforms showed that GSK-3 activity is required for optimal induction of antiviral innate immunity. Einsteinium 100-102 glycogen synthase kinase 3 beta Mus musculus 167-172 26151480-0 2015 ERK/GSK3beta signaling is involved in atractylenolide I-induced apoptosis and cell cycle arrest in melanoma cells. atractylenolide I 38-55 glycogen synthase kinase 3 beta Mus musculus 4-12 26151480-11 2015 Lithium chloride (LiCl, 5 mM), a GSK3beta inhibitor, treatment alone did not increase the apoptosis of B16 cells, while pretreatment with LiCl markedly reversed AT-I-induced apoptosis. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 33-41 26151480-11 2015 Lithium chloride (LiCl, 5 mM), a GSK3beta inhibitor, treatment alone did not increase the apoptosis of B16 cells, while pretreatment with LiCl markedly reversed AT-I-induced apoptosis. Lithium Chloride 18-22 glycogen synthase kinase 3 beta Mus musculus 33-41 26151480-13 2015 In conclusion, ERK/GSK3beta signaling was involved in the apoptotic and G1 phase arrest effects of AT-I in melanoma cells. Astatine 99-101 glycogen synthase kinase 3 beta Mus musculus 19-27 26151480-13 2015 In conclusion, ERK/GSK3beta signaling was involved in the apoptotic and G1 phase arrest effects of AT-I in melanoma cells. Iodine 0-1 glycogen synthase kinase 3 beta Mus musculus 19-27 26089345-9 2015 At the same time, LY294002 also inhibited phosphorylation of ERK, glycogen synthase kinase3beta and tyrosine 654 of beta-catenin induced by TDI. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 18-26 glycogen synthase kinase 3 beta Mus musculus 66-95 26089345-9 2015 At the same time, LY294002 also inhibited phosphorylation of ERK, glycogen synthase kinase3beta and tyrosine 654 of beta-catenin induced by TDI. Toluene 2,4-Diisocyanate 140-143 glycogen synthase kinase 3 beta Mus musculus 66-95 26311765-7 2015 The brains of Trpm2(-/-) mice showed a marked increase in phosphorylated glycogen synthase kinase-3 (GSK-3), a key element in BD-like behavior and a target of lithium. Lithium 159-166 glycogen synthase kinase 3 beta Mus musculus 73-106 26311765-17 2015 TRPM2 actively regulates the phosphorylation of GSK-3, which is a main target of lithium, a primary medicine for treating BD. Lithium 81-88 glycogen synthase kinase 3 beta Mus musculus 48-53 26068144-5 2015 In addition, we demonstrated that chronic treatment with PF inhibited the activation of glycogen synthase kinase 3beta (GSK-3beta) and reversed neuroinflammtory-induced activation of nuclear factor-kappa B (NF-kappaB) signaling pathways. peoniflorin 57-59 glycogen synthase kinase 3 beta Mus musculus 88-118 26092126-4 2015 Pharmacological inhibition of GSK3 using TDZD-8 starting before or after ischemia-reperfusion significantly suppressed renal fibrosis by reducing the myofibroblast population, collagen-1 and fibronectin deposition, inflammatory cytokines, and macrophage infiltration. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 41-47 glycogen synthase kinase 3 beta Mus musculus 30-34 25892506-6 2015 ERalpha activation by its agonist 4,4",4""-(4-Propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT) protected dopamine neurons, an effect associated with activation of striatal Akt signaling and an increase in Bcl-2 and BDNF levels; the GPER1 antagonist G15 inhibited the decrease in glycogen synthase kinase 3beta activity and the increase in BDNF induced by PPT. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 34-89 glycogen synthase kinase 3 beta Mus musculus 280-310 25892506-6 2015 ERalpha activation by its agonist 4,4",4""-(4-Propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT) protected dopamine neurons, an effect associated with activation of striatal Akt signaling and an increase in Bcl-2 and BDNF levels; the GPER1 antagonist G15 inhibited the decrease in glycogen synthase kinase 3beta activity and the increase in BDNF induced by PPT. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 91-94 glycogen synthase kinase 3 beta Mus musculus 280-310 25892506-6 2015 ERalpha activation by its agonist 4,4",4""-(4-Propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT) protected dopamine neurons, an effect associated with activation of striatal Akt signaling and an increase in Bcl-2 and BDNF levels; the GPER1 antagonist G15 inhibited the decrease in glycogen synthase kinase 3beta activity and the increase in BDNF induced by PPT. Dopamine 106-114 glycogen synthase kinase 3 beta Mus musculus 280-310 25754463-0 2015 Salidroside ameliorates insulin resistance through activation of a mitochondria-associated AMPK/PI3K/Akt/GSK3beta pathway. rhodioloside 0-11 glycogen synthase kinase 3 beta Mus musculus 105-113 25912432-7 2015 Western blot revealed that the levels of p-Ser9-glycogensynthase kinase-3beta (p-GSK-3beta) and beta-catenin were remarkably downregulated during TPEN-induced C17.2 proliferative impairment. N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine 146-150 glycogen synthase kinase 3 beta Mus musculus 81-90 25912432-9 2015 Furthermore, application with GSK-3beta inhibitor lithium chloride (LiCl) reversed TPEN-induced downregulation of beta-catenin and impairment of cell proliferation. Lithium Chloride 50-66 glycogen synthase kinase 3 beta Mus musculus 30-39 25912432-9 2015 Furthermore, application with GSK-3beta inhibitor lithium chloride (LiCl) reversed TPEN-induced downregulation of beta-catenin and impairment of cell proliferation. Lithium Chloride 68-72 glycogen synthase kinase 3 beta Mus musculus 30-39 25912432-9 2015 Furthermore, application with GSK-3beta inhibitor lithium chloride (LiCl) reversed TPEN-induced downregulation of beta-catenin and impairment of cell proliferation. N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine 83-87 glycogen synthase kinase 3 beta Mus musculus 30-39 25975268-5 2015 Downstream activation of the beta-catenin pathway using a pharmacological inhibitor of GSK-3beta ameliorates the Pb inhibition of Wnt signaling activity in the TOPGAL reporter mouse. Lead 113-115 glycogen synthase kinase 3 beta Mus musculus 87-96 25869780-9 2015 Furthermore, flupirtine (10mg/kg and 25mg/kg) treatment significantly decreased the expression of Bax and increased the p-Akt and p-GSK-3beta, and flupirtine (25mg/kg) treatment up-regulated the p-Erk1/2 in the hippocampus of CRS mice. flupirtine 13-23 glycogen synthase kinase 3 beta Mus musculus 132-141 25869780-10 2015 These results suggested that flupirtine exerted protective effects on the CRS-induced cognitive impairment and hippocampal neuronal apoptosis, which is possibly associated with the activation of Akt/GSK-3beta and Erk1/2 signaling pathways. flupirtine 29-39 glycogen synthase kinase 3 beta Mus musculus 199-208 25869780-10 2015 These results suggested that flupirtine exerted protective effects on the CRS-induced cognitive impairment and hippocampal neuronal apoptosis, which is possibly associated with the activation of Akt/GSK-3beta and Erk1/2 signaling pathways. 3-cresol 74-77 glycogen synthase kinase 3 beta Mus musculus 199-208 25802191-8 2015 These data demonstrate anti-diabetic efficacy of KICG1338, a novel GSK3beta inhibitor. KICG1338 49-57 glycogen synthase kinase 3 beta Mus musculus 67-75 25754463-10 2015 In vitro, salidroside dose-dependently induced an increase in the phosphorylations of AMPK and PI3K/Akt, as well as glycogen synthase kinase 3beta (GSK3beta) in hepatocytes. rhodioloside 10-21 glycogen synthase kinase 3 beta Mus musculus 116-146 25754463-10 2015 In vitro, salidroside dose-dependently induced an increase in the phosphorylations of AMPK and PI3K/Akt, as well as glycogen synthase kinase 3beta (GSK3beta) in hepatocytes. rhodioloside 10-21 glycogen synthase kinase 3 beta Mus musculus 148-156 25754463-14 2015 CONCLUSIONS AND IMPLICATIONS: Salidroside exerts an antidiabetic effect by improving the cellular metabolic flux through the activation of a mitochondria-related AMPK/PI3K/Akt/GSK3beta pathway. rhodioloside 30-41 glycogen synthase kinase 3 beta Mus musculus 176-184 25901028-8 2015 Compromised HSF1 activation was a result of HSF1 phosphorylation at serine 303, which was catalyzed by glycogen synthase kinase 3beta (GSK3beta). Serine 68-74 glycogen synthase kinase 3 beta Mus musculus 103-133 26093960-5 2015 MC-LR exposure at 10 or 20 mug/kg/d also altered mRNA and protein expression of downstream factors and genes of ER stress signaling pathways, including the downregulation of sterol regulatory element binding protein 1c (SREBP-1c) and fatty acid synthase (FASn), and upregulation of acetyl-coenzyme A carboxylase alpha (ACACA) and glycogen synthase kinase 3beta (Gsk-3beta). cyanoginosin LR 0-5 glycogen synthase kinase 3 beta Mus musculus 330-360 26093960-5 2015 MC-LR exposure at 10 or 20 mug/kg/d also altered mRNA and protein expression of downstream factors and genes of ER stress signaling pathways, including the downregulation of sterol regulatory element binding protein 1c (SREBP-1c) and fatty acid synthase (FASn), and upregulation of acetyl-coenzyme A carboxylase alpha (ACACA) and glycogen synthase kinase 3beta (Gsk-3beta). cyanoginosin LR 0-5 glycogen synthase kinase 3 beta Mus musculus 362-371 26170951-6 2015 In addition, propofol was shown to downregulate the phosphoinositide 3-kinase (PI3K)/Akt/GSK-3beta signaling pathway and inhibit glycogen synthesis in hepatocytes. Propofol 13-21 glycogen synthase kinase 3 beta Mus musculus 89-98 26170951-8 2015 Notably, pretreatment with propofol in tumor necrosis factor (TNF)-alpha-induced primary mouse hepatocytes with insulin resistance was demonstrated to alleviate the inhibitory effects of TNF-alpha on the PI3K/Akt/GSK-3beta signaling pathway and glycogen synthesis. Propofol 27-35 glycogen synthase kinase 3 beta Mus musculus 213-222 25869056-0 2015 Andrographolide suppresses melanin synthesis through Akt/GSK3beta/beta-catenin signal pathway. andrographolide 0-15 glycogen synthase kinase 3 beta Mus musculus 57-65 25869056-0 2015 Andrographolide suppresses melanin synthesis through Akt/GSK3beta/beta-catenin signal pathway. Melanins 27-34 glycogen synthase kinase 3 beta Mus musculus 57-65 25869056-10 2015 6-Bromoindirubin-3"-oxime (BIO, inhibitor of GSK3beta) and insulin-like growth factors-1 (IGF-1, activator of Akt) could reverse the decline of beta-catenin in B16F10 cells induced by andrographolide. 6-bromoindirubin-3'-oxime 0-25 glycogen synthase kinase 3 beta Mus musculus 45-53 25092247-7 2015 In vivo pharmacology and western blot experiments argue for increased serotonin tonus as a main mechanism for impaired GSK3beta signaling in OCT2(-/-) mice brain during acute response to stress. Serotonin 70-79 glycogen synthase kinase 3 beta Mus musculus 119-127 25901028-8 2015 Compromised HSF1 activation was a result of HSF1 phosphorylation at serine 303, which was catalyzed by glycogen synthase kinase 3beta (GSK3beta). Serine 68-74 glycogen synthase kinase 3 beta Mus musculus 135-143 25901028-9 2015 Testosterone was necessary for bicyclol to inhibit hepatic GSK3beta activity. Testosterone 0-12 glycogen synthase kinase 3 beta Mus musculus 59-67 25901028-9 2015 Testosterone was necessary for bicyclol to inhibit hepatic GSK3beta activity. bicyclol 31-39 glycogen synthase kinase 3 beta Mus musculus 59-67 25901028-10 2015 Administration of testosterone or GSK3beta inhibitors restored bicyclol-induced protection in females. bicyclol 63-71 glycogen synthase kinase 3 beta Mus musculus 34-42 25901028-11 2015 Bicyclol induces sex-specific hepatoprotection based on a sex-specific HSF1/Hsp70 response, in which testosterone and GSK3beta play key roles. bicyclol 0-8 glycogen synthase kinase 3 beta Mus musculus 118-126 25881103-5 2015 Blebbistatin enhanced Akt and GSK3beta phosphorylation and inhibited NF-kappaB p65 nuclear translocation and IkappaBalpha degradation. blebbistatin 0-12 glycogen synthase kinase 3 beta Mus musculus 30-38 25881103-10 2015 Importantly, blebbistatin decreased endothelium NMMHC IIA and TF expression, deactivated GSK3beta by inducing its phosphorylation, suppressed p65 nuclear translocation, and inhibited thrombus formation in a mouse deep venous thrombosis model.Our findings provide solid evidence that inhibition of NMMHC II, most likely NMMHC IIA, impedes TF expression and venous thrombosis via Akt/GSK3beta-NF-kappaB signalling pathways in the endothelium both in vitro and in vivo. blebbistatin 13-25 glycogen synthase kinase 3 beta Mus musculus 89-97 25881103-10 2015 Importantly, blebbistatin decreased endothelium NMMHC IIA and TF expression, deactivated GSK3beta by inducing its phosphorylation, suppressed p65 nuclear translocation, and inhibited thrombus formation in a mouse deep venous thrombosis model.Our findings provide solid evidence that inhibition of NMMHC II, most likely NMMHC IIA, impedes TF expression and venous thrombosis via Akt/GSK3beta-NF-kappaB signalling pathways in the endothelium both in vitro and in vivo. blebbistatin 13-25 glycogen synthase kinase 3 beta Mus musculus 382-390 26056233-8 2015 Co-treatment of skin wounds with PTD-DBM and valproic acid (VPA), a glycogen synthase kinase 3beta (GSK3beta) inhibitor which activates the Wnt/beta-catenin pathway, synergistically accelerated cutaneous wound healing in mice. ptd-dbm 33-40 glycogen synthase kinase 3 beta Mus musculus 68-98 26056233-8 2015 Co-treatment of skin wounds with PTD-DBM and valproic acid (VPA), a glycogen synthase kinase 3beta (GSK3beta) inhibitor which activates the Wnt/beta-catenin pathway, synergistically accelerated cutaneous wound healing in mice. ptd-dbm 33-40 glycogen synthase kinase 3 beta Mus musculus 100-108 26056233-8 2015 Co-treatment of skin wounds with PTD-DBM and valproic acid (VPA), a glycogen synthase kinase 3beta (GSK3beta) inhibitor which activates the Wnt/beta-catenin pathway, synergistically accelerated cutaneous wound healing in mice. Valproic Acid 45-58 glycogen synthase kinase 3 beta Mus musculus 68-98 26056233-8 2015 Co-treatment of skin wounds with PTD-DBM and valproic acid (VPA), a glycogen synthase kinase 3beta (GSK3beta) inhibitor which activates the Wnt/beta-catenin pathway, synergistically accelerated cutaneous wound healing in mice. Valproic Acid 45-58 glycogen synthase kinase 3 beta Mus musculus 100-108 26056233-8 2015 Co-treatment of skin wounds with PTD-DBM and valproic acid (VPA), a glycogen synthase kinase 3beta (GSK3beta) inhibitor which activates the Wnt/beta-catenin pathway, synergistically accelerated cutaneous wound healing in mice. Valproic Acid 60-63 glycogen synthase kinase 3 beta Mus musculus 68-98 26056233-8 2015 Co-treatment of skin wounds with PTD-DBM and valproic acid (VPA), a glycogen synthase kinase 3beta (GSK3beta) inhibitor which activates the Wnt/beta-catenin pathway, synergistically accelerated cutaneous wound healing in mice. Valproic Acid 60-63 glycogen synthase kinase 3 beta Mus musculus 100-108 26059557-7 2015 Biochemical analysis revealed that PMQ inhibited collagen-, thrombin- and U46619-induced activation of Syk, PLCgamma2, Akt, GSK3beta and Erk1/2. pmq 35-38 glycogen synthase kinase 3 beta Mus musculus 124-132 25592083-2 2015 6-Bromoindirubin-3"-oxime (BIO), a glycogen synthase kinase 3 (GSK3) inhibitor, could facilitate the maintenance of pluripotency of ESCs. 6-bromoindirubin-3'-oxime 0-25 glycogen synthase kinase 3 beta Mus musculus 35-61 25592083-2 2015 6-Bromoindirubin-3"-oxime (BIO), a glycogen synthase kinase 3 (GSK3) inhibitor, could facilitate the maintenance of pluripotency of ESCs. 6-bromoindirubin-3'-oxime 0-25 glycogen synthase kinase 3 beta Mus musculus 63-67 25063079-7 2015 Interestingly, sildenafil enhanced both Akt and glycogen synthase kinase-3beta (ser9) phosphorylation, which could be mediating the reduction in cathepsin B levels found in the hippocampus of sildenafil-treated SAMP8 mice. Sildenafil Citrate 15-25 glycogen synthase kinase 3 beta Mus musculus 48-78 25063079-7 2015 Interestingly, sildenafil enhanced both Akt and glycogen synthase kinase-3beta (ser9) phosphorylation, which could be mediating the reduction in cathepsin B levels found in the hippocampus of sildenafil-treated SAMP8 mice. Sildenafil Citrate 192-202 glycogen synthase kinase 3 beta Mus musculus 48-78 25629551-4 2015 In contrast, blockade of GSK3beta by lithium or 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) mitigated the expression of podocytopathic mediators, ameliorated podocyte injury, but barely affected Bcl-xL expression or sensitized apoptosis. Lithium 37-44 glycogen synthase kinase 3 beta Mus musculus 25-33 26459714-6 2015 This shows that mood stabilizers lamotrigine, lithium and valproate can exert behavioral effects in mice by disrupting the beta-arrestin 2-mediated regulation of Akt/GSK3 signaling by D2 dopamine receptors, thereby suggesting a shared mechanism for mood stabilizer selectivity. Lamotrigine 33-44 glycogen synthase kinase 3 beta Mus musculus 166-170 26459714-6 2015 This shows that mood stabilizers lamotrigine, lithium and valproate can exert behavioral effects in mice by disrupting the beta-arrestin 2-mediated regulation of Akt/GSK3 signaling by D2 dopamine receptors, thereby suggesting a shared mechanism for mood stabilizer selectivity. Lithium 46-53 glycogen synthase kinase 3 beta Mus musculus 166-170 26459714-6 2015 This shows that mood stabilizers lamotrigine, lithium and valproate can exert behavioral effects in mice by disrupting the beta-arrestin 2-mediated regulation of Akt/GSK3 signaling by D2 dopamine receptors, thereby suggesting a shared mechanism for mood stabilizer selectivity. Valproic Acid 58-67 glycogen synthase kinase 3 beta Mus musculus 166-170 25629551-4 2015 In contrast, blockade of GSK3beta by lithium or 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) mitigated the expression of podocytopathic mediators, ameliorated podocyte injury, but barely affected Bcl-xL expression or sensitized apoptosis. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 48-97 glycogen synthase kinase 3 beta Mus musculus 25-33 25629551-4 2015 In contrast, blockade of GSK3beta by lithium or 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) mitigated the expression of podocytopathic mediators, ameliorated podocyte injury, but barely affected Bcl-xL expression or sensitized apoptosis. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 99-105 glycogen synthase kinase 3 beta Mus musculus 25-33 25629551-5 2015 Mechanistically, GSK3beta was sufficient and essential for RelA/p65 phosphorylation, specifically at serine 467, which specifies the expression of selective NFkappaB target molecules, including podocytopathic mediators, but not Bcl-xL. Serine 101-107 glycogen synthase kinase 3 beta Mus musculus 17-25 25629553-4 2015 We previously found that GSK3beta, a regulator of cell proliferation, is also crucial for cAMP generation and vasopressin-mediated urine concentration by the kidneys. Cyclic AMP 90-94 glycogen synthase kinase 3 beta Mus musculus 25-33 25629553-8 2015 GSK3 inactivation inhibited cAMP generation and cell proliferation resulting in reduced cyst expansion, improved renal function, and extended life span. Cyclic AMP 28-32 glycogen synthase kinase 3 beta Mus musculus 0-4 25716948-0 2015 Berberine regulates melanin synthesis by activating PI3K/AKT, ERK and GSK3beta in B16F10 melanoma cells. Berberine 0-9 glycogen synthase kinase 3 beta Mus musculus 70-78 25845281-0 2015 Discovery of new acylaminopyridines as GSK-3 inhibitors by a structure guided in-depth exploration of chemical space around a pyrrolopyridinone core. acylaminopyridines 17-35 glycogen synthase kinase 3 beta Mus musculus 39-44 25845281-0 2015 Discovery of new acylaminopyridines as GSK-3 inhibitors by a structure guided in-depth exploration of chemical space around a pyrrolopyridinone core. pyrrolopyridone 126-143 glycogen synthase kinase 3 beta Mus musculus 39-44 25845281-4 2015 We identified several series of promising new GSK-3beta inhibitors from a coherent design around a pyrrolopyridinone core structure. pyrrolopyridone 99-116 glycogen synthase kinase 3 beta Mus musculus 46-55 25661065-11 2015 Thus, these data demonstrated that miR-346 participated in the epithelial-mesenchymal transition in mouse podocytes under high-glucose conditions and that miR-346 could indirectly regulate the expression of GSK-3beta in mouse podocytes. Glucose 127-134 glycogen synthase kinase 3 beta Mus musculus 207-216 25512114-3 2015 METHODS: Thiadiazolidinone 8 (TDZD-8), a selective inhibitor of GSK-3beta, was administered intraperitoneally to 12-week-old MRL/lpr mice for 8 weeks or to 22-week-old (NZB x NZW)F1 mice for 12 weeks. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 9-28 glycogen synthase kinase 3 beta Mus musculus 64-73 25512114-3 2015 METHODS: Thiadiazolidinone 8 (TDZD-8), a selective inhibitor of GSK-3beta, was administered intraperitoneally to 12-week-old MRL/lpr mice for 8 weeks or to 22-week-old (NZB x NZW)F1 mice for 12 weeks. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 30-36 glycogen synthase kinase 3 beta Mus musculus 64-73 25512114-8 2015 TDZD-8 inhibited the activation of GSK-3beta and caspase 1, with a concomitant decrease in interleukin-1beta (IL-1beta) synthesis. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 0-6 glycogen synthase kinase 3 beta Mus musculus 35-44 25716948-6 2015 The results showed that treatment with berberine resulted in a reduction in the phosphorylation of PI3K/AKT, ERK, and GSK3beta. Berberine 39-48 glycogen synthase kinase 3 beta Mus musculus 118-126 25950476-5 2015 Geniposide protected beta-cell through activating Wnt signaling, enhanced expressions of TCF7L2 and GLP-1R, activated AKT, inhibited GSK3beta activity, and promoted beta-catenin nuclear translocation. geniposide 0-10 glycogen synthase kinase 3 beta Mus musculus 133-141 25906473-8 2015 Treatment with AMPK or GSK3 inhibitors reverse the inhibitory effect of neuroinflammation by paeonol in microglial cells. paeonol 93-100 glycogen synthase kinase 3 beta Mus musculus 23-27 25716948-0 2015 Berberine regulates melanin synthesis by activating PI3K/AKT, ERK and GSK3beta in B16F10 melanoma cells. Melanins 20-27 glycogen synthase kinase 3 beta Mus musculus 70-78 25655048-9 2015 In immortalized mouse podocytes (iMPs), high glucose (HG), silencing RNA (siRNA) or blocking LRP6 (DKK-1) reduced p-LRP6 expression, leading to high GSK3beta-p53, p53 expression, apoptosis and increased albumin influx. Glucose 45-52 glycogen synthase kinase 3 beta Mus musculus 149-157 24788685-0 2015 Linoleic acid derivative DCP-LA ameliorates stress-induced depression-related behavior by promoting cell surface 5-HT1A receptor translocation, stimulating serotonin release, and inactivating GSK-3beta. Linoleic Acid 0-13 glycogen synthase kinase 3 beta Mus musculus 192-201 24915968-7 2015 The role of phosphorylation of glycogen synthesis kinase 3 beta (GSK-3beta) at Ser-9 in the EA pretreatment was also assessed. Serine 79-82 glycogen synthase kinase 3 beta Mus musculus 65-74 24788685-0 2015 Linoleic acid derivative DCP-LA ameliorates stress-induced depression-related behavior by promoting cell surface 5-HT1A receptor translocation, stimulating serotonin release, and inactivating GSK-3beta. 8-(2-(2-pentyl-cyclopropylmethyl)cyclopropyl)octanoic acid 25-31 glycogen synthase kinase 3 beta Mus musculus 192-201 24788685-5 2015 Moreover, DCP-LA stimulated serotonin release from hypothalamic slices and cancelled restraint stress-induced reduction of GSK-3beta phosphorylation at Ser9. 8-(2-(2-pentyl-cyclopropylmethyl)cyclopropyl)octanoic acid 10-16 glycogen synthase kinase 3 beta Mus musculus 123-132 25329250-0 2015 Small-molecule inhibitor of glycogen synthase kinase 3beta 6-Bromoindirubin-3-oxime inhibits hematopoietic regeneration in stem cell recipient mice. 6-bromoindirubin-3'-oxime 59-83 glycogen synthase kinase 3 beta Mus musculus 28-58 25781227-0 2015 Pregnenolone sulfate normalizes schizophrenia-like behaviors in dopamine transporter knockout mice through the AKT/GSK3beta pathway. pregnenolone sulfate 0-20 glycogen synthase kinase 3 beta Mus musculus 115-123 25781227-7 2015 Moreover, we found that acute treatment with pregnenolone sulfate increased the phosphorylation levels of striatal AKT and GSK3beta in DAT-KO mice, and that long-term treatment with pregnenolone sulfate increased expression levels of NR1 subunit of the NMDA receptor in hippocampus. pregnenolone sulfate 45-65 glycogen synthase kinase 3 beta Mus musculus 123-131 25781227-7 2015 Moreover, we found that acute treatment with pregnenolone sulfate increased the phosphorylation levels of striatal AKT and GSK3beta in DAT-KO mice, and that long-term treatment with pregnenolone sulfate increased expression levels of NR1 subunit of the NMDA receptor in hippocampus. pregnenolone sulfate 182-202 glycogen synthase kinase 3 beta Mus musculus 123-131 25781227-8 2015 Thus, pregnenolone sulfate was able to rescue the behavioral anomalies of DAT-KO mice through the NMDA receptor-mediated, AKT/GSK3beta signaling pathway. pregnenolone sulfate 6-26 glycogen synthase kinase 3 beta Mus musculus 126-134 25662052-11 2015 Additionally, the regulation of the Akt/GSK3beta/beta-catenin pathway is severely disturbed in TG at baseline where a significant activation of Akt is found that coincides with the typical phosphorylation of GSK3beta. Thioguanine 95-97 glycogen synthase kinase 3 beta Mus musculus 40-48 25662052-11 2015 Additionally, the regulation of the Akt/GSK3beta/beta-catenin pathway is severely disturbed in TG at baseline where a significant activation of Akt is found that coincides with the typical phosphorylation of GSK3beta. Thioguanine 95-97 glycogen synthase kinase 3 beta Mus musculus 208-216 25852508-0 2015 Glycogen synthase kinase-3beta inhibition in the medial prefrontal cortex mediates paradoxical amphetamine action in a mouse model of ADHD. Amphetamine 95-106 glycogen synthase kinase 3 beta Mus musculus 0-30 25852508-7 2015 Instead, the calming activity of amphetamine corresponded to the inhibition of glycogen synthase kinase 3beta (GSK3beta) activity, specifically in the mPFC. Amphetamine 33-44 glycogen synthase kinase 3 beta Mus musculus 79-109 25852508-7 2015 Instead, the calming activity of amphetamine corresponded to the inhibition of glycogen synthase kinase 3beta (GSK3beta) activity, specifically in the mPFC. Amphetamine 33-44 glycogen synthase kinase 3 beta Mus musculus 111-119 25852508-8 2015 Accordingly, not only systemic administration of the GSK3beta inhibitor TDZD-8 (20 mg/kg), but also local microinjections of TDZD-8 and amphetamine into the mPFC, but not into the striatum, decreased locomotor activity in LAB mice. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 72-78 glycogen synthase kinase 3 beta Mus musculus 53-61 25852508-9 2015 Amphetamine effects seem to depend on NMDA receptor signaling, since pre- or co-treatment with MK-801 (0.3 mg/kg) abolished the effects of amphetamine (1 mg/kg) on the locomotion and on the phosphorylation of GSK3beta at the level of the mPFC. Amphetamine 0-11 glycogen synthase kinase 3 beta Mus musculus 209-217 25852508-9 2015 Amphetamine effects seem to depend on NMDA receptor signaling, since pre- or co-treatment with MK-801 (0.3 mg/kg) abolished the effects of amphetamine (1 mg/kg) on the locomotion and on the phosphorylation of GSK3beta at the level of the mPFC. Dizocilpine Maleate 95-101 glycogen synthase kinase 3 beta Mus musculus 209-217 25852508-9 2015 Amphetamine effects seem to depend on NMDA receptor signaling, since pre- or co-treatment with MK-801 (0.3 mg/kg) abolished the effects of amphetamine (1 mg/kg) on the locomotion and on the phosphorylation of GSK3beta at the level of the mPFC. Amphetamine 139-150 glycogen synthase kinase 3 beta Mus musculus 209-217 25852508-10 2015 Taken together, the paradoxical calming effect of amphetamine in hyperactive LAB mice concurs with a decreased GSK3beta activity in the mPFC. Amphetamine 50-61 glycogen synthase kinase 3 beta Mus musculus 111-119 25608967-2 2015 GSK3beta has been shown to play a role in the ability of kidneys to concentrate urine by regulating vasopressin-mediated water permeability of collecting ducts, whereas the role of GSK3alpha has yet to be discerned. Water 121-126 glycogen synthase kinase 3 beta Mus musculus 0-8 25608967-9 2015 When treated with LiCl, an isoform nonselective inhibitor of GSK3 and known inducer of polyuria, WT mice developed significant polyuria within 6 days. Lithium Chloride 18-22 glycogen synthase kinase 3 beta Mus musculus 61-65 25329250-2 2015 Here, we investigated the effect of GSK3beta inhibitor 6-Bromoindirubin-3-oxime (BIO) previously shown to inhibit leukemia cell growth in vitro and of animal models on hematopoietic regeneration in recipients of stem cell transplant. 6-bromoindirubin-3'-oxime 55-79 glycogen synthase kinase 3 beta Mus musculus 36-44 25727520-0 2015 GSK3 inhibitors CHIR99021 and 6-bromoindirubin-3"-oxime inhibit microRNA maturation in mouse embryonic stem cells. 6-bromoindirubin-3'-oxime 30-55 glycogen synthase kinase 3 beta Mus musculus 0-4 25788881-8 2015 Acute 1 h pretreatment with the GSK3 inhibitor TDZD-8 also improved novel object recognition and temporal ordering in male and female GSK3 knockin mice. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 47-53 glycogen synthase kinase 3 beta Mus musculus 32-36 25788881-8 2015 Acute 1 h pretreatment with the GSK3 inhibitor TDZD-8 also improved novel object recognition and temporal ordering in male and female GSK3 knockin mice. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 47-53 glycogen synthase kinase 3 beta Mus musculus 134-138 25740518-5 2015 This relative suppression in axon growth behaviors is due to Coronin-1-dependent calcium release via PLC-gamma1 signaling, which releases PI3K-dependent suppression of GSK3beta. Calcium 81-88 glycogen synthase kinase 3 beta Mus musculus 168-176 25560828-3 2015 Western blottings revealed that protein kinase B (AKT)-mediated glucose signaling was down-regulated in diabetic testes and further decreased in FGF21-KO diabetic group both 10 days and 2 months after diabetes onset, reflected by reduced glycogen synthase (GS) kinase (GSK)-3beta phosphorylation and increased GS phosphorylation. Glucose 64-71 glycogen synthase kinase 3 beta Mus musculus 238-279 25733715-3 2015 Front-end electron transfer dissociation mass spectrometry analyses of DP revealed six novel serine phosphorylation sites dependent on GSK3 signaling and four novel arginine methylation sites including R2834, the mutation of which has been associated with arrhythmogenic cardiomyopathy (AC). Serine 93-99 glycogen synthase kinase 3 beta Mus musculus 135-139 24760579-4 2015 The tibias were treated with dimethylsulfoxide (control) or GSK-3 inhibitor SB415286 (SB86). 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 76-84 glycogen synthase kinase 3 beta Mus musculus 60-65 25179772-0 2015 Therapeutic concentration of lithium stimulates complement C3 production in dendritic cells and microglia via GSK-3 inhibition. Lithium 29-36 glycogen synthase kinase 3 beta Mus musculus 110-115 25617668-5 2015 Upstream signaling involving phosphorylation of Akt and GSK-3beta was induced by RANKL, of which the signaling was inhibited by DTCM-glutarimide. 3-((dodecylthiocarbonyl)methyl)glutarimide 128-144 glycogen synthase kinase 3 beta Mus musculus 56-65 25617668-7 2015 Thus, DTCM-glutarimide inhibited osteoclastogenesis by blocking both the Akt-GSK3beta-NFATc1 and NF-kappaB-NFATc1 pathways. 3-((dodecylthiocarbonyl)methyl)glutarimide 6-22 glycogen synthase kinase 3 beta Mus musculus 77-85 25565601-4 2015 In this study, we showed that glycogen synthase kinase 3beta (GSK3beta) inhibitors - SB216763, LiCl and azakenpaullone - enhanced LPS-induced OPN expression in mouse peritoneal macrophages. SB 216763 85-93 glycogen synthase kinase 3 beta Mus musculus 30-60 25565601-4 2015 In this study, we showed that glycogen synthase kinase 3beta (GSK3beta) inhibitors - SB216763, LiCl and azakenpaullone - enhanced LPS-induced OPN expression in mouse peritoneal macrophages. SB 216763 85-93 glycogen synthase kinase 3 beta Mus musculus 62-70 25565601-4 2015 In this study, we showed that glycogen synthase kinase 3beta (GSK3beta) inhibitors - SB216763, LiCl and azakenpaullone - enhanced LPS-induced OPN expression in mouse peritoneal macrophages. Lithium Chloride 95-99 glycogen synthase kinase 3 beta Mus musculus 30-60 25565601-4 2015 In this study, we showed that glycogen synthase kinase 3beta (GSK3beta) inhibitors - SB216763, LiCl and azakenpaullone - enhanced LPS-induced OPN expression in mouse peritoneal macrophages. Lithium Chloride 95-99 glycogen synthase kinase 3 beta Mus musculus 62-70 25565601-4 2015 In this study, we showed that glycogen synthase kinase 3beta (GSK3beta) inhibitors - SB216763, LiCl and azakenpaullone - enhanced LPS-induced OPN expression in mouse peritoneal macrophages. 1-Azakenpaullone 104-118 glycogen synthase kinase 3 beta Mus musculus 30-60 25565601-4 2015 In this study, we showed that glycogen synthase kinase 3beta (GSK3beta) inhibitors - SB216763, LiCl and azakenpaullone - enhanced LPS-induced OPN expression in mouse peritoneal macrophages. 1-Azakenpaullone 104-118 glycogen synthase kinase 3 beta Mus musculus 62-70 25262943-4 2015 KEY RESULTS: TDZD-8 therapy prominently ameliorated the proteinuria and glomerular sclerosis in mice with adriamycin nephropathy; this was associated with a correction of GSK3beta overactivity in the glomerulus and attenuation of podocyte injuries, including foot process effacement and podocyte death. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 13-19 glycogen synthase kinase 3 beta Mus musculus 171-179 25262943-5 2015 Consistently, in adriamycin-injured podocytes, TDZD-8 treatment counteracted GSK3beta overactivity, improved cell viability and prevented death, concomitant with diminished oxidative stress, improved mitochondrial dysfunction and desensitized MPT. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 47-53 glycogen synthase kinase 3 beta Mus musculus 77-85 25262943-7 2015 TDZD-8 treatment prevented the GSK3beta-controlled phosphorylation and activation of cyclophilin F, desensitized MPT and alleviated the damage to mitochondria in podocytes induced by adriamycin in vivo and in vitro. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 0-6 glycogen synthase kinase 3 beta Mus musculus 31-39 25262943-7 2015 TDZD-8 treatment prevented the GSK3beta-controlled phosphorylation and activation of cyclophilin F, desensitized MPT and alleviated the damage to mitochondria in podocytes induced by adriamycin in vivo and in vitro. Doxorubicin 183-193 glycogen synthase kinase 3 beta Mus musculus 31-39 25555252-13 2015 CONCLUSION: Our findings show that LiCl-mediated GSK3beta inhibition prevents palatal fusion and osteogenic differentiation in palatal shelves by increased beta-catenin signaling. Lithium Chloride 35-39 glycogen synthase kinase 3 beta Mus musculus 49-57 25625347-7 2015 Depending upon gestational age, corticosterone treatment increased phosphorylation of the insulin-signalling proteins, protein kinase B (Akt) and glycogen synthase-kinase 3beta, in maternal liver (P < 0.05) but not placenta (P > 0.05). Corticosterone 32-46 glycogen synthase kinase 3 beta Mus musculus 146-176 25713323-4 2015 In the liver, there was a 2.5-fold increase in insulin stimulated Akt(SER) (473) phosphorylation, and a threefold increase in insulin-stimulated (0.5 U/kg) GSK3beta(SER) (9) phosphorylation in RUN compared to SED mice. Serine 165-168 glycogen synthase kinase 3 beta Mus musculus 156-164 25644393-11 2015 Moreover, DFO attenuated elevated expression of caspase-3, modulated GSK3beta activity, and prevented LPS-induced increases of MDA and SOD levels in the hippocampus. Deferoxamine 10-13 glycogen synthase kinase 3 beta Mus musculus 69-77 25053111-0 2015 Lithium chloride suppresses LPS-mediated matrix metalloproteinase-9 expression in macrophages through phosphorylation of GSK-3beta. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 121-130 25053111-2 2015 We report that lithium chloride (LiCl) or CHIR99021, inhibitors of Wnt signaling pathway, enhance phosphorylation of glycogen synthase kinase-3beta and suppress lipopolysaccharide-mediated upregulation of MMP-9 expression in murine macrophage RAW264.7 cells in a dose-dependent manner. Lithium Chloride 15-31 glycogen synthase kinase 3 beta Mus musculus 117-147 25053111-2 2015 We report that lithium chloride (LiCl) or CHIR99021, inhibitors of Wnt signaling pathway, enhance phosphorylation of glycogen synthase kinase-3beta and suppress lipopolysaccharide-mediated upregulation of MMP-9 expression in murine macrophage RAW264.7 cells in a dose-dependent manner. Lithium Chloride 33-37 glycogen synthase kinase 3 beta Mus musculus 117-147 25504636-3 2015 We previously reported that inhibition of GSK3beta compromises the survival and proliferation of glioblastoma cells, induces their apoptosis, and sensitizes them to temozolomide and radiation. Temozolomide 165-177 glycogen synthase kinase 3 beta Mus musculus 42-50 25192664-10 2015 Meanwhile, LiCl further up-regulated phospho-Akt Ser473 and phospho-GSK3beta Ser9 expression. Lithium Chloride 11-15 glycogen synthase kinase 3 beta Mus musculus 68-76 25192664-14 2015 LiCl treatment exerted a neuroprotective effect on learning and memory by potentiating the Akt/GSK3beta cell-signaling pathway. Lithium Chloride 0-4 glycogen synthase kinase 3 beta Mus musculus 95-103 25692006-3 2015 The mood stabilizer lithium influences behavior and Akt/GSK-3 signaling in mice and many antipsychotics have been shown to more potently antagonize the activity of the beta-arrestin-2 pathway relative to the G protein-dependent pathway. Lithium 20-27 glycogen synthase kinase 3 beta Mus musculus 56-61 25541422-4 2015 Extracellular perfusion and subsequent internalization of Abeta42 increase spike discharge and promote GSK-3-dependent phosphorylation of the Kv4.2 alpha-subunit, a molecular determinant of A-type K(+) currents, at Ser-616. Serine 215-218 glycogen synthase kinase 3 beta Mus musculus 103-108 25541422-6 2015 Collectively, these data suggest that intraneuronal Abeta42 accumulation leads to an intracellular cascade culminating into caspases activation and GSK-3-dependent phosphorylation of Kv4.2 channels. UNII-042A8N37WH 52-59 glycogen synthase kinase 3 beta Mus musculus 148-153 25477508-6 2015 Dyrk1A-mediated phosphorylation at the Thr(356) residue inhibits GSK3beta activity. Threonine 39-42 glycogen synthase kinase 3 beta Mus musculus 65-73 25477508-9 2015 The level of Thr(P)(356)-GSK3beta was higher in the white adipose tissue of Dyrk1A TG mice compared with control mice. Threonine 13-16 glycogen synthase kinase 3 beta Mus musculus 25-33 26317159-5 2015 Interestingly, the pathways involving Per2 and Cry1, which regulate the behavior in the FST and the response to lithium, are distinct as evidenced by the phosphorylation of GSK3beta after lithium treatment and the modulation of dopamine levels in the striatum. Lithium 112-119 glycogen synthase kinase 3 beta Mus musculus 173-181 25468908-4 2015 GSK3beta overactivity induced by adriamycin injury or by a constitutively active mutant of GSK3beta augmented phosphorylation of Tau and CRMP2, concomitant with microtubule depolymerization, cell body shrinkage, and shortening of podocyte processes. Doxorubicin 33-43 glycogen synthase kinase 3 beta Mus musculus 0-8 25468908-5 2015 Conversely, inhibition of GSK3beta by a dominant negative mutant or by lithium, a Food and Drug Administration-approved neuroprotective mood stabilizer, diminished Tau and CRMP2 phosphorylation, resulting in microtubule polymerization, podocyte expansion, and lengthening of podocyte processes. Lithium 71-78 glycogen synthase kinase 3 beta Mus musculus 26-34 25468908-7 2015 Mechanistically, lithium therapy obliterated GSK3beta overactivity, mitigated phosphorylation of Tau and CRMP2, and enhanced microtubule polymerization and stabilization in glomeruli in adriamycin-injured kidneys, associated with elongation of podocyte major processes. Lithium 17-24 glycogen synthase kinase 3 beta Mus musculus 45-53 28649528-8 2015 Further, Akt/GSK3/cyclin D1 signaling pathways in the liver of treated mice were altered, which may help prevent homocysteine-induced cell cycle dysfunction. Homocysteine 113-125 glycogen synthase kinase 3 beta Mus musculus 13-17 25559887-8 2015 In the ex-vivo model, we showed that n-3 FAs increased phosphorylation of AKT and GSK3beta proteins (p<0.05). Fatty Acids 41-44 glycogen synthase kinase 3 beta Mus musculus 82-90 26317159-5 2015 Interestingly, the pathways involving Per2 and Cry1, which regulate the behavior in the FST and the response to lithium, are distinct as evidenced by the phosphorylation of GSK3beta after lithium treatment and the modulation of dopamine levels in the striatum. Lithium 188-195 glycogen synthase kinase 3 beta Mus musculus 173-181 25630719-9 2015 4-PBA also decreased GSK3beta activity in the livers of ALF mice. 4-phenylbutyric acid 0-5 glycogen synthase kinase 3 beta Mus musculus 21-29 26278531-0 2015 N-(4-bromophenethyl) Caffeamide Inhibits Melanogenesis by Regulating AKT/Glycogen Synthase Kinase 3 Beta/Microphthalmia-associated Transcription Factor and Tyrosinase-related Protein 1/Tyrosinase. n-(4-bromophenethyl) 0-20 glycogen synthase kinase 3 beta Mus musculus 73-151 26278531-0 2015 N-(4-bromophenethyl) Caffeamide Inhibits Melanogenesis by Regulating AKT/Glycogen Synthase Kinase 3 Beta/Microphthalmia-associated Transcription Factor and Tyrosinase-related Protein 1/Tyrosinase. caffeamide 21-31 glycogen synthase kinase 3 beta Mus musculus 73-151 25630719-11 2015 ER stress promoted LPS-triggered inflammation depending on GSK3beta activation because inhibition of GSK3beta by SB216763, the specific inhibitor of GSK3beta, resulted in downregulation of pro-inflammatory genes. SB 216763 113-121 glycogen synthase kinase 3 beta Mus musculus 59-67 25630719-11 2015 ER stress promoted LPS-triggered inflammation depending on GSK3beta activation because inhibition of GSK3beta by SB216763, the specific inhibitor of GSK3beta, resulted in downregulation of pro-inflammatory genes. SB 216763 113-121 glycogen synthase kinase 3 beta Mus musculus 101-109 25630719-11 2015 ER stress promoted LPS-triggered inflammation depending on GSK3beta activation because inhibition of GSK3beta by SB216763, the specific inhibitor of GSK3beta, resulted in downregulation of pro-inflammatory genes. SB 216763 113-121 glycogen synthase kinase 3 beta Mus musculus 101-109 24997566-6 2015 The results suggest that anthocyanins significantly reversed the ethanol-induced inhibition of glutamatergic neurotransmission, synaptic dysfunction, GABAB1R activation, and neuronal apoptosis by stimulating the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/v-akt murine thymoma viral oncogene (Akt)/glycogen synthase kinase 3 beta (GSK3beta) pathway in the hippocampus of postnatal rat brain. Anthocyanins 25-37 glycogen synthase kinase 3 beta Mus musculus 308-339 25908255-4 2015 The administration of Fasudil exhibited neuroprotective effects against the dopaminergic neurons and improved the motor function recovery in the MPTP-PD mice, accompanied by the suppression of inflammatory responses (IL-1beta, TNF-alpha, NF-kappaB-p65 and TLR-2), and oxidative stress (iNOS and gp91Phox), which might be associated with the inhibition of ROCK and GSK-3beta activity. fasudil 22-29 glycogen synthase kinase 3 beta Mus musculus 364-373 24997566-6 2015 The results suggest that anthocyanins significantly reversed the ethanol-induced inhibition of glutamatergic neurotransmission, synaptic dysfunction, GABAB1R activation, and neuronal apoptosis by stimulating the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/v-akt murine thymoma viral oncogene (Akt)/glycogen synthase kinase 3 beta (GSK3beta) pathway in the hippocampus of postnatal rat brain. Anthocyanins 25-37 glycogen synthase kinase 3 beta Mus musculus 341-349 24997566-6 2015 The results suggest that anthocyanins significantly reversed the ethanol-induced inhibition of glutamatergic neurotransmission, synaptic dysfunction, GABAB1R activation, and neuronal apoptosis by stimulating the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/v-akt murine thymoma viral oncogene (Akt)/glycogen synthase kinase 3 beta (GSK3beta) pathway in the hippocampus of postnatal rat brain. Ethanol 65-72 glycogen synthase kinase 3 beta Mus musculus 308-339 24997566-6 2015 The results suggest that anthocyanins significantly reversed the ethanol-induced inhibition of glutamatergic neurotransmission, synaptic dysfunction, GABAB1R activation, and neuronal apoptosis by stimulating the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/v-akt murine thymoma viral oncogene (Akt)/glycogen synthase kinase 3 beta (GSK3beta) pathway in the hippocampus of postnatal rat brain. Ethanol 65-72 glycogen synthase kinase 3 beta Mus musculus 341-349 25237909-8 2015 CONCLUSIONS: Luteolin + Gem promoted apoptotic cell death in pancreatic tumor cells in vivo through inhibition of the K-ras/GSK-3beta/NF-kappaB signaling pathway, leading to a reduction in the Bcl-2/Bax ratio, release of cytochrome c, and activation of caspase 3. luteolin + gem 13-27 glycogen synthase kinase 3 beta Mus musculus 124-133 26798521-2 2015 We have recently determined that ANDRO is a competitive inhibitor of glycogen synthase kinase-3beta (GSK-3beta), a key enzyme of the Wnt/beta-catenin signaling cascade. andrographolide 33-38 glycogen synthase kinase 3 beta Mus musculus 69-99 25565776-15 2015 Coff or Caff, plus Mel inhibited GSK3beta, Akt, PI3K p55, and Tau phosphorylation but enhanced PI3K p85 and Erk1/2 phosphorylation in N2a/APP cells. Caffeine 8-12 glycogen synthase kinase 3 beta Mus musculus 33-41 25565776-15 2015 Coff or Caff, plus Mel inhibited GSK3beta, Akt, PI3K p55, and Tau phosphorylation but enhanced PI3K p85 and Erk1/2 phosphorylation in N2a/APP cells. Melatonin 19-22 glycogen synthase kinase 3 beta Mus musculus 33-41 25565776-19 2015 Taken together, combination of Caff or Coff, before treatment with Mel elicits an additive antiamyloidogenic effects in N2a/APP cells, probably through inhibition of Abeta oligomerization and modulation of the Akt/GSK3beta/Tau signaling pathway. Caffeine 31-35 glycogen synthase kinase 3 beta Mus musculus 214-222 25463972-7 2014 Fluoxetine stimulated phosphorylation of Akt(Thr308) and GSK-3beta(Ser9) in the hippocampus and prefrontal cortex (PFC) of wild-type mice but not in db/db mice. Fluoxetine 0-10 glycogen synthase kinase 3 beta Mus musculus 57-66 25467150-0 2014 Novel benzothiazinones (BTOs) as allosteric modulator or substrate competitive inhibitor of glycogen synthase kinase 3beta (GSK-3beta) with cellular activity of promoting glucose uptake. benzothiazinones 6-22 glycogen synthase kinase 3 beta Mus musculus 92-122 25467150-0 2014 Novel benzothiazinones (BTOs) as allosteric modulator or substrate competitive inhibitor of glycogen synthase kinase 3beta (GSK-3beta) with cellular activity of promoting glucose uptake. benzothiazinones 6-22 glycogen synthase kinase 3 beta Mus musculus 124-133 25467150-0 2014 Novel benzothiazinones (BTOs) as allosteric modulator or substrate competitive inhibitor of glycogen synthase kinase 3beta (GSK-3beta) with cellular activity of promoting glucose uptake. btos 24-28 glycogen synthase kinase 3 beta Mus musculus 92-122 25467150-0 2014 Novel benzothiazinones (BTOs) as allosteric modulator or substrate competitive inhibitor of glycogen synthase kinase 3beta (GSK-3beta) with cellular activity of promoting glucose uptake. btos 24-28 glycogen synthase kinase 3 beta Mus musculus 124-133 25467150-0 2014 Novel benzothiazinones (BTOs) as allosteric modulator or substrate competitive inhibitor of glycogen synthase kinase 3beta (GSK-3beta) with cellular activity of promoting glucose uptake. Glucose 171-178 glycogen synthase kinase 3 beta Mus musculus 92-122 25467150-0 2014 Novel benzothiazinones (BTOs) as allosteric modulator or substrate competitive inhibitor of glycogen synthase kinase 3beta (GSK-3beta) with cellular activity of promoting glucose uptake. Glucose 171-178 glycogen synthase kinase 3 beta Mus musculus 124-133 25467150-4 2014 Here we reported two benzothiazinone compounds (BTO), named BTO-5h (IC50=8 muM) and BTO-5s (IC50=10 muM) as novel allosteric modulator and substrate competitive inhibitor of GSK-3beta, respectively. benzothiazinone 21-36 glycogen synthase kinase 3 beta Mus musculus 174-183 25467150-4 2014 Here we reported two benzothiazinone compounds (BTO), named BTO-5h (IC50=8 muM) and BTO-5s (IC50=10 muM) as novel allosteric modulator and substrate competitive inhibitor of GSK-3beta, respectively. bto 48-51 glycogen synthase kinase 3 beta Mus musculus 174-183 25467150-4 2014 Here we reported two benzothiazinone compounds (BTO), named BTO-5h (IC50=8 muM) and BTO-5s (IC50=10 muM) as novel allosteric modulator and substrate competitive inhibitor of GSK-3beta, respectively. bto-5h 60-66 glycogen synthase kinase 3 beta Mus musculus 174-183 25467150-4 2014 Here we reported two benzothiazinone compounds (BTO), named BTO-5h (IC50=8 muM) and BTO-5s (IC50=10 muM) as novel allosteric modulator and substrate competitive inhibitor of GSK-3beta, respectively. bto-5s 84-90 glycogen synthase kinase 3 beta Mus musculus 174-183 25339176-2 2014 We have previously shown that high glucose-induced matrix protein synthesis is associated with inactivation of glycogen synthase kinase 3beta (GSK3beta) in renal cells and in the kidneys of diabetic mice. Glucose 35-42 glycogen synthase kinase 3 beta Mus musculus 111-141 25339176-2 2014 We have previously shown that high glucose-induced matrix protein synthesis is associated with inactivation of glycogen synthase kinase 3beta (GSK3beta) in renal cells and in the kidneys of diabetic mice. Glucose 35-42 glycogen synthase kinase 3 beta Mus musculus 143-151 25339176-3 2014 We tested whether activation of GSK3beta by sodium nitroprusside (SNP) mitigates kidney injury in diabetes. Nitroprusside 44-64 glycogen synthase kinase 3 beta Mus musculus 32-40 25331948-9 2014 We show that Syk inhibition induces an increased phosphorylation of the inhibitory Ser-9 residue of glycogen synthase kinase-3beta, a primary Tau kinase involved in Tau phosphorylation, by activating protein kinase A, providing a mechanism explaining the reduction of Tau phosphorylation at GSK3beta-dependent epitopes following Syk inhibition. Serine 83-86 glycogen synthase kinase 3 beta Mus musculus 100-130 25331948-9 2014 We show that Syk inhibition induces an increased phosphorylation of the inhibitory Ser-9 residue of glycogen synthase kinase-3beta, a primary Tau kinase involved in Tau phosphorylation, by activating protein kinase A, providing a mechanism explaining the reduction of Tau phosphorylation at GSK3beta-dependent epitopes following Syk inhibition. Serine 83-86 glycogen synthase kinase 3 beta Mus musculus 291-299 25270429-0 2014 Chronic phencyclidine induces inflammatory responses and activates GSK3beta in mice. Phencyclidine 8-21 glycogen synthase kinase 3 beta Mus musculus 67-75 25223889-5 2014 Here we demonstrate that, the TLR4 agonist 29 KDa beta 1,4-galactose terminal glycoprotein (GP29) of LD activated GSK3beta through TLR4 to induce IL-12-mediated Nitric oxide (NO) production that resulted in effective parasite clearance from macrophages. Nitric Oxide 161-173 glycogen synthase kinase 3 beta Mus musculus 114-122 25223889-8 2014 Complete absence of GP29 mediated protection with down regulated NO and IL-12 production and dominant IL-10 production in presence of the GSK3beta inhibitor, Lithium chloride reiterated the role of GSK3beta in disease resolution in the murine model of visceral leishmaniasis. Lithium Chloride 158-174 glycogen synthase kinase 3 beta Mus musculus 138-146 25223889-8 2014 Complete absence of GP29 mediated protection with down regulated NO and IL-12 production and dominant IL-10 production in presence of the GSK3beta inhibitor, Lithium chloride reiterated the role of GSK3beta in disease resolution in the murine model of visceral leishmaniasis. Lithium Chloride 158-174 glycogen synthase kinase 3 beta Mus musculus 198-206 25270429-10 2014 Furthermore, PCP treatment decreased ratio of the phospho-Ser9 epitope of glycogen synthase kinase-3beta (GSK3beta) over total GSK3beta, which is indicative of increased GSK3beta activity. Phencyclidine 13-16 glycogen synthase kinase 3 beta Mus musculus 74-104 25270429-10 2014 Furthermore, PCP treatment decreased ratio of the phospho-Ser9 epitope of glycogen synthase kinase-3beta (GSK3beta) over total GSK3beta, which is indicative of increased GSK3beta activity. Phencyclidine 13-16 glycogen synthase kinase 3 beta Mus musculus 106-114 25270429-10 2014 Furthermore, PCP treatment decreased ratio of the phospho-Ser9 epitope of glycogen synthase kinase-3beta (GSK3beta) over total GSK3beta, which is indicative of increased GSK3beta activity. Phencyclidine 13-16 glycogen synthase kinase 3 beta Mus musculus 127-135 25270429-10 2014 Furthermore, PCP treatment decreased ratio of the phospho-Ser9 epitope of glycogen synthase kinase-3beta (GSK3beta) over total GSK3beta, which is indicative of increased GSK3beta activity. Phencyclidine 13-16 glycogen synthase kinase 3 beta Mus musculus 127-135 25270429-11 2014 These data demonstrate that chronic PCP in mouse produces inflammatory responses and GSK3beta activation. Phencyclidine 36-39 glycogen synthase kinase 3 beta Mus musculus 85-93 25239914-5 2014 GSK3beta inhibitors BIO (6-bromoindirubin-3"-oxime), SB216763, or siRNA knockdown of GSK3beta, but not the PI3K/AKT inhibitor LY294002, prevented Thr172-AMPK dephosphorylation. 6-bromoindirubin-3'-oxime 25-50 glycogen synthase kinase 3 beta Mus musculus 0-8 25239914-5 2014 GSK3beta inhibitors BIO (6-bromoindirubin-3"-oxime), SB216763, or siRNA knockdown of GSK3beta, but not the PI3K/AKT inhibitor LY294002, prevented Thr172-AMPK dephosphorylation. SB 216763 53-61 glycogen synthase kinase 3 beta Mus musculus 0-8 25003317-0 2014 Regulation of methylglyoxal-elicited leukocyte recruitment by endothelial SGK1/GSK3 signaling. Pyruvaldehyde 14-27 glycogen synthase kinase 3 beta Mus musculus 79-83 24949891-7 2014 Treatment with LiCl, a GSK-3beta inhibitor, and inhibition of PPARgamma expression suppressed the accelerated adipogenesis of shPP2A cells. Lithium Chloride 15-19 glycogen synthase kinase 3 beta Mus musculus 23-32 25003317-4 2014 Using intravital microscopy of mouse cremasteric microvasculature, we demonstrate that GSK3 inhibitors lithium and SB216763 mitigate MG-elicited leukocyte recruitment and microvascular hyperpermeability. Lithium 103-110 glycogen synthase kinase 3 beta Mus musculus 87-91 25003317-4 2014 Using intravital microscopy of mouse cremasteric microvasculature, we demonstrate that GSK3 inhibitors lithium and SB216763 mitigate MG-elicited leukocyte recruitment and microvascular hyperpermeability. SB 216763 115-123 glycogen synthase kinase 3 beta Mus musculus 87-91 25003317-4 2014 Using intravital microscopy of mouse cremasteric microvasculature, we demonstrate that GSK3 inhibitors lithium and SB216763 mitigate MG-elicited leukocyte recruitment and microvascular hyperpermeability. Pyruvaldehyde 133-135 glycogen synthase kinase 3 beta Mus musculus 87-91 25003317-6 2014 At later time points (>=1h), MG induces GSK3 deactivation which is dissipated by siRNA silencing of SGK. Hydrogen 27-29 glycogen synthase kinase 3 beta Mus musculus 43-47 25003317-6 2014 At later time points (>=1h), MG induces GSK3 deactivation which is dissipated by siRNA silencing of SGK. Pyruvaldehyde 32-34 glycogen synthase kinase 3 beta Mus musculus 43-47 25258031-11 2014 BEZ235 also blocked the activation of Akt and GSK-3beta dramatically, whereas rapamycin has been shown to increase further upregulation of phosphorylated Akt on Ser473 both in vitro and in vivo. dactolisib 0-6 glycogen synthase kinase 3 beta Mus musculus 46-55 25135708-6 2014 Furthermore, Glycogen synthase kinase-3beta (GSK-3beta) phosphorylation significantly increased in the hesperidin-treated (100 mg/kg per day) group. Hesperidin 103-113 glycogen synthase kinase 3 beta Mus musculus 13-43 25294938-2 2014 We report that canonical Wnt signaling introduced either by forced expression of activated beta-catenin, or the small-molecule inhibitor of Gsk3, CHIR99021, satisfied the need for Wnt3a signaling, and that the small-molecule inhibitor of BMP type I receptors, LDN193189, was able to replace Nog. LDN 193189 260-269 glycogen synthase kinase 3 beta Mus musculus 140-144 25146901-8 2014 Further, lithium treatment significantly offset ACR-induced depletion in p-GSK-3beta (Ser9) levels in hippocampus. Lithium 9-16 glycogen synthase kinase 3 beta Mus musculus 75-84 25313506-0 2014 Peripherally triggered and GSK-3beta-driven brain inflammation differentially skew adult hippocampal neurogenesis, behavioral pattern separation and microglial activation in response to ibuprofen. Ibuprofen 186-195 glycogen synthase kinase 3 beta Mus musculus 27-36 25313506-4 2014 Here we studied the effects of ibuprofen administration on a familial AD mouse model overexpressing GSK-3beta that presents severe brain inflammation. Ibuprofen 31-40 glycogen synthase kinase 3 beta Mus musculus 100-109 25313506-9 2014 These data may be clinically relevant for AD therapies, as GSK-3beta appears to determine the efficacy of ibuprofen treatment. Ibuprofen 106-115 glycogen synthase kinase 3 beta Mus musculus 59-68 25336920-0 2014 (R)-(+)-alpha-lipoic acid protected NG108-15 cells against H2O2-induced cell death through PI3K-Akt/GSK-3beta pathway and suppression of NF-kappabeta-cytokines. Thioctic Acid 0-25 glycogen synthase kinase 3 beta Mus musculus 100-109 25336920-0 2014 (R)-(+)-alpha-lipoic acid protected NG108-15 cells against H2O2-induced cell death through PI3K-Akt/GSK-3beta pathway and suppression of NF-kappabeta-cytokines. Hydrogen Peroxide 59-63 glycogen synthase kinase 3 beta Mus musculus 100-109 25336920-6 2014 Moreover, pretreatment with R-LA stimulated the activation of PI3K-Akt through mTORC1 and mTORC2 components (mTOR, rictor and raptor) and production of antiinflammatory cytokine, IL-10 which led to the inactivation of glycogen synthase kinase-3beta (GSK-3beta) and reduction of both Bax/Bcl2 and Bax/Bcl-xL ratios, accompanied by inhibition of the cleaved caspase-3. Thioctic Acid 28-32 glycogen synthase kinase 3 beta Mus musculus 218-248 25336920-6 2014 Moreover, pretreatment with R-LA stimulated the activation of PI3K-Akt through mTORC1 and mTORC2 components (mTOR, rictor and raptor) and production of antiinflammatory cytokine, IL-10 which led to the inactivation of glycogen synthase kinase-3beta (GSK-3beta) and reduction of both Bax/Bcl2 and Bax/Bcl-xL ratios, accompanied by inhibition of the cleaved caspase-3. Thioctic Acid 28-32 glycogen synthase kinase 3 beta Mus musculus 250-259 25239564-0 2014 Glycogen synthase kinase 3beta dictates podocyte motility and focal adhesion turnover by modulating paxillin activity: implications for the protective effect of low-dose lithium in podocytopathy. Lithium 170-177 glycogen synthase kinase 3 beta Mus musculus 0-30 25239564-4 2014 In doxorubicin (Adriamycin)-injured podocytes, lithium, a GSK3beta inhibitor and neuroprotective mood stabilizer, obliterated the accelerated focal adhesion turnover, rectified podocyte hypermotility, and restored actin cytoskeleton integrity. Doxorubicin 3-14 glycogen synthase kinase 3 beta Mus musculus 58-66 25239564-4 2014 In doxorubicin (Adriamycin)-injured podocytes, lithium, a GSK3beta inhibitor and neuroprotective mood stabilizer, obliterated the accelerated focal adhesion turnover, rectified podocyte hypermotility, and restored actin cytoskeleton integrity. Doxorubicin 16-26 glycogen synthase kinase 3 beta Mus musculus 58-66 25239564-4 2014 In doxorubicin (Adriamycin)-injured podocytes, lithium, a GSK3beta inhibitor and neuroprotective mood stabilizer, obliterated the accelerated focal adhesion turnover, rectified podocyte hypermotility, and restored actin cytoskeleton integrity. Lithium 47-54 glycogen synthase kinase 3 beta Mus musculus 58-66 25239564-5 2014 Mechanistically, lithium counteracted the doxorubicin-elicited GSK3beta overactivity and the hyperphosphorylation and overactivation of paxillin, a focal adhesion-associated adaptor protein. Lithium 17-24 glycogen synthase kinase 3 beta Mus musculus 63-71 25239564-5 2014 Mechanistically, lithium counteracted the doxorubicin-elicited GSK3beta overactivity and the hyperphosphorylation and overactivation of paxillin, a focal adhesion-associated adaptor protein. Doxorubicin 42-53 glycogen synthase kinase 3 beta Mus musculus 63-71 25239564-6 2014 Moreover, forced expression of a dominant negative kinase dead mutant of GSK3beta highly mimicked, whereas ectopic expression of a constitutively active GSK3beta mutant abolished, the effect of lithium in doxorubicin-injured podocytes, suggesting that the effect of lithium is mediated, at least in part, through inhibition of GSK3beta. Lithium 194-201 glycogen synthase kinase 3 beta Mus musculus 73-81 25239564-6 2014 Moreover, forced expression of a dominant negative kinase dead mutant of GSK3beta highly mimicked, whereas ectopic expression of a constitutively active GSK3beta mutant abolished, the effect of lithium in doxorubicin-injured podocytes, suggesting that the effect of lithium is mediated, at least in part, through inhibition of GSK3beta. Lithium 194-201 glycogen synthase kinase 3 beta Mus musculus 153-161 25239564-6 2014 Moreover, forced expression of a dominant negative kinase dead mutant of GSK3beta highly mimicked, whereas ectopic expression of a constitutively active GSK3beta mutant abolished, the effect of lithium in doxorubicin-injured podocytes, suggesting that the effect of lithium is mediated, at least in part, through inhibition of GSK3beta. Lithium 194-201 glycogen synthase kinase 3 beta Mus musculus 153-161 25239564-6 2014 Moreover, forced expression of a dominant negative kinase dead mutant of GSK3beta highly mimicked, whereas ectopic expression of a constitutively active GSK3beta mutant abolished, the effect of lithium in doxorubicin-injured podocytes, suggesting that the effect of lithium is mediated, at least in part, through inhibition of GSK3beta. Doxorubicin 205-216 glycogen synthase kinase 3 beta Mus musculus 153-161 25239564-6 2014 Moreover, forced expression of a dominant negative kinase dead mutant of GSK3beta highly mimicked, whereas ectopic expression of a constitutively active GSK3beta mutant abolished, the effect of lithium in doxorubicin-injured podocytes, suggesting that the effect of lithium is mediated, at least in part, through inhibition of GSK3beta. Doxorubicin 205-216 glycogen synthase kinase 3 beta Mus musculus 153-161 25239564-9 2014 Consistently, lithium therapy abrogated GSK3beta overactivity, blunted paxillin hyperphosphorylation, and reinstated actin cytoskeleton integrity in glomeruli associated with an early attenuation of podocyte foot process effacement. Lithium 14-21 glycogen synthase kinase 3 beta Mus musculus 40-48 24997455-8 2014 Additionally, oleanolic acid normalized the MK-801-induced alterations of signaling molecules including phosphorylation levels of Akt and GSK-3beta in the frontal cortex. Oleanolic Acid 14-28 glycogen synthase kinase 3 beta Mus musculus 138-147 24997455-8 2014 Additionally, oleanolic acid normalized the MK-801-induced alterations of signaling molecules including phosphorylation levels of Akt and GSK-3beta in the frontal cortex. Dizocilpine Maleate 44-50 glycogen synthase kinase 3 beta Mus musculus 138-147 25302618-5 2014 Then, Polymerase chain reaction and Western blot analysis were used to determine the expression of beta-catenin, GSK-3beta, SOX2, and OCT4 in TSA-treated cells. tanshinone 142-145 glycogen synthase kinase 3 beta Mus musculus 113-122 25302618-9 2014 Activation of the Wnt signaling pathway in TSA-pretreated cells was characterized by the upregulation of beta-catenin and the downregulation of GSK-3beta. tanshinone 43-46 glycogen synthase kinase 3 beta Mus musculus 144-153 25148938-0 2014 Inhibition of invasion and metastasis by DMBT, a novel trehalose derivative, through Akt/GSK-3beta/beta-catenin pathway in B16BL6 cells. dmbt 41-45 glycogen synthase kinase 3 beta Mus musculus 89-98 25148938-10 2014 Results from immunohistochemical staining, Western blotting and real-time PCR indicated that the chemopreventive effect of DMBT was attributed to the inhibition of the VEGF and MMP-9 through Akt/GSK-3beta/beta-catenin and Akt/mTOR signaling pathways. dmbt 123-127 glycogen synthase kinase 3 beta Mus musculus 195-204 24815917-3 2014 We investigated the effects of indirubin-3"-oxime (I3O), the GSK3beta inhibitor that activates Wnt/beta-catenin signaling, on trabecular bone in high-fat diet (HFD)-induced obese male mice. indirubin-3'-monoxime 31-49 glycogen synthase kinase 3 beta Mus musculus 61-69 25046438-5 2014 Importantly, these effects were reversed upon pretreatment with GSK-3 inhibitor SB415286. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 80-88 glycogen synthase kinase 3 beta Mus musculus 64-69 25070263-5 2014 In the present study, it was identified that the activation of AKT and glycogen synthase kinase 3 (GSK-3), and the expression levels of glycogen, were reduced in mouse NCTC 1469 hepatocytes and mouse primary hepatocytes, following exposure to 25 mM glucose for 48 h. Furthermore, it was demonstrated that high glucose levels suppressed the expression of miR-152 in hepatocytes. Glycogen 71-79 glycogen synthase kinase 3 beta Mus musculus 99-104 25070263-5 2014 In the present study, it was identified that the activation of AKT and glycogen synthase kinase 3 (GSK-3), and the expression levels of glycogen, were reduced in mouse NCTC 1469 hepatocytes and mouse primary hepatocytes, following exposure to 25 mM glucose for 48 h. Furthermore, it was demonstrated that high glucose levels suppressed the expression of miR-152 in hepatocytes. Glucose 249-256 glycogen synthase kinase 3 beta Mus musculus 99-104 25070263-5 2014 In the present study, it was identified that the activation of AKT and glycogen synthase kinase 3 (GSK-3), and the expression levels of glycogen, were reduced in mouse NCTC 1469 hepatocytes and mouse primary hepatocytes, following exposure to 25 mM glucose for 48 h. Furthermore, it was demonstrated that high glucose levels suppressed the expression of miR-152 in hepatocytes. Glucose 310-317 glycogen synthase kinase 3 beta Mus musculus 99-104 25186638-9 2014 Activation of the Wnt signaling pathway in TSA-pretreated cells was characterized by the upregulation of beta-catenin and the downregulation of GSK-3beta. tanshinone 43-46 glycogen synthase kinase 3 beta Mus musculus 144-153 24787352-0 2014 Sevoflurane induces tau phosphorylation and glycogen synthase kinase 3beta activation in young mice. Sevoflurane 0-11 glycogen synthase kinase 3 beta Mus musculus 44-74 24787352-7 2014 RESULTS: Anesthesia with 3% sevoflurane 2 h daily for 3 days induced Tau phosphorylation (257 vs. 100%, P = 0.0025, n = 6) and enhanced activation of glycogen synthase kinase 3beta, which is the kinase related to Tau phosphorylation in the hippocampus of postnatal day-8 wild-type mice. Sevoflurane 28-39 glycogen synthase kinase 3 beta Mus musculus 150-180 24787352-9 2014 Glycogen synthase kinase 3beta inhibitor lithium inhibited the sevoflurane-induced glycogen synthase kinase 3beta activation, Tau phosphorylation, increased levels of interleukin-6, and cognitive impairment in the wild-type young mice. Lithium 41-48 glycogen synthase kinase 3 beta Mus musculus 0-30 24787352-9 2014 Glycogen synthase kinase 3beta inhibitor lithium inhibited the sevoflurane-induced glycogen synthase kinase 3beta activation, Tau phosphorylation, increased levels of interleukin-6, and cognitive impairment in the wild-type young mice. Lithium 41-48 glycogen synthase kinase 3 beta Mus musculus 83-113 24787352-9 2014 Glycogen synthase kinase 3beta inhibitor lithium inhibited the sevoflurane-induced glycogen synthase kinase 3beta activation, Tau phosphorylation, increased levels of interleukin-6, and cognitive impairment in the wild-type young mice. Sevoflurane 63-74 glycogen synthase kinase 3 beta Mus musculus 0-30 24787352-9 2014 Glycogen synthase kinase 3beta inhibitor lithium inhibited the sevoflurane-induced glycogen synthase kinase 3beta activation, Tau phosphorylation, increased levels of interleukin-6, and cognitive impairment in the wild-type young mice. Sevoflurane 63-74 glycogen synthase kinase 3 beta Mus musculus 83-113 24787352-11 2014 CONCLUSIONS: These data suggested that sevoflurane induced Tau phosphorylation, glycogen synthase kinase 3beta activation, increase in interleukin-6 and reduction in postsynaptic density protein-95 levels in hippocampus of young mice, and cognitive impairment in the mice. Sevoflurane 39-50 glycogen synthase kinase 3 beta Mus musculus 80-110 24969778-7 2014 Furthermore, PECAM-1 cross-linking led to a significant reduction in the phosphorylation of glycogen synthase kinase-3beta Ser(9), but interestingly an increase in glycogen synthase kinase-3alpha pSer(21). Serine 123-126 glycogen synthase kinase 3 beta Mus musculus 92-122 24659139-12 2014 Our findings suggest that treatment of neuroblastoma cells with hispidulin-protected neural cells from Bupivacaine-induced injury via the activation of the AMPK/GSK3beta signaling pathway. Bupivacaine 103-114 glycogen synthase kinase 3 beta Mus musculus 161-169 24952295-4 2014 The present study aimed to determine whether pre-treatment with ABT-239, a novel H3R antagonist, and its combinations with sodium valproate (SVP) and TDZD-8 (glycogen synthase kinase-3beta (GSK3beta) inhibitor) can prevent the excitotoxic events in mice exposed to KA (10 mg/kg i.p.). benzonitrile, 4-(2-(2-((2r)-2-methyl-1-pyrrolidinyl)ethyl)-5-benzofuranyl)- 64-71 glycogen synthase kinase 3 beta Mus musculus 158-188 24952295-4 2014 The present study aimed to determine whether pre-treatment with ABT-239, a novel H3R antagonist, and its combinations with sodium valproate (SVP) and TDZD-8 (glycogen synthase kinase-3beta (GSK3beta) inhibitor) can prevent the excitotoxic events in mice exposed to KA (10 mg/kg i.p.). 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 150-156 glycogen synthase kinase 3 beta Mus musculus 158-188 24955980-8 2014 These results suggested that local application of lithium (or other GSK-3 inhibitors) might effectively facilitate recovery from bone injury by promoting osteoblastogenesis and inhibiting osteoclastogenesis. Lithium 50-57 glycogen synthase kinase 3 beta Mus musculus 68-73 24951331-0 2014 Syntheses, neural protective activities, and inhibition of glycogen synthase kinase-3beta of substituted quinolines. Quinolines 105-115 glycogen synthase kinase 3 beta Mus musculus 59-89 25036031-5 2014 Further, perifosine and MK-2206, two Akt-specific inhibitors, suppressed TGF-beta1-induced GSK3beta phosphorylation and beta-catenin nuclear translocation. perifosine 9-19 glycogen synthase kinase 3 beta Mus musculus 91-99 24595501-0 2014 Reactivation of cocaine reward memory engages the Akt/GSK3/mTOR signaling pathway and can be disrupted by GSK3 inhibition. Cocaine 16-23 glycogen synthase kinase 3 beta Mus musculus 54-58 24595501-0 2014 Reactivation of cocaine reward memory engages the Akt/GSK3/mTOR signaling pathway and can be disrupted by GSK3 inhibition. Cocaine 16-23 glycogen synthase kinase 3 beta Mus musculus 106-110 24595501-7 2014 Since reduced phosphorylation of GSK3 indicates heightened enzyme activity, the effect of a selective GSK3 inhibitor, SB216763, on reconsolidation was tested. SB 216763 118-126 glycogen synthase kinase 3 beta Mus musculus 102-106 24595501-8 2014 Administration of SB216763 immediately after exposure to an environment previously paired with cocaine abrogated a previously established place preference, suggesting that GSK3 inhibition interfered with reconsolidation of cocaine-associated reward memories. SB 216763 18-26 glycogen synthase kinase 3 beta Mus musculus 172-176 24595501-8 2014 Administration of SB216763 immediately after exposure to an environment previously paired with cocaine abrogated a previously established place preference, suggesting that GSK3 inhibition interfered with reconsolidation of cocaine-associated reward memories. Cocaine 223-230 glycogen synthase kinase 3 beta Mus musculus 172-176 24595501-9 2014 CONCLUSIONS: These findings suggest that the Akt/GSK3/mTORC1 signaling pathway in the nucleus accumbens, hippocampus, and/or prefrontal cortex is critically involved in the reconsolidation of cocaine contextual reward memory. Cocaine 192-199 glycogen synthase kinase 3 beta Mus musculus 49-53 24634145-4 2014 Inhibitory phosphorylation of GSK3 (pGSK3) was elevated in mhtt cells and this appeared related to an overall energy metabolism deficit as the mhtt cells had less ATP and inhibiting ATP production in control cells expressing non-pathogenic htt with paraquat also increased pGSK3. Adenosine Triphosphate 163-166 glycogen synthase kinase 3 beta Mus musculus 30-34 24634145-4 2014 Inhibitory phosphorylation of GSK3 (pGSK3) was elevated in mhtt cells and this appeared related to an overall energy metabolism deficit as the mhtt cells had less ATP and inhibiting ATP production in control cells expressing non-pathogenic htt with paraquat also increased pGSK3. Adenosine Triphosphate 182-185 glycogen synthase kinase 3 beta Mus musculus 30-34 25036031-5 2014 Further, perifosine and MK-2206, two Akt-specific inhibitors, suppressed TGF-beta1-induced GSK3beta phosphorylation and beta-catenin nuclear translocation. MK 2206 24-31 glycogen synthase kinase 3 beta Mus musculus 91-99 24859647-3 2014 This study demonstrated that DDT-induced apoptosis of mouse embryonic neuronal cells is a caspase-9-, caspase-3-, and GSK-3beta-dependent process, which involves p,p"-DDT-specific impairment of classical ERs. DDT 29-32 glycogen synthase kinase 3 beta Mus musculus 118-127 24713149-8 2014 The beneficial effects of cotinine in preventing various consequences of chronic stress were underscored by the inhibition of the glycogen synthase kinase 3 beta in the hippocampus and prefrontal cortex. Cotinine 26-34 glycogen synthase kinase 3 beta Mus musculus 130-161 24969790-1 2014 PURPOSE: To quantify the effectiveness of SB415286, a specific inhibitor of GSK-3beta, as a neuroprotectant against radiation-induced central nervous system (brain) necrosis in a mouse model. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 42-50 glycogen synthase kinase 3 beta Mus musculus 76-85 24969790-11 2014 Effectiveness of SB415286 as a neuroprotectant against necrosis motivates potential clinical trials of it or other GSK-3beta inhibitors. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 17-25 glycogen synthase kinase 3 beta Mus musculus 115-124 24937184-4 2014 These active compounds were also evaluated in vitro as kinase inhibitors against CDK2/cyclin E1, CDK4/cyclin D1 and GSK-3beta and the best inhibition was displayed against GSK-3beta with the allylfurochalcone derivative 9b exhibiting 80% decrease in GSK-3beta catalytic activity. allylfurochalcone 191-208 glycogen synthase kinase 3 beta Mus musculus 172-181 24937184-4 2014 These active compounds were also evaluated in vitro as kinase inhibitors against CDK2/cyclin E1, CDK4/cyclin D1 and GSK-3beta and the best inhibition was displayed against GSK-3beta with the allylfurochalcone derivative 9b exhibiting 80% decrease in GSK-3beta catalytic activity. allylfurochalcone 191-208 glycogen synthase kinase 3 beta Mus musculus 172-181 24937184-5 2014 On the other hand, the styrylfurochromone 25e interestingly showed a 13% enhancement of GSK-3beta catalytic power and a 12% reduction in CDK4/cyclin D1 activity. styrylfurochromone 23-41 glycogen synthase kinase 3 beta Mus musculus 88-97 24859647-3 2014 This study demonstrated that DDT-induced apoptosis of mouse embryonic neuronal cells is a caspase-9-, caspase-3-, and GSK-3beta-dependent process, which involves p,p"-DDT-specific impairment of classical ERs. DDT 162-170 glycogen synthase kinase 3 beta Mus musculus 118-127 25316136-0 2014 Pharmacological GSK-3beta inhibition improves osteoblast differentiation on titanium surfaces. Titanium 76-84 glycogen synthase kinase 3 beta Mus musculus 16-25 27152166-5 2014 However, mice deficient in GSK3beta in D2R-expressing neurons show a significantly reduced locomotor response to only amphetamine but not morphine. Amphetamine 118-129 glycogen synthase kinase 3 beta Mus musculus 27-35 27152166-5 2014 However, mice deficient in GSK3beta in D2R-expressing neurons show a significantly reduced locomotor response to only amphetamine but not morphine. Morphine 138-146 glycogen synthase kinase 3 beta Mus musculus 27-35 24627571-12 2014 Alcohol also increased callus associated activated GSK-3beta at post-injury day 9. Alcohols 0-7 glycogen synthase kinase 3 beta Mus musculus 51-60 24627571-13 2014 Lithium chloride (an inhibitor of GSK-3beta) treatment increased activated beta-catenin protein levels, significantly decreased activated GSK-3beta and restored cartilaginous callus formation and endochondral ossification. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 34-43 24627571-13 2014 Lithium chloride (an inhibitor of GSK-3beta) treatment increased activated beta-catenin protein levels, significantly decreased activated GSK-3beta and restored cartilaginous callus formation and endochondral ossification. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 138-147 25316136-2 2014 The present study investigated the effects of GSK3b-inhibitor (2"Z,3"E)- 6-Bromoindirubin-3"-oxime (BIO) on osteoblastic differentiation on titanium surfaces with different topography and wettability. (2"z,3"e)- 6-bromoindirubin-3"-oxime 62-98 glycogen synthase kinase 3 beta Mus musculus 46-51 24636797-6 2014 We restored GSK3beta phosphorylation in trisomic aNPCs using either lithium, a well-known GSK3beta inhibitor, or using a 5-HT receptor agonist or fluoxetine, which activated the serotonin receptor 5-HT1A. Lithium 68-75 glycogen synthase kinase 3 beta Mus musculus 12-20 24601954-9 2014 Luprolide acetate rescues ovariectomy-dependent cognitive function, increases signaling events associated with synaptic plasticity including GSK3 beta inhibition, but does not alter AD pathology. luprolide acetate 0-17 glycogen synthase kinase 3 beta Mus musculus 141-150 24636797-6 2014 We restored GSK3beta phosphorylation in trisomic aNPCs using either lithium, a well-known GSK3beta inhibitor, or using a 5-HT receptor agonist or fluoxetine, which activated the serotonin receptor 5-HT1A. Fluoxetine 146-156 glycogen synthase kinase 3 beta Mus musculus 12-20 24636797-8 2014 In agreement with results obtained in vitro, we found that early treatment with fluoxetine, which was previously shown to rescue neurogenesis and behavior in Ts65Dn mice, restored GSK3beta phosphorylation. Fluoxetine 80-90 glycogen synthase kinase 3 beta Mus musculus 180-188 24636797-11 2014 Results suggest that drugs that increase GSK3beta phosphorylation, such as lithium or fluoxetine, may represent useful tools for the improvement of neurogenesis in DS. Lithium 75-82 glycogen synthase kinase 3 beta Mus musculus 41-49 24636797-11 2014 Results suggest that drugs that increase GSK3beta phosphorylation, such as lithium or fluoxetine, may represent useful tools for the improvement of neurogenesis in DS. Fluoxetine 86-96 glycogen synthase kinase 3 beta Mus musculus 41-49 24922070-6 2014 We found that the activation of P2X7R by BzATP caused the death of AEC I by suppressing Wnt/beta-catenin signaling through stimulating glycogen synthase kinase-3beta (GSK-3beta) and proteasome. BzATP 41-46 glycogen synthase kinase 3 beta Mus musculus 135-165 25165785-0 2014 The antidepressant effects of ginseng total saponins in male C57BL/6N mice by enhancing hippocampal inhibitory phosphorylation of GSK-3beta. Saponins 44-52 glycogen synthase kinase 3 beta Mus musculus 130-139 24987368-5 2014 In HEK293/tau and N2a/tau cells, silencing [Formula: see text] by [Formula: see text] also significantly reduced tau hyperphosphorylation with restoration of PP2A activity and inhibition of GSK-3beta, demonstrated by the decreased GSK-3beta total protein and mRNA levels, and the increased inhibitory phosphorylation of GSK-3beta at serine-9. Serine 333-339 glycogen synthase kinase 3 beta Mus musculus 190-199 24987368-5 2014 In HEK293/tau and N2a/tau cells, silencing [Formula: see text] by [Formula: see text] also significantly reduced tau hyperphosphorylation with restoration of PP2A activity and inhibition of GSK-3beta, demonstrated by the decreased GSK-3beta total protein and mRNA levels, and the increased inhibitory phosphorylation of GSK-3beta at serine-9. Serine 333-339 glycogen synthase kinase 3 beta Mus musculus 231-240 24987368-5 2014 In HEK293/tau and N2a/tau cells, silencing [Formula: see text] by [Formula: see text] also significantly reduced tau hyperphosphorylation with restoration of PP2A activity and inhibition of GSK-3beta, demonstrated by the decreased GSK-3beta total protein and mRNA levels, and the increased inhibitory phosphorylation of GSK-3beta at serine-9. Serine 333-339 glycogen synthase kinase 3 beta Mus musculus 231-240 24922070-6 2014 We found that the activation of P2X7R by BzATP caused the death of AEC I by suppressing Wnt/beta-catenin signaling through stimulating glycogen synthase kinase-3beta (GSK-3beta) and proteasome. BzATP 41-46 glycogen synthase kinase 3 beta Mus musculus 167-176 24670930-5 2014 Repeated oral administration of DIF-1 markedly reduced the number and size of intestinal tumors that developed in Mutyh-deficient mice, reducing the phosphorylation level of GSK-3beta Ser(9) and the expression levels of early growth response-1 (Egr-1), transcription factor 7-like 2 (TCF7L2) and cyclin D1. Serine 184-187 glycogen synthase kinase 3 beta Mus musculus 174-183 24901984-5 2014 We found that GSK3beta directly phosphorylates the endogenous NM1 on a single serine residue (Ser-1020) located within the NM1 C-terminus. Serine 78-84 glycogen synthase kinase 3 beta Mus musculus 14-22 24901984-5 2014 We found that GSK3beta directly phosphorylates the endogenous NM1 on a single serine residue (Ser-1020) located within the NM1 C-terminus. Serine 94-97 glycogen synthase kinase 3 beta Mus musculus 14-22 24892905-0 2014 CMZ reversed chronic ethanol-induced disturbance of PPAR-alpha possibly by suppressing oxidative stress and PGC-1alpha acetylation, and activating the MAPK and GSK3beta pathway. Ethanol 21-28 glycogen synthase kinase 3 beta Mus musculus 160-168 24892905-13 2014 CONCLUSION: These results suggested that CMZ suppressed chronic ethanol-induced oxidative stress, TNF-alpha overproduction, decline of p300 protein level and deacetylation of PGC1-alpha, and activated AMPK, MAPK, and PI3K/Akt/GSK3beta pathway, which might contribute to the activation of PPAR-alpha and account for the protection of CMZ against AFL. Ethanol 64-71 glycogen synthase kinase 3 beta Mus musculus 226-234 24263322-10 2014 Furthermore, phosphorylation and inactivation of neuronal GSK3beta was significantly enhanced after atorvastatin treatment. Atorvastatin 100-112 glycogen synthase kinase 3 beta Mus musculus 58-66 24670930-6 2014 DIF-1 also inhibited the growth of HCT-116- and HeLa-xenograft tumors together with decreasing phosphorylation level of GSK-3beta Ser(9), although it was not statistically significant in HeLa-xenograft tumors. Serine 130-133 glycogen synthase kinase 3 beta Mus musculus 120-129 24777252-4 2014 In resting macrophages, CKIP-1 was phosphorylated at Serine 342 by constitutively active GSK3beta, the downstream target of Akt. Serine 53-59 glycogen synthase kinase 3 beta Mus musculus 89-97 24496925-3 2014 Here, we show that a low-dose of 6-bromoindirubin-3"-oxime (BIO), a competitive inhibitor of glycogen synthase kinase-3beta, induced the stabilization of beta-catenin and its subsequent direct interaction with the transcription factor NANOG in the nucleus of ECs. 6-bromoindirubin-3'-oxime 33-58 glycogen synthase kinase 3 beta Mus musculus 93-123 24458356-4 2014 Treatment of atrial myocytes with the GSK3beta inhibitor Kenpaullone increased levels of SREBP-1 and expression of GIRK4 and IKACh, whereas a dominant-active GSK3beta mutant decreased SREBP-1 and GIRK4 expression. kenpaullone 57-68 glycogen synthase kinase 3 beta Mus musculus 38-46 24458356-4 2014 Treatment of atrial myocytes with the GSK3beta inhibitor Kenpaullone increased levels of SREBP-1 and expression of GIRK4 and IKACh, whereas a dominant-active GSK3beta mutant decreased SREBP-1 and GIRK4 expression. kenpaullone 57-68 glycogen synthase kinase 3 beta Mus musculus 158-166 24477332-4 2014 Further, we show that the effects of CO are dependent on inhibition of phosphorylation of glycogen synthase kinase-3 beta (GSK3beta), activation of haem synthesis, and increased expression of Rev-erbalpha. Carbon Monoxide 37-39 glycogen synthase kinase 3 beta Mus musculus 90-121 24477332-4 2014 Further, we show that the effects of CO are dependent on inhibition of phosphorylation of glycogen synthase kinase-3 beta (GSK3beta), activation of haem synthesis, and increased expression of Rev-erbalpha. Carbon Monoxide 37-39 glycogen synthase kinase 3 beta Mus musculus 123-131 24597671-6 2014 Zn supplement prevented the effects of TPEN and also increased Akt and GSK-3beta phosphorylation with a decrease in Nrf2 nuclear exporter, Fyn. Zinc 0-2 glycogen synthase kinase 3 beta Mus musculus 71-80 24677550-5 2014 Intraventricular infusion of the GSK3beta inhibitor ARA-014418 in mice aged postnatal day (P) 8-11 significantly increased generation of OPs in the dorsal microdomain of the SVZ, as shown by expression of cell specific markers using rt-qPCR and immunolabelling. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 52-62 glycogen synthase kinase 3 beta Mus musculus 33-41 24462916-8 2014 PSVII-induced growth inhibitory effect was associated with disturbance of MAPK pathway by down-regulating MEK1/2, ERK1/2 phosphorylation, and suppression of AKT pathway by reducing AKT and GSK-3beta phosphorylation. Paris saponin VII 0-5 glycogen synthase kinase 3 beta Mus musculus 189-198 24720754-9 2014 Collectively, our results demonstrate that the GSK-3 inhibitor SB216763 is an effective medical countermeasure against acute radiation injury of the hematopoietic system. SB 216763 63-71 glycogen synthase kinase 3 beta Mus musculus 47-52 24522749-7 2014 Furthermore, lithium significantly increased the level of phospho-glycogen synthase kinase-3 beta (GSK-3beta), the non-activated GSK-3beta. Lithium 13-20 glycogen synthase kinase 3 beta Mus musculus 99-108 24522749-7 2014 Furthermore, lithium significantly increased the level of phospho-glycogen synthase kinase-3 beta (GSK-3beta), the non-activated GSK-3beta. Lithium 13-20 glycogen synthase kinase 3 beta Mus musculus 129-138 24623780-5 2014 GSK-3 binds to and directly phosphorylates SRF on a highly conserved serine residue. Serine 69-75 glycogen synthase kinase 3 beta Mus musculus 0-5 24614172-5 2014 The present study also revealed that ZBPYR strengthened brain leptin and insulin signaling and inhibited GSK3beta overactivity, which may be the potential mechanism or underlying targets of ZBPYR. zbpyr 37-42 glycogen synthase kinase 3 beta Mus musculus 105-113 24580743-0 2014 The potential dual effects of sevoflurane on AKT/GSK3beta signaling pathway. Sevoflurane 30-41 glycogen synthase kinase 3 beta Mus musculus 49-57 24580743-3 2014 However, whether sevoflurane can induce a dual effect (increase versus decrease) on the activation of AKT/GSK3beta signaling pathway remains to be determined. Sevoflurane 17-28 glycogen synthase kinase 3 beta Mus musculus 106-114 24580743-4 2014 We therefore set out to assess the effects of sevoflurane on AKT/GSK3beta signaling pathway in vivo and in vitro. Sevoflurane 46-57 glycogen synthase kinase 3 beta Mus musculus 65-73 24580743-7 2014 We then determined the effects of different sevoflurane treatments on the levels of phosphorylated (P)-GSK3beta(ser9) and P-AKT(ser473) by using Western blot analysis. Sevoflurane 44-55 glycogen synthase kinase 3 beta Mus musculus 103-111 24580743-10 2014 CONCLUSIONS: Anesthetic sevoflurane might induce a dual effect (increase versus decrease) on the activation of the AKT/GSK3beta signaling pathway. Sevoflurane 24-35 glycogen synthase kinase 3 beta Mus musculus 119-127 24094580-0 2014 beta-amyloid impairs the regulation of N-methyl-D-aspartate receptors by glycogen synthase kinase 3. beta-amyloid 0-12 glycogen synthase kinase 3 beta Mus musculus 73-99 24408869-2 2014 Here, delayed treatment with a single dose of lithium, a selective inhibitor of GSK3beta and a US Food and Drug Administration-approved mood stabilizer, accelerated recovery of renal function, promoted repopulation of renal tubular epithelia, and improved kidney repair in murine models of cisplatin- and ischemia/reperfusion-induced AKI. Lithium 46-53 glycogen synthase kinase 3 beta Mus musculus 80-88 24408869-4 2014 In cultured renal tubular cells, cisplatin exposure led to transient repression of GSK3beta activity followed by a prolonged upregulation of activity. Cisplatin 33-42 glycogen synthase kinase 3 beta Mus musculus 83-91 24408869-5 2014 Rescue treatment with lithium inhibited GSK3beta activity, enhanced nuclear expression of cyclin D1, c-Myc, and HIF-1alpha, and boosted cellular proliferation. Lithium 22-29 glycogen synthase kinase 3 beta Mus musculus 40-48 24408869-6 2014 Similarly, ectopic expression of a kinase-dead mutant of GSK3beta enhanced the expression of cyclin D1, c-Myc, and HIF-1alpha and amplified cellular proliferation after cisplatin injury, whereas forced expression of a constitutively active mutant of GSK3beta abrogated the effects of lithium. Cisplatin 169-178 glycogen synthase kinase 3 beta Mus musculus 57-65 24408869-6 2014 Similarly, ectopic expression of a kinase-dead mutant of GSK3beta enhanced the expression of cyclin D1, c-Myc, and HIF-1alpha and amplified cellular proliferation after cisplatin injury, whereas forced expression of a constitutively active mutant of GSK3beta abrogated the effects of lithium. Lithium 284-291 glycogen synthase kinase 3 beta Mus musculus 57-65 24408869-10 2014 Collectively, our findings suggest that pharmacologic targeting of GSK3beta by lithium may be a novel therapeutic strategy to improve renal salvage after AKI. Lithium 79-86 glycogen synthase kinase 3 beta Mus musculus 67-75 24374173-12 2014 Furthermore, we found that the level of beta-catenin together with GSK-3beta phosphorylation was inhibited by celecoxib. Celecoxib 110-119 glycogen synthase kinase 3 beta Mus musculus 67-76 24374173-13 2014 In conclusion, celecoxib inhibits metastasis of A549 cells in the circulation enhanced by PGE2 after surgery by not only inhibiting endogenous PGE2 expression, but also by suppression downstream of PGE2 via the GSK-3beta-beta-catenin pathway. Celecoxib 15-24 glycogen synthase kinase 3 beta Mus musculus 211-220 23439485-1 2014 Glycogen synthase kinase 3 (GSK3), a prominent enzyme in carbohydrate metabolism, also has a major role in brain function. Carbohydrates 57-69 glycogen synthase kinase 3 beta Mus musculus 0-26 23439485-1 2014 Glycogen synthase kinase 3 (GSK3), a prominent enzyme in carbohydrate metabolism, also has a major role in brain function. Carbohydrates 57-69 glycogen synthase kinase 3 beta Mus musculus 28-32 23439485-3 2014 Inositol hexakisphosphate-1 (IP6K1) generates the inositol pyrophosphate diphosphoinositol pentakisphosphate (IP7), which physiologically inhibits Akt leading to enhanced GSK3 activity. inositol pyrophosphate diphosphoinositol pentakisphosphate 50-108 glycogen synthase kinase 3 beta Mus musculus 171-175 23439485-3 2014 Inositol hexakisphosphate-1 (IP6K1) generates the inositol pyrophosphate diphosphoinositol pentakisphosphate (IP7), which physiologically inhibits Akt leading to enhanced GSK3 activity. ip7 110-113 glycogen synthase kinase 3 beta Mus musculus 171-175 24094580-0 2014 beta-amyloid impairs the regulation of N-methyl-D-aspartate receptors by glycogen synthase kinase 3. N-Methylaspartate 39-59 glycogen synthase kinase 3 beta Mus musculus 73-99 24094580-6 2014 Consequently, GSK-3 inhibitor lost the capability of protecting neurons against N-methyl-D-aspartate-induced excitotoxicity in Abeta-treated neurons. N-Methylaspartate 80-100 glycogen synthase kinase 3 beta Mus musculus 14-19 24013758-1 2014 Lithium, an inhibitor of glycogen synthase kinase 3 (GSK3), is widely used for the treatment of mood disorders. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 25-51 24013758-1 2014 Lithium, an inhibitor of glycogen synthase kinase 3 (GSK3), is widely used for the treatment of mood disorders. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 53-57 24013758-8 2014 Lithium treatment significantly increased renal GSK3 phosphorylation, enhanced serum ADH and FGF23 concentrations, downregulated renal Klotho expression, stimulated renal calcium and phosphate excretion, and decreased serum 1,25(OH)2D3 and phosphate concentrations. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 48-52 24577082-8 2014 TNFalpha/zVAD treatment induced cell death within 4 h. Cell death was preceded by RIPK1-RIPK3-pAkt assembly, and phosphorylation of Thr-308 and Thr473 of AKT and its direct substrate glycogen synthase kinase-3beta, as well as mTOR and its direct substrate S6 ribosomal protein (S6), suggesting activation of Akt/mTOR pathways. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 9-13 glycogen synthase kinase 3 beta Mus musculus 183-213 24523925-7 2014 As a result, thapsigargin-induced CRIS and SOCE were significantly blunted by GSK3-inhibitors SB216763 (1-10 microM, 30 min) or GSK-XIII (10 microM, 30 min) but were significantly lower in gsk3(WT) than in gsk3(KI) DCs. Thapsigargin 13-25 glycogen synthase kinase 3 beta Mus musculus 78-82 24519956-6 2014 Inhibition of GSK-3 with SB415286 in PC3 cells resulted in impaired motility, proliferation and colony formation. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 25-33 glycogen synthase kinase 3 beta Mus musculus 14-19 24519956-9 2014 Together, we provide novel insight into the Src-mediated Y216GSK-3 phosphorylation and activation in prostate cancer cells and reveal the potential benefits of targeting Src-GSK-3 axis using drugs such as dasatinib. Dasatinib 205-214 glycogen synthase kinase 3 beta Mus musculus 61-66 24523925-7 2014 As a result, thapsigargin-induced CRIS and SOCE were significantly blunted by GSK3-inhibitors SB216763 (1-10 microM, 30 min) or GSK-XIII (10 microM, 30 min) but were significantly lower in gsk3(WT) than in gsk3(KI) DCs. Thapsigargin 13-25 glycogen synthase kinase 3 beta Mus musculus 189-193 24523925-7 2014 As a result, thapsigargin-induced CRIS and SOCE were significantly blunted by GSK3-inhibitors SB216763 (1-10 microM, 30 min) or GSK-XIII (10 microM, 30 min) but were significantly lower in gsk3(WT) than in gsk3(KI) DCs. Thapsigargin 13-25 glycogen synthase kinase 3 beta Mus musculus 206-218 24396420-7 2014 By contrast, the BF group demonstrated significant reductions in the expression levels of mTOR and Camk2gamma and a significant increase in the expression levels of GSK-3beta, compared with those in the F group (P<0.01). benzo(b)fluoranthene 17-19 glycogen synthase kinase 3 beta Mus musculus 165-174 24505362-0 2014 The GSK3 signaling pathway is activated by cocaine and is critical for cocaine conditioned reward in mice. Cocaine 43-50 glycogen synthase kinase 3 beta Mus musculus 4-8 24505362-0 2014 The GSK3 signaling pathway is activated by cocaine and is critical for cocaine conditioned reward in mice. Cocaine 71-78 glycogen synthase kinase 3 beta Mus musculus 4-8 24505362-2 2014 Here, the ability of cocaine to regulate the activity of Akt and GSK3 was investigated by measuring the phosphorylation states of the two kinases. Cocaine 21-28 glycogen synthase kinase 3 beta Mus musculus 65-69 24505362-4 2014 As GSK3 activity was found to be increased by cocaine, subsequent experiments investigated the importance of GSK3 activation in cocaine conditioned reward. Cocaine 46-53 glycogen synthase kinase 3 beta Mus musculus 3-7 23905999-5 2014 Now we have investigated the effect GSK-3beta overexpression on the (18)F-fluoro-deoxyglucose (FDG) uptake by positron emission tomography (PET), taking advantage from this non-invasive technique which has allowed us to track individually the same animals throughout their lives. f-fluoro-deoxyglucose 72-93 glycogen synthase kinase 3 beta Mus musculus 36-45 23905999-5 2014 Now we have investigated the effect GSK-3beta overexpression on the (18)F-fluoro-deoxyglucose (FDG) uptake by positron emission tomography (PET), taking advantage from this non-invasive technique which has allowed us to track individually the same animals throughout their lives. Fluorodeoxyglucose F18 95-98 glycogen synthase kinase 3 beta Mus musculus 36-45 23905999-8 2014 This effect seems to be reverted in a satellite group of 3-month transgenic animals treated with the classical GSK-3 inhibitor lithium, as they show higher FDG uptake values compared with untreated age-matched transgenic animals. Lithium 127-134 glycogen synthase kinase 3 beta Mus musculus 111-116 24396420-0 2014 Effects of BD1047, a sigma1 receptor antagonist, on the expression of mTOR, Camk2gamma and GSK-3beta in fluvoxamine-treated N2a cells. Fluvoxamine 104-115 glycogen synthase kinase 3 beta Mus musculus 91-100 24462873-10 2014 Furthermore, the phosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser(9) and cytosolic beta-catenin level were increased in Adipo-KO mice and they were significantly reduced by Ad-Adipo treatment. Serine 81-84 glycogen synthase kinase 3 beta Mus musculus 36-66 24462873-10 2014 Furthermore, the phosphorylation of glycogen synthase kinase 3beta (GSK3beta) at Ser(9) and cytosolic beta-catenin level were increased in Adipo-KO mice and they were significantly reduced by Ad-Adipo treatment. Serine 81-84 glycogen synthase kinase 3 beta Mus musculus 68-76 24365490-10 2014 Consistently, exposure to rotigotine induced the activation of Akt by phosphorylation followed by phosphorylation, and thus inactivation, of the pro-apoptotic factor glycogen synthase kinase-3-beta (GSK-3-beta). rotigotine 26-36 glycogen synthase kinase 3 beta Mus musculus 199-209 24505362-6 2014 Acute administration of cocaine significantly decreased the phosphorylation of Akt-Thr308 (pAkt-Thr308) and GSK3beta in the caudate putamen and nucleus accumbens core, without altering pAkt-Ser473 and pGSK3alpha. Cocaine 24-31 glycogen synthase kinase 3 beta Mus musculus 108-116 24505362-7 2014 To investigate the role of dopamine and NMDA receptors in the regulation of Akt and GSK3 by cocaine, specific receptor antagonists were administered prior to cocaine. Cocaine 92-99 glycogen synthase kinase 3 beta Mus musculus 84-88 24505362-9 2014 The potential importance of GSK3 activity in the rewarding actions of cocaine was determined using a cocaine conditioned place preference procedure. Cocaine 70-77 glycogen synthase kinase 3 beta Mus musculus 28-32 24505362-10 2014 Administration of the selective GSK3 inhibitor, SB 216763, prior to cocaine conditioning sessions blocked the development of cocaine place preference. SB 216763 48-57 glycogen synthase kinase 3 beta Mus musculus 32-36 24505362-10 2014 Administration of the selective GSK3 inhibitor, SB 216763, prior to cocaine conditioning sessions blocked the development of cocaine place preference. Cocaine 68-75 glycogen synthase kinase 3 beta Mus musculus 32-36 24505362-10 2014 Administration of the selective GSK3 inhibitor, SB 216763, prior to cocaine conditioning sessions blocked the development of cocaine place preference. Cocaine 125-132 glycogen synthase kinase 3 beta Mus musculus 32-36 24505362-12 2014 The results of this study indicate that phosphorylation of GSK3beta is reduced, hence GSK3beta activity is increased following acute cocaine, an effect that is contingent upon both dopaminergic and glutamatergic receptors. Cocaine 133-140 glycogen synthase kinase 3 beta Mus musculus 59-67 24505362-12 2014 The results of this study indicate that phosphorylation of GSK3beta is reduced, hence GSK3beta activity is increased following acute cocaine, an effect that is contingent upon both dopaminergic and glutamatergic receptors. Cocaine 133-140 glycogen synthase kinase 3 beta Mus musculus 86-94 24505362-13 2014 Further, GSK3 activity is required for the development of cocaine conditioned reward. Cocaine 58-65 glycogen synthase kinase 3 beta Mus musculus 9-13 24041505-5 2014 Furthermore, synaptosomes from the dentate gyrus of FX mice displayed decreased inhibitory serine-phosphorylation of GSK3beta compared with wild-type littermates. Serine 91-97 glycogen synthase kinase 3 beta Mus musculus 117-125 24396420-8 2014 These results suggest that sigma1 receptors mediate fluvoxamine-elicited changes in the expression levels of mTOR, Camk2gamma and GSK-3beta in N2a cells, which indicates that sigma1 receptors are likely to be involved in the pharmacological effects of fluvoxamine. Fluvoxamine 52-63 glycogen synthase kinase 3 beta Mus musculus 130-139 24387036-9 2014 Phosphorylation of Akt and GSK3beta protein expression levels in the LPS-induced PTEN overexpression transfected cells were significantly lower than those in the LPS-induced non-transfected cells, which can be reversed by the PTEN inhibitor, bpV(phen). bromopyruvate 242-245 glycogen synthase kinase 3 beta Mus musculus 27-35 24296131-4 2014 Allantoin treatment (3 or 10 mg/kg, for 7 days) also increased the expression levels of phosphorylated phosphatidylinositide 3-kinase (PI3K), phosphorylated protein kinase B (Akt) and phosphorylated glycogen synthase kinase-3beta (GSK-3beta). Allantoin 0-9 glycogen synthase kinase 3 beta Mus musculus 199-229 24296131-4 2014 Allantoin treatment (3 or 10 mg/kg, for 7 days) also increased the expression levels of phosphorylated phosphatidylinositide 3-kinase (PI3K), phosphorylated protein kinase B (Akt) and phosphorylated glycogen synthase kinase-3beta (GSK-3beta). Allantoin 0-9 glycogen synthase kinase 3 beta Mus musculus 231-240 24296131-6 2014 In conclusion, allantoin has memory-enhancing effects, and these effects may be partly mediated by the PI3K-Akt-GSK-3beta signal pathway. Allantoin 15-24 glycogen synthase kinase 3 beta Mus musculus 112-121 24067926-6 2014 Our data also suggest that 5-HT plays a critical role in mediating the effects of ethanol on Akt/GSK3beta signaling in the nucleus accumbens. Ethanol 82-89 glycogen synthase kinase 3 beta Mus musculus 97-105 24338011-5 2014 We also found that the Panx3 hemichannel inhibited cell growth by promoting beta-catenin degradation through GSK3beta activation. hemichannel 29-40 glycogen synthase kinase 3 beta Mus musculus 109-117 24989012-6 2014 Furthermore, Western blot analysis revealed that the expression levels of phosphorylated extracellular signal-regulated kinase 1/2 (pERK) and phosphorylated glycogen synthase kinase-3beta (pGSK-3beta) were significantly enhanced by a single administration of alpha- and beta-amyrin in the hippocampus. pgsk-3beta 189-199 glycogen synthase kinase 3 beta Mus musculus 157-187 24989012-6 2014 Furthermore, Western blot analysis revealed that the expression levels of phosphorylated extracellular signal-regulated kinase 1/2 (pERK) and phosphorylated glycogen synthase kinase-3beta (pGSK-3beta) were significantly enhanced by a single administration of alpha- and beta-amyrin in the hippocampus. beta-amyrin 274-281 glycogen synthase kinase 3 beta Mus musculus 157-187 24989012-8 2014 The present study suggests that alpha- and beta-amyrin may ameliorate the cognitive impairment induced by hypocholinergic neurotransmission via the activation of ERK as well as GSK-3beta signaling. alpha- and beta-amyrin 32-54 glycogen synthase kinase 3 beta Mus musculus 177-186 24732862-0 2014 GSK-3beta and vitamin D receptor are involved in beta-catenin and snail signaling in high glucose-induced epithelial-mesenchymal transition of mouse podocytes. Glucose 90-97 glycogen synthase kinase 3 beta Mus musculus 0-9 24577479-7 2014 Additionally, the expression and activity of glycogen synthase kinase 3beta and protein phosphatase 2A, two important enzymes involved in tau phosphorylation, were markedly decreased and increased respectively by Se-Met treatment. Selenomethionine 213-219 glycogen synthase kinase 3 beta Mus musculus 45-102 25269915-12 2014 CONCLUSION: GSK-3 kinase is closely related to retinal neuron apoptosis, and the application of the GSK-3 inhibitor lithium chloride can reduce retinal neuron apoptosis in early diabetic retinopathy. Lithium Chloride 116-132 glycogen synthase kinase 3 beta Mus musculus 12-17 25269915-12 2014 CONCLUSION: GSK-3 kinase is closely related to retinal neuron apoptosis, and the application of the GSK-3 inhibitor lithium chloride can reduce retinal neuron apoptosis in early diabetic retinopathy. Lithium Chloride 116-132 glycogen synthase kinase 3 beta Mus musculus 100-105 25024327-7 2014 Lastly, THC was tested to determine its effects on glycogen synthase kinase-3beta (GSK-3beta) and related signaling pathways. Dronabinol 8-11 glycogen synthase kinase 3 beta Mus musculus 51-81 25024327-7 2014 Lastly, THC was tested to determine its effects on glycogen synthase kinase-3beta (GSK-3beta) and related signaling pathways. Dronabinol 8-11 glycogen synthase kinase 3 beta Mus musculus 83-92 25024327-11 2014 Furthermore, THC was effective at lowering both total GSK-3beta levels and phosphorylated GSK-3beta in a dose-dependent manner at low concentrations. Dronabinol 13-16 glycogen synthase kinase 3 beta Mus musculus 54-63 24164738-8 2014 Importantly, a diet supplemented with 0.04% simvastatin for one month (at 7 months) positively affected synaptic plasticity in AbetaPPswe/PS1dE9 mice and did not significantly alter levels of water-soluble, detergent-soluble, or FA-soluble Abeta, but did increase phosphorylation of both Akt and GSK-3, while tau and tau phosphorylation were unaltered. Simvastatin 44-55 glycogen synthase kinase 3 beta Mus musculus 296-301 24209999-9 2014 These results indicate that the antidepressant-like effect of ascorbic acid in the TST might be dependent on the activation of PI3K and mTOR, inhibition of GSK-3beta as well as induction of HO-1, reinforcing the notion that these are important targets for antidepressant activity and contributing to better elucidate the mechanisms underlying the antidepressant-like effect of ascorbic acid. Ascorbic Acid 62-75 glycogen synthase kinase 3 beta Mus musculus 156-165 25024327-11 2014 Furthermore, THC was effective at lowering both total GSK-3beta levels and phosphorylated GSK-3beta in a dose-dependent manner at low concentrations. Dronabinol 13-16 glycogen synthase kinase 3 beta Mus musculus 90-99 24006282-12 2013 GSK3 phosphorylation was altered in the presence of H89, a PKA inhibitor. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 52-55 glycogen synthase kinase 3 beta Mus musculus 0-4 24176395-0 2013 2-(2-Phenylmorpholin-4-yl)pyrimidin-4(3H)-ones; a new class of potent, selective and orally active glycogen synthase kinase-3beta inhibitors. 2-(2-phenylmorpholin-4-yl)pyrimidin-4(3h)-ones 0-46 glycogen synthase kinase 3 beta Mus musculus 99-129 24176395-1 2013 A series of 2-(2-phenylmorpholin-4-yl)pyrimidin-4(3H)-ones was synthesized and examined for their inhibitory activity against glycogen synthase kinase-3beta (GSK-3beta). 2-(2-phenylmorpholin-4-yl)pyrimidin-4(3h)-ones 12-58 glycogen synthase kinase 3 beta Mus musculus 126-156 24176395-1 2013 A series of 2-(2-phenylmorpholin-4-yl)pyrimidin-4(3H)-ones was synthesized and examined for their inhibitory activity against glycogen synthase kinase-3beta (GSK-3beta). 2-(2-phenylmorpholin-4-yl)pyrimidin-4(3h)-ones 12-58 glycogen synthase kinase 3 beta Mus musculus 158-167 24340001-7 2013 In addition, we also observed a number of novel isoproterenol-induced protein dephosphorylation events in target substrates of the PI3K/AKT pathway: GSK3beta(S9), 4E-BP1(S65), and p70s6k(T389). Isoproterenol 48-61 glycogen synthase kinase 3 beta Mus musculus 149-157 24105484-3 2013 We previously demonstrated that glycogen-synthase-kinase-3beta (GSK-3beta), the key enzyme of the WNT pathway, is increased in the hypothalamus during obesity and exacerbates high-fat diet-induced weight gain as well as glucose intolerance. Glucose 220-227 glycogen synthase kinase 3 beta Mus musculus 32-62 24105484-3 2013 We previously demonstrated that glycogen-synthase-kinase-3beta (GSK-3beta), the key enzyme of the WNT pathway, is increased in the hypothalamus during obesity and exacerbates high-fat diet-induced weight gain as well as glucose intolerance. Glucose 220-227 glycogen synthase kinase 3 beta Mus musculus 64-73 24391509-11 2014 Furthermore, the survival of MYCN transgenic mice bearing neuroblastoma was improved by treatment with NVP-BEZ235, a dual PI3K/mTOR inhibitor shown to destabilize MYCN via GSK3beta activation. dactolisib 106-113 glycogen synthase kinase 3 beta Mus musculus 172-180 25243109-0 2014 Prenatal alcohol exposure alters p35, CDK5 and GSK3beta in the medial frontal cortex and hippocampus of adolescent mice. Alcohols 9-16 glycogen synthase kinase 3 beta Mus musculus 47-55 25243109-5 2014 We investigated whether levels of GSK3beta and CDK5 are affected by moderate prenatal alcohol exposure (PAE), specifically in the hippocampus and medial frontal cortex of the adolescent mouse. Alcohols 86-93 glycogen synthase kinase 3 beta Mus musculus 34-42 25243109-5 2014 We investigated whether levels of GSK3beta and CDK5 are affected by moderate prenatal alcohol exposure (PAE), specifically in the hippocampus and medial frontal cortex of the adolescent mouse. 2-(Isopropylamino)ethanol 104-107 glycogen synthase kinase 3 beta Mus musculus 34-42 23992368-5 2013 KEY RESULTS: Enzastaurin inhibited the serine-threonine kinase p90RSK which has downstream effects on GSK3beta. enzastaurin 13-24 glycogen synthase kinase 3 beta Mus musculus 102-110 24018603-8 2013 In this study, we demonstrate that the GSK-3beta inhibitor 6-bromoindirubin 3"-oxime (BIO) activates Wnt/beta-catenin signaling, elevates the proportion of naive T cells, and delays T cell differentiation during homeostatic T cell expansion in lymphodepleted mice transplanted with human hematopoietic stem cells. 6-bromoindirubin-3'-oxime 59-84 glycogen synthase kinase 3 beta Mus musculus 39-48 23807397-2 2013 Recent evidence has suggested that acute and chronic administration of antidepressants led to inhibition of GSK-3beta via phosphorylation of Serine9 residue. serine9 141-148 glycogen synthase kinase 3 beta Mus musculus 108-117 23832395-6 2013 We found that STZ-induced diabetes resulted in decreased hippocampal expression of genes involved in epigenetic regulation and synaptic plasticity, for example, histone deacetylases and glycogen synthase kinase 3 beta (HDACs and GSK3beta). Streptozocin 14-17 glycogen synthase kinase 3 beta Mus musculus 229-237 23971735-6 2013 Here we show for the first time that 4.1%, but not 2.0%, sevoflurane reduced mouse NPC proliferation, increased Glycogen synthase kinase-3beta(GSK-3beta) levels, and decreased levels of beta-Catenin in mouse NPCs. Sevoflurane 57-68 glycogen synthase kinase 3 beta Mus musculus 112-142 23815613-8 2013 In addition, GlcN increased Akt glycosylation and glycogen synthase kinase-3beta (GSK-3beta) phosphorylation, and then Snail1 glycosylation. Glucosamine 13-17 glycogen synthase kinase 3 beta Mus musculus 50-80 23815613-8 2013 In addition, GlcN increased Akt glycosylation and glycogen synthase kinase-3beta (GSK-3beta) phosphorylation, and then Snail1 glycosylation. Glucosamine 13-17 glycogen synthase kinase 3 beta Mus musculus 82-91 23815613-12 2013 In conclusion, GlcN contributed to migration and proliferation of mESCs through integrin beta4/plectin complex reduction via Ca2+/PKC, as well as the Sp1/CaM and Akt/GSK-3beta/Snail1 signaling pathway. Glucosamine 15-19 glycogen synthase kinase 3 beta Mus musculus 166-175 24260576-9 2013 Furthermore, we show that alterations in healing in Cx43 deficient fractures can be rescued by inhibiting GSK-3beta activity using Lithium Chloride (LiCl). Lithium Chloride 131-147 glycogen synthase kinase 3 beta Mus musculus 106-115 24260576-9 2013 Furthermore, we show that alterations in healing in Cx43 deficient fractures can be rescued by inhibiting GSK-3beta activity using Lithium Chloride (LiCl). Lithium Chloride 149-153 glycogen synthase kinase 3 beta Mus musculus 106-115 24223757-8 2013 The mechanistic study about FLZ"s inhibitory effect on tau phosphorylation revealed t the involvement of Akt/glycogen synthase kinase 3beta (GSK3beta) pathway. flz 28-31 glycogen synthase kinase 3 beta Mus musculus 109-139 23971735-6 2013 Here we show for the first time that 4.1%, but not 2.0%, sevoflurane reduced mouse NPC proliferation, increased Glycogen synthase kinase-3beta(GSK-3beta) levels, and decreased levels of beta-Catenin in mouse NPCs. Sevoflurane 57-68 glycogen synthase kinase 3 beta Mus musculus 143-152 23971735-7 2013 The GSK-3beta inhibitor Lithium attenuated the sevoflurane-induced reduction in mouse NPC proliferation. Lithium 24-31 glycogen synthase kinase 3 beta Mus musculus 4-13 23971735-7 2013 The GSK-3beta inhibitor Lithium attenuated the sevoflurane-induced reduction in mouse NPC proliferation. Sevoflurane 47-58 glycogen synthase kinase 3 beta Mus musculus 4-13 24043902-1 2013 Lithium salt is a widely used glycogen synthase kinase-3beta inhibitor and effective drug for the treatment of psychiatric diseases. lithium salt 0-12 glycogen synthase kinase 3 beta Mus musculus 30-60 24204656-5 2013 Knockdown of Sirt2 expression also leads to the activation of GSK3beta through decreased phosphorylation of the serine at position 9 (Ser9) but not tyrosine at position 216 (Tyr216). Serine 112-118 glycogen synthase kinase 3 beta Mus musculus 62-70 24033914-3 2013 We found that insulin/IGF1 and lithium chloride enhanced IL-17-induced expression of C-X-C motif ligand 1 (Cxcl1) and C-C motif ligand 20 (Ccl20) in the Gsk3b(+/+) , but not in Gsk3b(-/-) mouse embryonic fibroblast (MEF) cells. Lithium Chloride 31-47 glycogen synthase kinase 3 beta Mus musculus 153-158 24033914-3 2013 We found that insulin/IGF1 and lithium chloride enhanced IL-17-induced expression of C-X-C motif ligand 1 (Cxcl1) and C-C motif ligand 20 (Ccl20) in the Gsk3b(+/+) , but not in Gsk3b(-/-) mouse embryonic fibroblast (MEF) cells. Lithium Chloride 31-47 glycogen synthase kinase 3 beta Mus musculus 177-182 23884148-9 2013 Medullary levels of p-GSK3beta were increased in the renal medullas of lithium-treated mice and remained elevated following rapamycin treatment. Lithium 71-78 glycogen synthase kinase 3 beta Mus musculus 22-30 23884148-9 2013 Medullary levels of p-GSK3beta were increased in the renal medullas of lithium-treated mice and remained elevated following rapamycin treatment. Sirolimus 124-133 glycogen synthase kinase 3 beta Mus musculus 22-30 23860320-0 2013 Resistin disrupts glycogen synthesis under high insulin and high glucose levels by down-regulating the hepatic levels of GSK3beta. Glycogen 18-26 glycogen synthase kinase 3 beta Mus musculus 121-129 23860320-3 2013 Protein levels of factors in the insulin signaling pathway involved in glycogen synthesis were examined by Western blot analysis, with the only significant change observed being the level of phosphorylated (at Ser 9) glycogen synthase kinase-3beta (GSK-3beta) (P<0.001). Serine 210-213 glycogen synthase kinase 3 beta Mus musculus 217-247 24043902-3 2013 In this study, we show that lithium chloride attenuates LPS-, polyinosinic-polycytidylic acid-, and Sendai virus-induced IFN-beta production and IFN regulatory factor 3 activation in macrophages in a glycogen synthase kinase-3beta-independent manner. Lithium Chloride 28-44 glycogen synthase kinase 3 beta Mus musculus 200-230 24129178-7 2013 Gallic acid also increased GSK3beta and p-beta-catenin expression but down-regulated p-GSK3beta. Gallic Acid 0-11 glycogen synthase kinase 3 beta Mus musculus 27-35 24129178-7 2013 Gallic acid also increased GSK3beta and p-beta-catenin expression but down-regulated p-GSK3beta. Gallic Acid 0-11 glycogen synthase kinase 3 beta Mus musculus 87-95 24129178-8 2013 Moreover, GSK3beta-specific inhibitor (SB216763) restored gallic acid-induced melanin reduction. SB 216763 39-47 glycogen synthase kinase 3 beta Mus musculus 10-18 24129178-8 2013 Moreover, GSK3beta-specific inhibitor (SB216763) restored gallic acid-induced melanin reduction. Gallic Acid 58-69 glycogen synthase kinase 3 beta Mus musculus 10-18 24129178-8 2013 Moreover, GSK3beta-specific inhibitor (SB216763) restored gallic acid-induced melanin reduction. Melanins 78-85 glycogen synthase kinase 3 beta Mus musculus 10-18 24091664-7 2013 Here, we explored a pharmacological manipulation of a Wnt signaling pathway using lithium chloride (LiCl), a GSK-3beta inhibitor, and observed the enhanced expression of beta-catenin protein as well as the decreased cell death normally observed in an OPMD cell model of murine myoblast (C2C12) expressing the expanded and pathogenic form of the expPABPN1. Lithium Chloride 82-98 glycogen synthase kinase 3 beta Mus musculus 109-118 24091664-7 2013 Here, we explored a pharmacological manipulation of a Wnt signaling pathway using lithium chloride (LiCl), a GSK-3beta inhibitor, and observed the enhanced expression of beta-catenin protein as well as the decreased cell death normally observed in an OPMD cell model of murine myoblast (C2C12) expressing the expanded and pathogenic form of the expPABPN1. Lithium Chloride 100-104 glycogen synthase kinase 3 beta Mus musculus 109-118 23689589-8 2013 LiCl (a GSK3beta inhibitor)-treated cells also showed increased expression of Snail, with a reduced adipogenic potential. Lithium Chloride 0-4 glycogen synthase kinase 3 beta Mus musculus 8-16 23857515-8 2013 In addition, fucoxanthinol inhibited the phosphorylation of phosphoinositide-dependent kinase 1 and Akt and the downstream glycogen synthase kinase 3beta, resulting in downregulation of beta-catenin. fucoxanthinol 13-26 glycogen synthase kinase 3 beta Mus musculus 123-153 23640537-5 2013 Additionally, MLB prevented the decrease in phosphorylated Akt and glycogen synthase kinase-3beta (GSK-3beta) levels both in NMDA-injured neurons and KA-injured mouse brain. N-Methylaspartate 125-129 glycogen synthase kinase 3 beta Mus musculus 67-97 23640537-5 2013 Additionally, MLB prevented the decrease in phosphorylated Akt and glycogen synthase kinase-3beta (GSK-3beta) levels both in NMDA-injured neurons and KA-injured mouse brain. N-Methylaspartate 125-129 glycogen synthase kinase 3 beta Mus musculus 99-108 23640537-6 2013 This effect was blocked by phosphoinositide 3-kinase (PI3K) inhibitor LY294002 and Akt inhibitor triciribine, thus indicating the neuroprotective effects of MLB are most likely mediated by the PI3K/Akt/GSK-3beta pathway. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 70-78 glycogen synthase kinase 3 beta Mus musculus 202-211 23640537-6 2013 This effect was blocked by phosphoinositide 3-kinase (PI3K) inhibitor LY294002 and Akt inhibitor triciribine, thus indicating the neuroprotective effects of MLB are most likely mediated by the PI3K/Akt/GSK-3beta pathway. triciribine 97-108 glycogen synthase kinase 3 beta Mus musculus 202-211 23839051-7 2013 Furthermore, after the free consumption of alcohol, the activities of protein kinase B and glycogen synthase kinase 3beta (GSK3beta) increased in the dorsal striatum of WT mice, but not in KO mice, which showed high basal activity of Akt in the dorsal striatum. Alcohols 43-50 glycogen synthase kinase 3 beta Mus musculus 91-121 23707483-2 2013 Dopamine-associated neuropsychiatric illnesses such as schizophrenia and bipolar disorder seem to be characterized by impairments in the AKT/GSK3beta network. Dopamine 0-8 glycogen synthase kinase 3 beta Mus musculus 141-149 23707483-3 2013 Here, we sought evidence for the presence of molecular and functional changes in the AKT/GSK3beta pathway using an established infection-based mouse model of developmental neuropsychiatric disease that is based on prenatal administration of the viral mimetic poly(I:C) (=polyriboinosinic-polyribocytidilic acid). poly 259-263 glycogen synthase kinase 3 beta Mus musculus 89-97 23707483-7 2013 We further found that acute pre-treatment with the selective GSK3beta inhibitor TDZD-8 dose-dependently normalized aberrant behavior typically emerging following prenatal immune activation, including deficient spontaneous alternation in the Y-maze and increased locomotor responses to systemic amphetamine treatment. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 80-86 glycogen synthase kinase 3 beta Mus musculus 61-69 23707483-7 2013 We further found that acute pre-treatment with the selective GSK3beta inhibitor TDZD-8 dose-dependently normalized aberrant behavior typically emerging following prenatal immune activation, including deficient spontaneous alternation in the Y-maze and increased locomotor responses to systemic amphetamine treatment. Amphetamine 294-305 glycogen synthase kinase 3 beta Mus musculus 61-69 23850563-7 2013 Remarkably, the hyperactivity of the Cdk5 conditional knockouts can be ameliorated by the administration of lithium chloride, an inhibitor of GSK3beta signaling. Lithium Chloride 108-124 glycogen synthase kinase 3 beta Mus musculus 142-150 24141459-8 2013 Lithium ameliorated P-GSK3beta expression in the hippocampus of all the treatment groups in knockout mice (p<0.05). Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 22-30 23896029-5 2013 DEX administration initially reduced expression of GSK3B, GYS1, GBE1, FOXO1, UGP2 in both male and female placentas, but reduced histologically detectable glycogen storage in placentas of female fetuses only. Dexamethasone 0-3 glycogen synthase kinase 3 beta Mus musculus 51-56 23896029-6 2013 The DEX-induced reduction in expression of GSK3B and UGP2 persisted until day 37 of gestation, an effect that was significantly greater in the male placenta. Dexamethasone 4-7 glycogen synthase kinase 3 beta Mus musculus 43-48 23839051-7 2013 Furthermore, after the free consumption of alcohol, the activities of protein kinase B and glycogen synthase kinase 3beta (GSK3beta) increased in the dorsal striatum of WT mice, but not in KO mice, which showed high basal activity of Akt in the dorsal striatum. Alcohols 43-50 glycogen synthase kinase 3 beta Mus musculus 123-131 23839051-8 2013 These results suggest that beta-arrestin-2 negatively regulates alcohol preference and reward, likely through regulating the activation of signaling pathways including Akt/GSK3beta in the dorsal striatum. Alcohols 64-71 glycogen synthase kinase 3 beta Mus musculus 172-180 23851680-8 2013 Furthermore, activation of glycogen synthase kinase-3beta (GSK-3beta) was required for ceramide-induced NF-kappaB activation and iNOS expression. Ceramides 87-95 glycogen synthase kinase 3 beta Mus musculus 59-68 23919927-2 2013 Among several putative therapeutic molecular targets, direct inhibition of glycogen synthase kinase-3 beta (GSK3beta) by lithium has been proposed to underlie its effects on circadian physiology. Lithium 121-128 glycogen synthase kinase 3 beta Mus musculus 75-106 23919927-2 2013 Among several putative therapeutic molecular targets, direct inhibition of glycogen synthase kinase-3 beta (GSK3beta) by lithium has been proposed to underlie its effects on circadian physiology. Lithium 121-128 glycogen synthase kinase 3 beta Mus musculus 108-116 23919927-7 2013 Knowing that GSK3beta interacts with most of the core clock components, these data suggest that GSK3beta acts as a critical intrinsic regulator of the circadian clock and plays an important role in regulating its period in response to lithium treatment. Lithium 235-242 glycogen synthase kinase 3 beta Mus musculus 13-21 23919927-7 2013 Knowing that GSK3beta interacts with most of the core clock components, these data suggest that GSK3beta acts as a critical intrinsic regulator of the circadian clock and plays an important role in regulating its period in response to lithium treatment. Lithium 235-242 glycogen synthase kinase 3 beta Mus musculus 96-104 23848820-2 2013 By inhibiting glycogen synthase kinase-3 (GSK-3) and histone deacetylases (HDACs), respectively, lithium and valproate (VPA) have beneficial effects in diverse neurodegenerative diseases. Lithium 97-104 glycogen synthase kinase 3 beta Mus musculus 14-40 23848820-2 2013 By inhibiting glycogen synthase kinase-3 (GSK-3) and histone deacetylases (HDACs), respectively, lithium and valproate (VPA) have beneficial effects in diverse neurodegenerative diseases. Lithium 97-104 glycogen synthase kinase 3 beta Mus musculus 42-47 23848820-2 2013 By inhibiting glycogen synthase kinase-3 (GSK-3) and histone deacetylases (HDACs), respectively, lithium and valproate (VPA) have beneficial effects in diverse neurodegenerative diseases. Valproic Acid 109-118 glycogen synthase kinase 3 beta Mus musculus 14-40 23848820-2 2013 By inhibiting glycogen synthase kinase-3 (GSK-3) and histone deacetylases (HDACs), respectively, lithium and valproate (VPA) have beneficial effects in diverse neurodegenerative diseases. Valproic Acid 109-118 glycogen synthase kinase 3 beta Mus musculus 42-47 23848820-2 2013 By inhibiting glycogen synthase kinase-3 (GSK-3) and histone deacetylases (HDACs), respectively, lithium and valproate (VPA) have beneficial effects in diverse neurodegenerative diseases. Valproic Acid 120-123 glycogen synthase kinase 3 beta Mus musculus 14-40 23848820-2 2013 By inhibiting glycogen synthase kinase-3 (GSK-3) and histone deacetylases (HDACs), respectively, lithium and valproate (VPA) have beneficial effects in diverse neurodegenerative diseases. Valproic Acid 120-123 glycogen synthase kinase 3 beta Mus musculus 42-47 23892131-0 2013 Anti-inflammatory effects of lipoic acid through inhibition of GSK-3beta in lipopolysaccharide-induced BV-2 microglial cells. Thioctic Acid 29-40 glycogen synthase kinase 3 beta Mus musculus 63-72 23707771-10 2013 Furthermore, there was a marked induction of AKT, GSK-3beta, beta-catenin, mTOR, and carcinogenic markers in tumor tissues formed in mice after injection with Cr(VI)-stimulated cells. chromium hexavalent ion 159-165 glycogen synthase kinase 3 beta Mus musculus 50-59 23784744-0 2013 Naproxen and cromolyn as new glycogen synthase kinase 3beta inhibitors for amelioration of diabetes and obesity: an investigation by docking simulation and subsequent in vitro/in vivo biochemical evaluation. Naproxen 0-8 glycogen synthase kinase 3 beta Mus musculus 29-59 23784744-0 2013 Naproxen and cromolyn as new glycogen synthase kinase 3beta inhibitors for amelioration of diabetes and obesity: an investigation by docking simulation and subsequent in vitro/in vivo biochemical evaluation. Cromolyn Sodium 13-21 glycogen synthase kinase 3 beta Mus musculus 29-59 23784744-1 2013 Naproxen and cromolyn were investigated as new inhibitors of glycogen synthase kinase-3beta (GSK-3beta) in an attempt to explain their hypoglycemic properties. Naproxen 0-8 glycogen synthase kinase 3 beta Mus musculus 61-91 23784744-1 2013 Naproxen and cromolyn were investigated as new inhibitors of glycogen synthase kinase-3beta (GSK-3beta) in an attempt to explain their hypoglycemic properties. Naproxen 0-8 glycogen synthase kinase 3 beta Mus musculus 93-102 23784744-1 2013 Naproxen and cromolyn were investigated as new inhibitors of glycogen synthase kinase-3beta (GSK-3beta) in an attempt to explain their hypoglycemic properties. Cromolyn Sodium 13-21 glycogen synthase kinase 3 beta Mus musculus 61-91 23784744-1 2013 Naproxen and cromolyn were investigated as new inhibitors of glycogen synthase kinase-3beta (GSK-3beta) in an attempt to explain their hypoglycemic properties. Cromolyn Sodium 13-21 glycogen synthase kinase 3 beta Mus musculus 93-102 23784744-3 2013 Both drugs not only were optimally fitted within a GSK-3beta binding pocket via several attractive interactions with key amino acids but also exhibited potent in vitro enzymatic inhibitory activities of IC50 1.5 and 2.0 microM for naproxen and cromolyn, respectively. Naproxen 231-239 glycogen synthase kinase 3 beta Mus musculus 51-60 23784744-3 2013 Both drugs not only were optimally fitted within a GSK-3beta binding pocket via several attractive interactions with key amino acids but also exhibited potent in vitro enzymatic inhibitory activities of IC50 1.5 and 2.0 microM for naproxen and cromolyn, respectively. Cromolyn Sodium 244-252 glycogen synthase kinase 3 beta Mus musculus 51-60 23784744-6 2013 It can be concluded that naproxen and cromolyn are novel GSK-3beta inhibitors and can help in management of diabetes and obesity. Naproxen 25-33 glycogen synthase kinase 3 beta Mus musculus 57-66 23784744-6 2013 It can be concluded that naproxen and cromolyn are novel GSK-3beta inhibitors and can help in management of diabetes and obesity. Cromolyn Sodium 38-46 glycogen synthase kinase 3 beta Mus musculus 57-66 23853095-2 2013 At low glucose levels, glycogen synthase kinase 3beta (GSK3beta) is known to phosphorylate PDX-1 on C-terminal serine residues, which triggers PDX-1 proteasomal degradation. Glucose 7-14 glycogen synthase kinase 3 beta Mus musculus 23-53 23853095-2 2013 At low glucose levels, glycogen synthase kinase 3beta (GSK3beta) is known to phosphorylate PDX-1 on C-terminal serine residues, which triggers PDX-1 proteasomal degradation. Glucose 7-14 glycogen synthase kinase 3 beta Mus musculus 55-63 23853095-2 2013 At low glucose levels, glycogen synthase kinase 3beta (GSK3beta) is known to phosphorylate PDX-1 on C-terminal serine residues, which triggers PDX-1 proteasomal degradation. Serine 111-117 glycogen synthase kinase 3 beta Mus musculus 23-53 23853095-2 2013 At low glucose levels, glycogen synthase kinase 3beta (GSK3beta) is known to phosphorylate PDX-1 on C-terminal serine residues, which triggers PDX-1 proteasomal degradation. Serine 111-117 glycogen synthase kinase 3 beta Mus musculus 55-63 23853095-7 2013 In vitro, PASK directly phosphorylates GSK3beta on its inactivating phosphorylation site Ser(9). Serine 89-92 glycogen synthase kinase 3 beta Mus musculus 39-47 23853095-8 2013 Overexpression of a kinase-dead (KD), dominant negative version of PASK blocks glucose-induced Ser(9) phosphorylation of GSK3beta. Glucose 79-86 glycogen synthase kinase 3 beta Mus musculus 121-129 23853095-8 2013 Overexpression of a kinase-dead (KD), dominant negative version of PASK blocks glucose-induced Ser(9) phosphorylation of GSK3beta. Serine 95-98 glycogen synthase kinase 3 beta Mus musculus 121-129 23853095-9 2013 Accordingly, GSK3beta Ser(9) phosphorylation is reduced in islets from pask-null mice. Serine 22-25 glycogen synthase kinase 3 beta Mus musculus 13-21 23853095-12 2013 We conclude that PASK phosphorylates and inactivates GSK3beta, thereby preventing PDX-1 serine phosphorylation and alleviating GSK3beta-mediated PDX-1 protein degradation in pancreatic beta-cells. Serine 88-94 glycogen synthase kinase 3 beta Mus musculus 53-61 23940567-0 2013 Possible role of the glycogen synthase kinase-3 signaling pathway in trimethyltin-induced hippocampal neurodegeneration in mice. trimethyltin 69-81 glycogen synthase kinase 3 beta Mus musculus 21-47 22964642-9 2013 Pre-treatment of Keap1(-/-) MEFs or A549 cells with the LY294002 PI3K inhibitor or the MK-2206 PKB/Akt inhibitor increased their sensitivity to acrolein, chlorambucil and cisplatin between 1.9-fold and 3.1-fold, and this was substantially attenuated by simultaneous pre-treatment with the GSK-3 inhibitor CT99021. MK 2206 87-94 glycogen synthase kinase 3 beta Mus musculus 289-294 23940567-3 2013 In this study, we evaluated the therapeutic effect of lithium, a selective GSK-3 inhibitor, on the hippocampus of adult C57BL/6 mice with TMT treatment (2.6 mg/kg, intraperitoneal [i.p.]) Lithium 54-61 glycogen synthase kinase 3 beta Mus musculus 75-80 23940673-0 2013 Neuronal apoptosis and motor deficits in mice with genetic inhibition of GSK-3 are Fas-dependent. ammonium ferrous sulfate 83-86 glycogen synthase kinase 3 beta Mus musculus 73-78 23940567-7 2013 Additionally, the dynamic changes in GSK-3/beta-catenin signaling were observed in the mouse hippocampus and cultured hippocampal neurons after TMT treatment with or without lithium. Lithium 174-181 glycogen synthase kinase 3 beta Mus musculus 37-42 23940673-3 2013 Lithium, a non-selective GSK-3 inhibitor has been classically administered to treat bipolar patients but its prescription is decreasing due to its frequent side effects such as hand tremor. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 25-30 23940567-8 2013 Therefore, lithium inhibited the detrimental effects of TMT on the hippocampal neurons in vivo and in vitro, suggesting involvement of the GSK-3/beta-catenin signaling pathway in TMT-induced hippocampal cell degeneration and dysfunction. Lithium 11-18 glycogen synthase kinase 3 beta Mus musculus 139-144 23940673-7 2013 For this purpose we took advantage of a transgenic mouse line with decreased GSK-3 activity (Tet/DN-GSK-3 mice) that shows increased rate of neuronal apoptosis as well as motor deficits and brought it to a Fas deficient background (lpr mice). tetramethylenedisulfotetramine 93-96 glycogen synthase kinase 3 beta Mus musculus 77-82 23940673-7 2013 For this purpose we took advantage of a transgenic mouse line with decreased GSK-3 activity (Tet/DN-GSK-3 mice) that shows increased rate of neuronal apoptosis as well as motor deficits and brought it to a Fas deficient background (lpr mice). tetramethylenedisulfotetramine 93-96 glycogen synthase kinase 3 beta Mus musculus 100-105 23817039-10 2013 Conversely, GSK3 inhibitor SB216763 (3-[2,4-Dichlorophenyl]-4-[1-methyl-1H-indol-3-yl]-1H-pyrrole-2,5-dione, 10muM, 30min) significantly blunted the increase of cytosolic Ca(2+) concentration following LPS exposure. SB 216763 27-35 glycogen synthase kinase 3 beta Mus musculus 12-16 23940673-7 2013 For this purpose we took advantage of a transgenic mouse line with decreased GSK-3 activity (Tet/DN-GSK-3 mice) that shows increased rate of neuronal apoptosis as well as motor deficits and brought it to a Fas deficient background (lpr mice). ammonium ferrous sulfate 206-209 glycogen synthase kinase 3 beta Mus musculus 77-82 23940673-7 2013 For this purpose we took advantage of a transgenic mouse line with decreased GSK-3 activity (Tet/DN-GSK-3 mice) that shows increased rate of neuronal apoptosis as well as motor deficits and brought it to a Fas deficient background (lpr mice). ammonium ferrous sulfate 206-209 glycogen synthase kinase 3 beta Mus musculus 100-105 23940673-9 2013 Interestingly, motor deficits were also absent in Fas deficient Tet/DN-GSK-3 mice. ammonium ferrous sulfate 50-53 glycogen synthase kinase 3 beta Mus musculus 71-76 23940673-9 2013 Interestingly, motor deficits were also absent in Fas deficient Tet/DN-GSK-3 mice. tetramethylenedisulfotetramine 64-67 glycogen synthase kinase 3 beta Mus musculus 71-76 23940673-10 2013 These results demonstrate that Fas signaling contributes to the neurological toxicity of GSK-3 inhibition and suggest that a combination of GSK-3 inhibitors with blockers of Fas signaling could help to improve the application of GSK-3 inhibitors to clinics. ammonium ferrous sulfate 31-34 glycogen synthase kinase 3 beta Mus musculus 89-94 23817039-10 2013 Conversely, GSK3 inhibitor SB216763 (3-[2,4-Dichlorophenyl]-4-[1-methyl-1H-indol-3-yl]-1H-pyrrole-2,5-dione, 10muM, 30min) significantly blunted the increase of cytosolic Ca(2+) concentration following LPS exposure. SB 216763 37-107 glycogen synthase kinase 3 beta Mus musculus 12-16 23660953-10 2013 Furthermore, EGCG treatment inhibited TNF-alpha/JNK signaling and increased the phosphorylation of Akt and glycogen synthase kinase-3beta in the hippocampus of APP/PS1 mice. epigallocatechin gallate 13-17 glycogen synthase kinase 3 beta Mus musculus 107-137 23628704-8 2013 Significant accumulation of glycogen synthase kinase-3beta (GSK-3beta) in the nucleus of N2a and mouse brain cells, and elevation of its phosphorylation at Y216, was observed under formaldehyde stress. Formaldehyde 181-193 glycogen synthase kinase 3 beta Mus musculus 28-58 23628704-8 2013 Significant accumulation of glycogen synthase kinase-3beta (GSK-3beta) in the nucleus of N2a and mouse brain cells, and elevation of its phosphorylation at Y216, was observed under formaldehyde stress. Formaldehyde 181-193 glycogen synthase kinase 3 beta Mus musculus 60-69 23628704-9 2013 Formaldehyde-induced Tau hyperphosphorylation was blocked in the presence of LiCl and CT99021, inhibitors of GSK-3beta, and by RNAi interference. Formaldehyde 0-12 glycogen synthase kinase 3 beta Mus musculus 109-118 23628704-10 2013 CONCLUSIONS: Formaldehyde, which may cause age-related memory loss, can act as a factor triggering Tau hyperphosphorylation via GSK-3beta catalysis and induces polymerization of Tau. Formaldehyde 13-25 glycogen synthase kinase 3 beta Mus musculus 128-137 22626030-0 2013 GSK3b-inhibitor lithium chloride enhances activation of Wnt canonical signaling and osteoblast differentiation on hydrophilic titanium surfaces. Lithium Chloride 16-32 glycogen synthase kinase 3 beta Mus musculus 0-5 22626030-0 2013 GSK3b-inhibitor lithium chloride enhances activation of Wnt canonical signaling and osteoblast differentiation on hydrophilic titanium surfaces. Titanium 126-134 glycogen synthase kinase 3 beta Mus musculus 0-5 22626030-2 2013 This study investigated whether stimulation of Wnt signaling by GSK3b inhibitor lithium chloride (LiCl) could affect the response of mesenchymal or osteoblastic cells growing on titanium surfaces with different topography and wettability, and improve their differentiation along the osteoblastic lineage. Lithium Chloride 80-96 glycogen synthase kinase 3 beta Mus musculus 64-69 22626030-2 2013 This study investigated whether stimulation of Wnt signaling by GSK3b inhibitor lithium chloride (LiCl) could affect the response of mesenchymal or osteoblastic cells growing on titanium surfaces with different topography and wettability, and improve their differentiation along the osteoblastic lineage. Lithium Chloride 98-102 glycogen synthase kinase 3 beta Mus musculus 64-69 23687303-2 2013 The aim of this work was to investigate the participation of the PI3K/Akt pathway and its outcome on different molecular targets such as glycogen synthase kinase 3beta (GSK3beta) and Forkhead box-O (FoxO) transcription factors during mild oxidative stress triggered by iron overload. Iron 269-273 glycogen synthase kinase 3 beta Mus musculus 137-167 23595951-11 2013 PGE2 could stimulate phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase3beta signaling in VSMCs through Gbetagamma subunits on EP3alpha/beta activation. Dinoprostone 0-4 glycogen synthase kinase 3 beta Mus musculus 55-84 23687303-9 2013 Our results show that activation of the PI3K/Akt pathway during iron-induced neurotoxicity regulates multiple targets such as GSK3beta, FoxO transcriptional activity, and glutathione metabolism, thus modulating the neuronal response to oxidative stress. Iron 64-68 glycogen synthase kinase 3 beta Mus musculus 126-134 23823480-5 2013 These data show that (1) the immediate action of insulin to suppress hepatic glucose production functions via an Akt2-dependent redirection of glucose-6-phosphate to glycogen, and (2) insulin increases glucose phosphorylation and conversion to glycogen independent of GSK3. Glycogen 244-252 glycogen synthase kinase 3 beta Mus musculus 268-272 23194475-9 2013 One of the main kinases involved in tau phosphorylation, glycogen synthase kinase 3beta (GSK3beta), which is inactivated by phosphorylation by pAkt, was found to be decreased after corticosterone and increased after propranolol treatment. Corticosterone 181-195 glycogen synthase kinase 3 beta Mus musculus 57-87 23473804-3 2013 To this end, 158N murine oligodendrocytes were treated with 7KC or 7betaOHC inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving Mcl-1, and caspase-3 activation. 7betaohc 67-75 glycogen synthase kinase 3 beta Mus musculus 205-209 23473804-9 2013 Thus, in 158N cells, the ability of oxysterols to trigger a mode of cell death by apoptosis involving GSK-3 and caspase-3 activation is independent of the increase in the Ca(2+) level and of their accumulation in lipid raft microdomains. Oxysterols 36-46 glycogen synthase kinase 3 beta Mus musculus 102-107 23604046-0 2013 Ephedrine hydrochloride inhibits PGN-induced inflammatory responses by promoting IL-10 production and decreasing proinflammatory cytokine secretion via the PI3K/Akt/GSK3beta pathway. Ephedrine 0-23 glycogen synthase kinase 3 beta Mus musculus 165-173 23823480-0 2013 A noncanonical, GSK3-independent pathway controls postprandial hepatic glycogen deposition. Glycogen 71-79 glycogen synthase kinase 3 beta Mus musculus 16-20 23570858-5 2013 We further demonstrate that the number of differentiating, doublecortin-positive new neurons is reduced in GSK-3beta[S9A] mice, but not in GSK-3beta(n-/-) mice. doublecortin 59-71 glycogen synthase kinase 3 beta Mus musculus 107-116 23194475-9 2013 One of the main kinases involved in tau phosphorylation, glycogen synthase kinase 3beta (GSK3beta), which is inactivated by phosphorylation by pAkt, was found to be decreased after corticosterone and increased after propranolol treatment. Corticosterone 181-195 glycogen synthase kinase 3 beta Mus musculus 89-97 23194475-9 2013 One of the main kinases involved in tau phosphorylation, glycogen synthase kinase 3beta (GSK3beta), which is inactivated by phosphorylation by pAkt, was found to be decreased after corticosterone and increased after propranolol treatment. Propranolol 216-227 glycogen synthase kinase 3 beta Mus musculus 57-87 23194475-9 2013 One of the main kinases involved in tau phosphorylation, glycogen synthase kinase 3beta (GSK3beta), which is inactivated by phosphorylation by pAkt, was found to be decreased after corticosterone and increased after propranolol treatment. Propranolol 216-227 glycogen synthase kinase 3 beta Mus musculus 89-97 23896637-9 2013 Consistent with this, we have found by BrdU incorporation assay that combined treatments of small molecule GSK-3 inhibitor and mitogen/s lead to elevated proliferation of human beta-cells, which is caused partly due to p27(Kip1) downregulation. Bromodeoxyuridine 39-43 glycogen synthase kinase 3 beta Mus musculus 107-112 23604413-8 2013 After 8 weeks, mice pretreated or treated with IC3 developed smaller tumors compared to the untreated control group, and the protein expression of PI3K p110alpha, PI3K class III, Akt, p-Akt and the downstream signaling proteins p-c-Raf and GSK3-beta in the tumors were significantly downregulated. 5-AMINO-1-[2-NITRO-4-(TRIFLUOROMETHYL)PHENYL]-1H-PYRAZOLE-4-CARBONITRILE 47-50 glycogen synthase kinase 3 beta Mus musculus 240-249 23725591-0 2013 Characterization of maleimide-based glycogen synthase kinase-3 (GSK-3) inhibitors as stimulators of steroidogenesis. maleimide 20-29 glycogen synthase kinase 3 beta Mus musculus 36-62 23725591-0 2013 Characterization of maleimide-based glycogen synthase kinase-3 (GSK-3) inhibitors as stimulators of steroidogenesis. maleimide 20-29 glycogen synthase kinase 3 beta Mus musculus 64-69 23725591-1 2013 Inhibition of GSK-3beta has been well documented to account for the behavioral actions of the mood stabilizer lithium in various animal models of mood disorders. Lithium 110-117 glycogen synthase kinase 3 beta Mus musculus 14-23 23725591-3 2013 In our ongoing efforts to develop GSK-3beta inhibitors for the treatment of mood disorders, SAR studies on maleimide-based compounds were undertaken. maleimide 107-116 glycogen synthase kinase 3 beta Mus musculus 34-43 23725591-4 2013 We present herein for the first time that some of these GSK-3beta inhibitors, in particular analogues 1 and 9, were able to stimulate progesterone production in the MA-10 mouse tumor Leydig cell model of steroidogenesis without any significant toxicity. Progesterone 134-146 glycogen synthase kinase 3 beta Mus musculus 56-65 23725591-6 2013 Taken together, these results support the hypothesis that GSK-3beta inhibition could influence neuroactive steroid production thereby mediating the modulation of anxiety-like behavior in vivo. Steroids 107-114 glycogen synthase kinase 3 beta Mus musculus 58-67 23665028-4 2013 Among them, we found that Kenpaullone, a GSK3-beta and CDK inhibitor, efficiently suppressed TGF-beta-mediated RORgammat induction and enhanced Foxp3 induction in primary T cells. kenpaullone 26-37 glycogen synthase kinase 3 beta Mus musculus 41-50 23761900-0 2013 The sphingolipid psychosine inhibits fast axonal transport in Krabbe disease by activation of GSK3beta and deregulation of molecular motors. sphingolipid psychosine 4-27 glycogen synthase kinase 3 beta Mus musculus 94-102 23761900-3 2013 Myelin-free in vitro analyses showed that psychosine inhibited fast axonal transport through the activation of axonal PP1 and GSK3beta in the axon. Psychosine 42-52 glycogen synthase kinase 3 beta Mus musculus 126-134 23606540-5 2013 Administration of the selective GSK3 inhibitors TDZD-8, VP2.51, VP0.7, or L803-mts significantly reduced the clinical symptoms of myelin oligodendrocyte glycoprotein35-55-induced EAE in mice, nearly eliminating the chronic progressive phase, and reduced the number of Th17 and Th1 cells in the spinal cord. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 48-54 glycogen synthase kinase 3 beta Mus musculus 32-36 23402899-0 2013 Disease-modified glycogen synthase kinase-3beta intervention by melatonin arrests the pathology and memory deficits in an Alzheimer"s animal model. Melatonin 64-73 glycogen synthase kinase 3 beta Mus musculus 17-47 23402899-5 2013 We also found that the disease stage-specific alteration of glycogen synthase kinase-3beta (GSK-3beta) but not protein phosphatase-2A, was correlated with the alterations of the pathology and behavior, and the timely targeting of GSK-3beta was critical for the efficacy of melatonin. Melatonin 273-282 glycogen synthase kinase 3 beta Mus musculus 60-90 23474308-11 2013 In vitro study using the GSK3beta inhibitor SB216763 mimicked the response elicited by chronic Akt activation. SB 216763 44-52 glycogen synthase kinase 3 beta Mus musculus 25-33 23583326-0 2013 Paliperidone protects prefrontal cortical neurons from damages caused by MK-801 via Akt1/GSK3beta signaling pathway. Paliperidone Palmitate 0-12 glycogen synthase kinase 3 beta Mus musculus 89-97 23583326-0 2013 Paliperidone protects prefrontal cortical neurons from damages caused by MK-801 via Akt1/GSK3beta signaling pathway. Dizocilpine Maleate 73-79 glycogen synthase kinase 3 beta Mus musculus 89-97 23583326-7 2013 Moreover, paliperidone could significantly retard MK-801-mediated inhibition of neurite outgrowth (p<0.01) and reverse MK-801-induced decreases of gene expression and phosphorylation of Akt1 and GSK3beta (both p<0.01). Paliperidone Palmitate 10-22 glycogen synthase kinase 3 beta Mus musculus 198-206 23583326-7 2013 Moreover, paliperidone could significantly retard MK-801-mediated inhibition of neurite outgrowth (p<0.01) and reverse MK-801-induced decreases of gene expression and phosphorylation of Akt1 and GSK3beta (both p<0.01). Dizocilpine Maleate 50-56 glycogen synthase kinase 3 beta Mus musculus 198-206 23583326-7 2013 Moreover, paliperidone could significantly retard MK-801-mediated inhibition of neurite outgrowth (p<0.01) and reverse MK-801-induced decreases of gene expression and phosphorylation of Akt1 and GSK3beta (both p<0.01). Dizocilpine Maleate 122-128 glycogen synthase kinase 3 beta Mus musculus 198-206 23583326-9 2013 Taking together, our results demonstrated that paliperidone could protect prefrontal cortical neurons from MK-801-induced damages via Akt1/GSK3beta signaling pathway. Paliperidone Palmitate 47-59 glycogen synthase kinase 3 beta Mus musculus 139-147 23583326-9 2013 Taking together, our results demonstrated that paliperidone could protect prefrontal cortical neurons from MK-801-induced damages via Akt1/GSK3beta signaling pathway. Dizocilpine Maleate 107-113 glycogen synthase kinase 3 beta Mus musculus 139-147 24025512-4 2013 Western blot was used to detect the expression levels of GSK-3beta and phospho-GSK-3beta (ser-9). Serine 90-93 glycogen synthase kinase 3 beta Mus musculus 79-88 24025512-6 2013 The expression level of GSK-3beta at phospho-GSK-3beta (ser-9) was detected in APPL1-suppressed C2C12 myotube while that of APPL1 at phospho-APPL1 (ser-401) determined in GSK-3beta overexpressed/inhibited C2C12 cell. Serine 56-59 glycogen synthase kinase 3 beta Mus musculus 24-33 24025512-6 2013 The expression level of GSK-3beta at phospho-GSK-3beta (ser-9) was detected in APPL1-suppressed C2C12 myotube while that of APPL1 at phospho-APPL1 (ser-401) determined in GSK-3beta overexpressed/inhibited C2C12 cell. Serine 56-59 glycogen synthase kinase 3 beta Mus musculus 45-54 24025512-6 2013 The expression level of GSK-3beta at phospho-GSK-3beta (ser-9) was detected in APPL1-suppressed C2C12 myotube while that of APPL1 at phospho-APPL1 (ser-401) determined in GSK-3beta overexpressed/inhibited C2C12 cell. Serine 56-59 glycogen synthase kinase 3 beta Mus musculus 45-54 24025512-6 2013 The expression level of GSK-3beta at phospho-GSK-3beta (ser-9) was detected in APPL1-suppressed C2C12 myotube while that of APPL1 at phospho-APPL1 (ser-401) determined in GSK-3beta overexpressed/inhibited C2C12 cell. Serine 148-151 glycogen synthase kinase 3 beta Mus musculus 24-33 24025512-7 2013 RESULTS: Leptin time-dependently increased the phosphorylation level of GSK-3beta at ser-9 in C2C12 cell, and the pGSK-3beta level in cells incubated by leptin for 30 min was as 4.08 times as which in control cells (P < 0.01). Serine 85-88 glycogen synthase kinase 3 beta Mus musculus 72-81 24025512-10 2013 And the phosphorylation of APPL1 at ser-401 could be induced by GSK-3beta. Serine 36-39 glycogen synthase kinase 3 beta Mus musculus 64-73 24025512-11 2013 CONCLUSION: Leptin promotes muscle glycogen synthesis by inducing phosphorylation of GSK-3beta in C2C12 cell. Glycogen 35-43 glycogen synthase kinase 3 beta Mus musculus 85-94 24025512-13 2013 Meanwhile, GSK-3beta can also increase the phosphorylation of APPL1 at ser-401. Serine 71-74 glycogen synthase kinase 3 beta Mus musculus 11-20 23595215-8 2013 Furthermore, ischemic preconditioning (IPC, 4 cycles of 3.5 min of ischemia and 5 min of reperfusion) increased phosphorylation of ERK-1/2, GSK3beta, and STAT3 in all hearts without differences between groups (n = 5-6, p < 0.05), although Cx43 deficient mice were not protected by either IPC or pharmacological preconditioning with diazoxide. ipc 39-42 glycogen synthase kinase 3 beta Mus musculus 140-148 23661004-10 2013 APAP-treated PTP1B(-/-) hepatocytes showed enhanced antioxidant defense through the glycogen synthase kinase 3 (GSK3)beta/Src kinase family (SKF) axis, delaying tyrosine phosphorylation of the transcription factor nuclear factor-erythroid 2-related factor (Nrf2) and its nuclear exclusion, ubiquitination and degradation. 4-amino-N-acetyl-N-methylaniline 0-4 glycogen synthase kinase 3 beta Mus musculus 112-121 23661004-0 2013 Protein tyrosine phosphatase 1B modulates GSK3beta/Nrf2 and IGFIR signaling pathways in acetaminophen-induced hepatotoxicity. Acetaminophen 88-101 glycogen synthase kinase 3 beta Mus musculus 42-50 23410496-8 2013 In drd1a-EGFP transgenic mice, quinelorane activated Akt/GSK-3beta in both neurons expressing and lacking D1 receptor. quinelorane 31-42 glycogen synthase kinase 3 beta Mus musculus 57-66 23658842-5 2013 Odor stimulation, or blockade of peripheral olfactory inputs caused by either transgenic knock-out or ZnSO4 irrigation to the olfactory epithelium, all affected the expression level of GSK3beta in the OB. Zinc Sulfate 102-107 glycogen synthase kinase 3 beta Mus musculus 185-193 23239117-5 2013 Depletion of Akt1 and Akt2 resulted in a disconnection of APC/EB1 and a decrease in bone-resorbing activity along with reduced sealing zone formation, both of which were recovered upon the addition of LiCl, a glycogen synthase kinase-3beta (GSK-3beta) inhibitor. Lithium Chloride 201-205 glycogen synthase kinase 3 beta Mus musculus 241-250 23529610-6 2013 Knockdown of XBP1 or inositol requiring enzyme 1 alpha decreased endothelial cell proliferation via suppression of Akt/GSK3beta phosphorylation, beta-catenin nuclear translocation, and E2F2 expression. Inositol 21-29 glycogen synthase kinase 3 beta Mus musculus 119-127 23548624-2 2013 Recently, we demonstrated that factor-inhibiting hypoxia-inducible factor 1 (FIH-1) diminished glycogen stores in vitro and in vivo, working through the Akt/Glycogen Synthase Kinase (GSK)-3beta pathway. Glycogen 95-103 glycogen synthase kinase 3 beta Mus musculus 153-193 23630444-6 2013 RESULTS: Icaritin promoted osteogenic differentiation and maturation of MSCs as indicated by increased mRNA expression for Runx2, osteocalcin and BSP, and enhanced ALP activity and mineralization; Icaritin inhibited adipogenic differentiation, as indicated by decreased mRNA expression for PPARgamma, LPL, aP2, and suppressed formation of adipocyte-like cells; Icaritin inactivated GSK3beta and suppressed PPARgamma expression when promoting osteogenesis and suppressing adipogenesis of MSCs. icaritin 9-17 glycogen synthase kinase 3 beta Mus musculus 382-390 23630444-6 2013 RESULTS: Icaritin promoted osteogenic differentiation and maturation of MSCs as indicated by increased mRNA expression for Runx2, osteocalcin and BSP, and enhanced ALP activity and mineralization; Icaritin inhibited adipogenic differentiation, as indicated by decreased mRNA expression for PPARgamma, LPL, aP2, and suppressed formation of adipocyte-like cells; Icaritin inactivated GSK3beta and suppressed PPARgamma expression when promoting osteogenesis and suppressing adipogenesis of MSCs. icaritin 197-205 glycogen synthase kinase 3 beta Mus musculus 382-390 23630444-6 2013 RESULTS: Icaritin promoted osteogenic differentiation and maturation of MSCs as indicated by increased mRNA expression for Runx2, osteocalcin and BSP, and enhanced ALP activity and mineralization; Icaritin inhibited adipogenic differentiation, as indicated by decreased mRNA expression for PPARgamma, LPL, aP2, and suppressed formation of adipocyte-like cells; Icaritin inactivated GSK3beta and suppressed PPARgamma expression when promoting osteogenesis and suppressing adipogenesis of MSCs. icaritin 197-205 glycogen synthase kinase 3 beta Mus musculus 382-390 23630444-7 2013 CONCLUSION: This was the first study demonstrating that the novel semisynthetic molecule Icaritin could stimulate osteogenic differentiation and inhibit adipogenesis of MSCs, which was associated with the suppression of GSK3beta and PPARgamma. icaritin 89-97 glycogen synthase kinase 3 beta Mus musculus 220-228 23380502-7 2013 Furthermore, they responded to the D1/D2 agonist apomorphine with increased Akt and GSK3 phosphorylation. Apomorphine 49-60 glycogen synthase kinase 3 beta Mus musculus 84-88 23548624-11 2013 CONCLUSIONS: c-Kit signaling has been shown to affect glucose metabolism via the Akt/GSK-3beta pathway. Glucose 54-61 glycogen synthase kinase 3 beta Mus musculus 85-94 23324178-5 2013 High NaCl increases phosphorylation of GSK-3beta-S9, which inhibits GSK-3beta. Sodium Chloride 5-9 glycogen synthase kinase 3 beta Mus musculus 39-48 23369342-12 2013 6-Gingerol also inhibited differentiation in 3T3-L1 cells by attenuating the Akt/GSK3beta pathway. gingerol 0-10 glycogen synthase kinase 3 beta Mus musculus 81-89 23369342-10 2013 Meanwhile, 6-gingerol diminished the insulin-stimulated serine phosphorylation of Akt (Ser473) and GSK3beta (Ser9). gingerol 11-21 glycogen synthase kinase 3 beta Mus musculus 99-107 23593332-9 2013 Furthermore, GSK-3beta (Ser-9) phosphorylation increased in the DG of OBX mice possibly accounting for increased neurogenesis through Akt activation. Serine 24-27 glycogen synthase kinase 3 beta Mus musculus 13-22 23593332-11 2013 Overall, we conclude that sigma-1 receptor stimulation by DHEA ameliorates OBX-induced depressive-like behaviors by increasing neurogenesis in the DG through activation of the Akt/GSK-3beta/beta-catenin pathway. Dehydroepiandrosterone 58-62 glycogen synthase kinase 3 beta Mus musculus 180-189 23324178-0 2013 Inhibitory phosphorylation of GSK-3beta by AKT, PKA, and PI3K contributes to high NaCl-induced activation of the transcription factor NFAT5 (TonEBP/OREBP). Sodium Chloride 82-86 glycogen synthase kinase 3 beta Mus musculus 30-39 23324178-5 2013 High NaCl increases phosphorylation of GSK-3beta-S9, which inhibits GSK-3beta. Sodium Chloride 5-9 glycogen synthase kinase 3 beta Mus musculus 68-77 23324178-6 2013 In GSK-3beta-null mouse embryonic fibroblasts transfection of GSK-3beta, in which serine 9 is mutated to alanine, so that it cannot be inhibited by phosphorylation at that site, inhibits high NaCl-induced NFAT5 transcriptional activity more than transfection of wild-type GSK-3beta. Sodium Chloride 192-196 glycogen synthase kinase 3 beta Mus musculus 62-71 23324178-6 2013 In GSK-3beta-null mouse embryonic fibroblasts transfection of GSK-3beta, in which serine 9 is mutated to alanine, so that it cannot be inhibited by phosphorylation at that site, inhibits high NaCl-induced NFAT5 transcriptional activity more than transfection of wild-type GSK-3beta. Sodium Chloride 192-196 glycogen synthase kinase 3 beta Mus musculus 62-71 23324178-7 2013 High NaCl-induced phosphorylation of GSK-3beta-S9 depends on PKA, PI3K, and AKT, but not p38alpha. Sodium Chloride 5-9 glycogen synthase kinase 3 beta Mus musculus 37-46 23324178-10 2013 When activated by high NaCl, PKA, PI3K, and AKT1, but not p38alpha, increase phosphorylation of GSK-3beta-S9, which reduces the inhibitory effect of GSK-3beta on NFAT5, and thus contributes to activation of NFAT5. Sodium Chloride 23-27 glycogen synthase kinase 3 beta Mus musculus 96-105 23324178-10 2013 When activated by high NaCl, PKA, PI3K, and AKT1, but not p38alpha, increase phosphorylation of GSK-3beta-S9, which reduces the inhibitory effect of GSK-3beta on NFAT5, and thus contributes to activation of NFAT5. Sodium Chloride 23-27 glycogen synthase kinase 3 beta Mus musculus 149-158 23257288-8 2013 Unexpectedly, the decrease in the number of mature neurons and neuronal precursor cells of the subgranular zone of Tet/GSK3beta mice could not be reverted. tetramethylenedisulfotetramine 115-118 glycogen synthase kinase 3 beta Mus musculus 119-127 23478410-6 2013 Moreover, HSPC motility was regulated by norepinephrine and insulin-like growth factor-1 (IGF-1), which increased or reduced, respectively, GSK3beta expression in BM HSPCs and their subsequent egress. Norepinephrine 41-55 glycogen synthase kinase 3 beta Mus musculus 140-148 23021826-8 2013 In mice previously exposed to CMS, pre-injection of lentivirus-expressing GSK-3beta into the hippocampal dentate gyrus significantly decreased sucrose preferences in the sucrose intake test and increased immobility times in both forced swim and tail suspension tests. Sucrose 143-150 glycogen synthase kinase 3 beta Mus musculus 74-83 23393138-8 2013 When Wnt/beta-catenin signaling was reactivated by crossing with APC(min)(/+) mice or by treating with a GSK-3beta inhibitor, the number of Paneth cells was partially restored and the mortality caused by DSS-induced inflammatory bowel disease was strikingly reduced in Lgr4-deficient animals. Dextran Sulfate 204-207 glycogen synthase kinase 3 beta Mus musculus 105-114 23219964-0 2013 Involvement of GSK3 and PP2A in ginsenoside Rb1"s attenuation of aluminum-induced tau hyperphosphorylation. Aluminum 65-73 glycogen synthase kinase 3 beta Mus musculus 15-19 23021826-8 2013 In mice previously exposed to CMS, pre-injection of lentivirus-expressing GSK-3beta into the hippocampal dentate gyrus significantly decreased sucrose preferences in the sucrose intake test and increased immobility times in both forced swim and tail suspension tests. Sucrose 170-177 glycogen synthase kinase 3 beta Mus musculus 74-83 23021826-14 2013 Furthermore, chronic fluoxetine administration reversed these prodepressant-like effects and decreased neuronal apoptosis in the hippocampal DG in GSK-3beta-overexpressing mice. Fluoxetine 21-31 glycogen synthase kinase 3 beta Mus musculus 147-156 23138569-2 2013 The phosphorylation of beta-catenin by glycogen synthase kinase-3beta (GSK-3beta) at serine31/37/threonine41 regulates its stability and its role in canonical Wnt signaling. serine31 85-93 glycogen synthase kinase 3 beta Mus musculus 39-69 23266618-0 2013 Incorporation of beta-sitosterol into the membrane increases resistance to oxidative stress and lipid peroxidation via estrogen receptor-mediated PI3K/GSK3beta signaling. gamma-sitosterol 17-32 glycogen synthase kinase 3 beta Mus musculus 151-159 22950911-7 2013 Furthermore, quetiapine normalized the abnormal activity of glycogen synthase kinase-3beta (GSK-3beta), an AD-involved kinase, in the AD mice. Quetiapine Fumarate 13-23 glycogen synthase kinase 3 beta Mus musculus 60-90 22991247-8 2013 PGE2 treatment leads to activation of the Wnt/beta-catenin pathway by inactivation of glycogen synthase kinase 3beta of NKT cells. Dinoprostone 0-4 glycogen synthase kinase 3 beta Mus musculus 86-116 22903504-8 2013 Notably, LPS-induced ROS generation can partly facilitate p38 MAPK/JNK/AKT activation to regulate GSK-3beta-mediated Mcl-1 stability, apoptosis, and neutrophilia. ros 21-24 glycogen synthase kinase 3 beta Mus musculus 98-107 24356466-7 2013 METHODS: WT or IL-6(-/-)mice or cells were pretreated with SB216763, a GSK-3beta inhibitor, and survival of the mice was determined. SB 216763 59-67 glycogen synthase kinase 3 beta Mus musculus 71-80 23544329-6 2013 The activation of glycogen synthase kinase 3beta (GSK3beta) was associated with morphine tolerance, since an inhibitor of GSK3beta prevented it. Morphine 80-88 glycogen synthase kinase 3 beta Mus musculus 18-48 23544329-6 2013 The activation of glycogen synthase kinase 3beta (GSK3beta) was associated with morphine tolerance, since an inhibitor of GSK3beta prevented it. Morphine 80-88 glycogen synthase kinase 3 beta Mus musculus 50-58 23544329-6 2013 The activation of glycogen synthase kinase 3beta (GSK3beta) was associated with morphine tolerance, since an inhibitor of GSK3beta prevented it. Morphine 80-88 glycogen synthase kinase 3 beta Mus musculus 122-130 23313590-8 2013 Further study suggested that CA/CAPE showed protective effects against acrolein by modulating MAPKs and Akt/GSK3beta signaling pathways. caffeic acid phenethyl ester 32-36 glycogen synthase kinase 3 beta Mus musculus 108-116 23313590-8 2013 Further study suggested that CA/CAPE showed protective effects against acrolein by modulating MAPKs and Akt/GSK3beta signaling pathways. Acrolein 71-79 glycogen synthase kinase 3 beta Mus musculus 108-116 23283523-4 2013 HCA induces epithelial reversion at nanomolar concentrations by suppressing Snail via the nuclear translocalization of GSK-3beta, which results in the transcriptional upregulation of E-cadherin. hca 0-3 glycogen synthase kinase 3 beta Mus musculus 119-128 23099259-0 2013 Examination of methylphenidate-mediated behavior regulation by glycogen synthase kinase-3 in mice. Methylphenidate 15-30 glycogen synthase kinase 3 beta Mus musculus 63-89 23099259-2 2013 Amphetamine administration increases glycogen synthase kinase-3 (GSK3) activation, which is necessary for certain acute behavioral responses to amphetamine, including increased locomotor activity and impaired sensorimotor gating. Amphetamine 0-11 glycogen synthase kinase 3 beta Mus musculus 37-63 23099259-2 2013 Amphetamine administration increases glycogen synthase kinase-3 (GSK3) activation, which is necessary for certain acute behavioral responses to amphetamine, including increased locomotor activity and impaired sensorimotor gating. Amphetamine 0-11 glycogen synthase kinase 3 beta Mus musculus 65-69 23099259-2 2013 Amphetamine administration increases glycogen synthase kinase-3 (GSK3) activation, which is necessary for certain acute behavioral responses to amphetamine, including increased locomotor activity and impaired sensorimotor gating. Amphetamine 144-155 glycogen synthase kinase 3 beta Mus musculus 37-63 23099259-2 2013 Amphetamine administration increases glycogen synthase kinase-3 (GSK3) activation, which is necessary for certain acute behavioral responses to amphetamine, including increased locomotor activity and impaired sensorimotor gating. Amphetamine 144-155 glycogen synthase kinase 3 beta Mus musculus 65-69 23099259-3 2013 Here, we tested if modulating GSK3 by administration of the GSK3 inhibitor lithium or expression of constitutively active GSK3 altered behavioral responses to methylphenidate administered to mice acutely or daily for 8 days. Lithium 75-82 glycogen synthase kinase 3 beta Mus musculus 30-34 23099259-3 2013 Here, we tested if modulating GSK3 by administration of the GSK3 inhibitor lithium or expression of constitutively active GSK3 altered behavioral responses to methylphenidate administered to mice acutely or daily for 8 days. Lithium 75-82 glycogen synthase kinase 3 beta Mus musculus 60-64 23099259-3 2013 Here, we tested if modulating GSK3 by administration of the GSK3 inhibitor lithium or expression of constitutively active GSK3 altered behavioral responses to methylphenidate administered to mice acutely or daily for 8 days. Lithium 75-82 glycogen synthase kinase 3 beta Mus musculus 60-64 23099259-3 2013 Here, we tested if modulating GSK3 by administration of the GSK3 inhibitor lithium or expression of constitutively active GSK3 altered behavioral responses to methylphenidate administered to mice acutely or daily for 8 days. Methylphenidate 159-174 glycogen synthase kinase 3 beta Mus musculus 30-34 23099259-8 2013 In GSK3 knockin mice, expression of constitutively active GSK3beta, but not GSK3alpha, significantly increased locomotor hyperactivity after acute methylphenidate treatment, and significantly impaired PPI, preventing further methylphenidate-induced impairment of PPI that was evident in wild-type mice and GSK3alpha knockin mice. Methylphenidate 147-162 glycogen synthase kinase 3 beta Mus musculus 58-66 23099259-8 2013 In GSK3 knockin mice, expression of constitutively active GSK3beta, but not GSK3alpha, significantly increased locomotor hyperactivity after acute methylphenidate treatment, and significantly impaired PPI, preventing further methylphenidate-induced impairment of PPI that was evident in wild-type mice and GSK3alpha knockin mice. Methylphenidate 225-240 glycogen synthase kinase 3 beta Mus musculus 58-66 23138569-2 2013 The phosphorylation of beta-catenin by glycogen synthase kinase-3beta (GSK-3beta) at serine31/37/threonine41 regulates its stability and its role in canonical Wnt signaling. serine31 85-93 glycogen synthase kinase 3 beta Mus musculus 71-80 23138569-2 2013 The phosphorylation of beta-catenin by glycogen synthase kinase-3beta (GSK-3beta) at serine31/37/threonine41 regulates its stability and its role in canonical Wnt signaling. threonine41 97-108 glycogen synthase kinase 3 beta Mus musculus 39-69 23138569-2 2013 The phosphorylation of beta-catenin by glycogen synthase kinase-3beta (GSK-3beta) at serine31/37/threonine41 regulates its stability and its role in canonical Wnt signaling. threonine41 97-108 glycogen synthase kinase 3 beta Mus musculus 71-80 24080829-3 2013 Akt2 is a key protein in the phosphatidylinositide-3 (PI3K) / glycogen synthase 3 kinase (GSK3) signaling pathway, which in turn is involved in brain-derived neurotrophic factor (BDNF) effects on fear memory, mood stabilisation and action of several antidepressant drugs. phosphatidylinositide 29-50 glycogen synthase kinase 3 beta Mus musculus 90-94 23844319-0 2013 Antitumor Molecular Mechanism of Chlorogenic Acid on Inducting Genes GSK-3 beta and APC and Inhibiting Gene beta -Catenin. Chlorogenic Acid 33-49 glycogen synthase kinase 3 beta Mus musculus 69-79 23703152-5 2013 The tau phosphorylation correlated with activated GSK3, a prominent tau kinase normally kept inactive under the control of IIS. iis 123-126 glycogen synthase kinase 3 beta Mus musculus 50-54 22710914-2 2013 GSK3 phosphorylates tau in most serine and threonine residues hyperphosphorylated in paired helical filaments, and GSK3 activity contributes both to amyloid-beta production and amyloid-beta-mediated neuronal death. Serine 32-38 glycogen synthase kinase 3 beta Mus musculus 0-4 22710914-2 2013 GSK3 phosphorylates tau in most serine and threonine residues hyperphosphorylated in paired helical filaments, and GSK3 activity contributes both to amyloid-beta production and amyloid-beta-mediated neuronal death. Threonine 43-52 glycogen synthase kinase 3 beta Mus musculus 0-4 23844319-2 2013 Inhibiting gene beta -catenin and inducting genes GSK-3 beta and APC, promoting the tumor cell apoptosis in Wnt pathway, by chlorogenic acid were discussed (CGA). Chlorogenic Acid 124-140 glycogen synthase kinase 3 beta Mus musculus 50-60 23844319-9 2013 The results infer that the multimeric protein complex of beta -catenin could be increased by CGA upregulated genes GSK-3 beta and APC, which could inhibit the free beta -catenin into the nucleus to connect with TCF. tcf 211-214 glycogen synthase kinase 3 beta Mus musculus 115-125 23065380-11 2013 The activations of mitogen-activated protein kinase extracellular signal-regulated kinases, Akt, GSK3beta and STAT3 induced by PDGF-BB were also inhibited in sinomenine-treated VSMCs. sinomenine 158-168 glycogen synthase kinase 3 beta Mus musculus 97-105 23137781-11 2013 Interestingly, upon pharmacological p38MAPK inhibition (SB203580), GSK3beta inhibition loses its effect on MEF2 transcriptional activity suggesting potent cross-talk between the two pathways. SB 203580 56-64 glycogen synthase kinase 3 beta Mus musculus 67-75 23188702-3 2013 Absence of D2R signalling in the hippocampus leads to activation (dephosphorylation) of glycogen synthase kinase 3beta (GSK-3beta) after KA (20 mg/kg), which is not associated with a change in the phosphorylation of the GSK-3beta regulator Akt at the canonical threonine 308 residue. Threonine 261-270 glycogen synthase kinase 3 beta Mus musculus 88-118 23188702-3 2013 Absence of D2R signalling in the hippocampus leads to activation (dephosphorylation) of glycogen synthase kinase 3beta (GSK-3beta) after KA (20 mg/kg), which is not associated with a change in the phosphorylation of the GSK-3beta regulator Akt at the canonical threonine 308 residue. Threonine 261-270 glycogen synthase kinase 3 beta Mus musculus 120-129 24685987-6 2013 METHODS: UUO was induced in mice carrying a PKB/SGK-resistant GSK-3alpha/beta (gsk-3(KI)) and corresponding wild-type mice (gsk-3(WT)). uuo 9-12 glycogen synthase kinase 3 beta Mus musculus 79-84 24685987-6 2013 METHODS: UUO was induced in mice carrying a PKB/SGK-resistant GSK-3alpha/beta (gsk-3(KI)) and corresponding wild-type mice (gsk-3(WT)). uuo 9-12 glycogen synthase kinase 3 beta Mus musculus 124-129 22824191-8 2013 Interestingly, propranolol also phosphorylated Akt in SAMP8 mice, which was associated with an increase of glycogen synthase kinase-3beta phosphorylation, contributing therefore to the reductions in Tau hyperphosphorylation. Propranolol 15-26 glycogen synthase kinase 3 beta Mus musculus 107-137 22626981-6 2013 Moreover, huprine X and huperzine A activate protein kinase C/mitogen-activated protein kinase pathway signalling, alpha-secretases (ADAM 10 and TACE) and increase the fraction of phospho-glycogen synthase kinase 3-beta. huprine X 10-19 glycogen synthase kinase 3 beta Mus musculus 188-219 22626981-6 2013 Moreover, huprine X and huperzine A activate protein kinase C/mitogen-activated protein kinase pathway signalling, alpha-secretases (ADAM 10 and TACE) and increase the fraction of phospho-glycogen synthase kinase 3-beta. huperzine A 24-35 glycogen synthase kinase 3 beta Mus musculus 188-219 23262393-5 2013 Moreover, DFO intranasal administration also decreases Fe-induced the activities of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase 3beta (GSK3beta), which in turn suppressing tau phosphorylation. Deferoxamine 10-13 glycogen synthase kinase 3 beta Mus musculus 121-151 23262393-5 2013 Moreover, DFO intranasal administration also decreases Fe-induced the activities of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase 3beta (GSK3beta), which in turn suppressing tau phosphorylation. Iron 55-57 glycogen synthase kinase 3 beta Mus musculus 121-151 22796753-10 2013 CONCLUSION: Soluble Abeta(1-42) oligomers have long-lasting effects on tau phosphorylation in the rTg4510 model, possibly due to elevations in GSK3. rtg4510 98-105 glycogen synthase kinase 3 beta Mus musculus 143-147 23390559-3 2013 A recent study suggested that glycogen synthase kinase (GSK)-3 may underlie the rapid antidepressant action of ketamine, although the precise mechanisms are unclear. Ketamine 111-119 glycogen synthase kinase 3 beta Mus musculus 30-62 24349609-0 2013 Carbon monoxide attenuates dextran sulfate sodium-induced colitis via inhibition of GSK-3beta signaling. Carbon Monoxide 0-15 glycogen synthase kinase 3 beta Mus musculus 84-93 24349609-0 2013 Carbon monoxide attenuates dextran sulfate sodium-induced colitis via inhibition of GSK-3beta signaling. Dextran Sulfate 27-49 glycogen synthase kinase 3 beta Mus musculus 84-93 23393595-9 2013 The elevation of inhibitory glycogen synthase kinase 3beta Ser9 phosphorylation (pGSK3beta) was sustained until the neuronal differentiation stage at embryonic day 14.5, instead of pGSK3beta downregulation. pgsk3beta 81-90 glycogen synthase kinase 3 beta Mus musculus 28-58 23393595-9 2013 The elevation of inhibitory glycogen synthase kinase 3beta Ser9 phosphorylation (pGSK3beta) was sustained until the neuronal differentiation stage at embryonic day 14.5, instead of pGSK3beta downregulation. pgsk3beta 181-190 glycogen synthase kinase 3 beta Mus musculus 28-58 24454979-0 2013 Carbon monoxide protects against hepatic ischemia/reperfusion injury via ROS-dependent Akt signaling and inhibition of glycogen synthase kinase 3beta. Carbon Monoxide 0-15 glycogen synthase kinase 3 beta Mus musculus 119-149 24454979-7 2013 Furthermore, administration of LY294002, an inhibitor of PI3K, compromised the protective effect of CO and decreased the level of phospho-GSK3beta after I/R injury. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 31-39 glycogen synthase kinase 3 beta Mus musculus 138-146 23533594-6 2013 CONCLUSIONS: Our results provide the first evidences that Wnt1 plays an important role in CSCs" defenses against H2O2-induced apoptosis through the canonical Wnt1/GSK3beta/beta-catenin signaling pathway. Hydrogen Peroxide 113-117 glycogen synthase kinase 3 beta Mus musculus 163-171 23390559-4 2013 In this study, we examined the effects of ketamine and GSK-3 inhibitor SB216763 in the unpredictable, chronic mild stress (CMS) mouse model of mice. SB 216763 71-79 glycogen synthase kinase 3 beta Mus musculus 55-60 23390559-6 2013 Then, either vehicle, ketamine (10 mg/kg), or the established GSK-3 inhibitor, SB216763 (10 mg/kg), were administered into mice in the CMS group, while vehicle was administered to controls. SB 216763 79-87 glycogen synthase kinase 3 beta Mus musculus 62-67 23051669-0 2012 Lithium exacerbates hepatic ischemia/reperfusion injury by inhibiting GSK-3beta/NF-kappaB-mediated protective signaling in mice. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 70-79 23437106-8 2013 Basal (9)Ser-GSK3beta phosphorylation was increased by IR subjects serum with a smaller potentiating effect of insulin. Serine 9-12 glycogen synthase kinase 3 beta Mus musculus 13-21 23326414-0 2013 Control of Hes7 expression by Tbx6, the Wnt pathway and the chemical Gsk3 inhibitor LiCl in the mouse segmentation clock. Lithium Chloride 84-88 glycogen synthase kinase 3 beta Mus musculus 69-73 23051669-1 2012 Lithium (an inhibitor of GSK-3beta activity) has beneficial effects on ischemia/reperfusion (I/R) injury in the central nervous system, heart and kidney. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 25-34 23051669-4 2012 Previous studies showed that lithium chloride (LiCl) can phosphorylate residue Ser9, inhibit GSK-3beta activity, and improve I/R injury in other organs. Lithium Chloride 29-45 glycogen synthase kinase 3 beta Mus musculus 93-102 23051669-4 2012 Previous studies showed that lithium chloride (LiCl) can phosphorylate residue Ser9, inhibit GSK-3beta activity, and improve I/R injury in other organs. Lithium Chloride 47-51 glycogen synthase kinase 3 beta Mus musculus 93-102 23051669-5 2012 In the present study, mice were pretreated with either vehicle or LiCl, which had similar effects on GSK-3beta activity. Lithium Chloride 66-70 glycogen synthase kinase 3 beta Mus musculus 101-110 23051669-8 2012 To gain insight into the mechanism involved in this damage, the activity of nuclear factor-kappaB (NF-kappaB) (GSK-3beta can regulate the transcriptional complex of NF-kappaB) was analyzed, which revealed that LiCl treatment significantly down-regulated the activity of NF-kappaB. Lithium Chloride 210-214 glycogen synthase kinase 3 beta Mus musculus 111-120 23051669-11 2012 Taken together, these findings show that lithium exacerbates hepatic I/R injury by suppressing the expression of GSK-3beta/NF-kappaB-mediated protective genes. Lithium 41-48 glycogen synthase kinase 3 beta Mus musculus 113-122 23000630-0 2012 Glycogen synthase kinase 3-specific inhibitor AR-A014418 decreases neuropathic pain in mice: evidence for the mechanisms of action. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 46-56 glycogen synthase kinase 3 beta Mus musculus 0-26 22976998-4 2012 Gsk3beta specific inhibitor (SB216763) was used to activate Wnt/beta-catenin signaling. SB 216763 29-37 glycogen synthase kinase 3 beta Mus musculus 0-8 22986169-3 2012 We examined the hypothesis that rhythmic GSK3 activity is critical for robust circadian rhythmicity using GSK3alpha(21A/21A)/beta(9A/9A) knock-in mice with serine-alanine substitutions at the inhibitory phosphorylation sites, making both forms constitutively active. Serine 156-162 glycogen synthase kinase 3 beta Mus musculus 41-45 22986169-3 2012 We examined the hypothesis that rhythmic GSK3 activity is critical for robust circadian rhythmicity using GSK3alpha(21A/21A)/beta(9A/9A) knock-in mice with serine-alanine substitutions at the inhibitory phosphorylation sites, making both forms constitutively active. Alanine 163-170 glycogen synthase kinase 3 beta Mus musculus 41-45 22975730-0 2012 S632A3, a new glutarimide antibiotic, suppresses lipopolysaccharide-induced pro-inflammatory responses via inhibiting the activation of glycogen synthase kinase 3beta. glutarimide 14-25 glycogen synthase kinase 3 beta Mus musculus 136-166 23188793-0 2012 Deletion of GSK3beta in D2R-expressing neurons reveals distinct roles for beta-arrestin signaling in antipsychotic and lithium action. Lithium 119-126 glycogen synthase kinase 3 beta Mus musculus 12-20 23188793-2 2012 Recently it was demonstrated that GSK3beta through a beta-arrestin2/protein kinase B (PKB or Akt)/protein phosphatase 2A (PP2A) signaling complex regulates dopamine (DA)- and lithium-sensitive behaviors and is required to mediate endophenotypes of mania and depression in rodents. Dopamine 156-164 glycogen synthase kinase 3 beta Mus musculus 34-42 23188793-2 2012 Recently it was demonstrated that GSK3beta through a beta-arrestin2/protein kinase B (PKB or Akt)/protein phosphatase 2A (PP2A) signaling complex regulates dopamine (DA)- and lithium-sensitive behaviors and is required to mediate endophenotypes of mania and depression in rodents. Dopamine 166-168 glycogen synthase kinase 3 beta Mus musculus 34-42 23188793-2 2012 Recently it was demonstrated that GSK3beta through a beta-arrestin2/protein kinase B (PKB or Akt)/protein phosphatase 2A (PP2A) signaling complex regulates dopamine (DA)- and lithium-sensitive behaviors and is required to mediate endophenotypes of mania and depression in rodents. Lithium 175-182 glycogen synthase kinase 3 beta Mus musculus 34-42 23188793-4 2012 To elucidate the site of action of GSK3beta in regulating DA- or lithium-sensitive behaviors, we generated conditional knockouts of GSK3beta, where GSK3beta was deleted in either DA D1- or D2-receptor-expressing neurons. Lithium 65-72 glycogen synthase kinase 3 beta Mus musculus 35-43 23399843-5 2012 Furthermore, veratric acid facilitated the inactivation of glycogen synthase kinase-3beta (GSK-3beta), STAT-1, and STAT-3 in dose-dependent manner. veratric acid 13-26 glycogen synthase kinase 3 beta Mus musculus 59-89 23167932-5 2012 Inhibitory serine-phosphorylation of GSK3, particularly GSK3beta, was extremely high in the one-day postnatal mouse brain, and rapidly declined thereafter. Serine 11-17 glycogen synthase kinase 3 beta Mus musculus 37-41 23167932-5 2012 Inhibitory serine-phosphorylation of GSK3, particularly GSK3beta, was extremely high in the one-day postnatal mouse brain, and rapidly declined thereafter. Serine 11-17 glycogen synthase kinase 3 beta Mus musculus 56-64 23167932-7 2012 In contrast to the adult mouse brain, where administration of lithium or fluoxetine rapidly and robustly increased serine-phosphorylation of GSK3, in young mice these responses were blunted or absent. Lithium 62-69 glycogen synthase kinase 3 beta Mus musculus 141-145 23167932-7 2012 In contrast to the adult mouse brain, where administration of lithium or fluoxetine rapidly and robustly increased serine-phosphorylation of GSK3, in young mice these responses were blunted or absent. Fluoxetine 73-83 glycogen synthase kinase 3 beta Mus musculus 141-145 23167932-7 2012 In contrast to the adult mouse brain, where administration of lithium or fluoxetine rapidly and robustly increased serine-phosphorylation of GSK3, in young mice these responses were blunted or absent. Serine 115-121 glycogen synthase kinase 3 beta Mus musculus 141-145 23399843-5 2012 Furthermore, veratric acid facilitated the inactivation of glycogen synthase kinase-3beta (GSK-3beta), STAT-1, and STAT-3 in dose-dependent manner. veratric acid 13-26 glycogen synthase kinase 3 beta Mus musculus 91-100 22459600-6 2012 Glycogen synthase kinase (GSK)3, a major kinase involved in APP and tau phosphorylation, was significantly inhibited by BBR treatment. Berberine 120-123 glycogen synthase kinase 3 beta Mus musculus 0-31 22886144-9 2012 Treatment with a GSK3beta inhibitor attenuated Dex-induced inhibition of TCF/LEF-mediated transcriptional activity, but suppressed Dex-induced adipocyte differentiation, indicating that adipocyte differentiation and inhibition of Wnt/beta-catenin activity by Dex are mediated by GSK3beta activity. Dexamethasone 47-50 glycogen synthase kinase 3 beta Mus musculus 279-287 22886144-9 2012 Treatment with a GSK3beta inhibitor attenuated Dex-induced inhibition of TCF/LEF-mediated transcriptional activity, but suppressed Dex-induced adipocyte differentiation, indicating that adipocyte differentiation and inhibition of Wnt/beta-catenin activity by Dex are mediated by GSK3beta activity. Dexamethasone 131-134 glycogen synthase kinase 3 beta Mus musculus 17-25 22886144-9 2012 Treatment with a GSK3beta inhibitor attenuated Dex-induced inhibition of TCF/LEF-mediated transcriptional activity, but suppressed Dex-induced adipocyte differentiation, indicating that adipocyte differentiation and inhibition of Wnt/beta-catenin activity by Dex are mediated by GSK3beta activity. Dexamethasone 131-134 glycogen synthase kinase 3 beta Mus musculus 17-25 22886144-6 2012 Dex decreased phosphorylation of Ser9-GSK3beta and expression of active beta-catenin protein. Dexamethasone 0-3 glycogen synthase kinase 3 beta Mus musculus 38-46 22886144-9 2012 Treatment with a GSK3beta inhibitor attenuated Dex-induced inhibition of TCF/LEF-mediated transcriptional activity, but suppressed Dex-induced adipocyte differentiation, indicating that adipocyte differentiation and inhibition of Wnt/beta-catenin activity by Dex are mediated by GSK3beta activity. Dexamethasone 47-50 glycogen synthase kinase 3 beta Mus musculus 17-25 23443104-8 2012 The expression of certain potential target genes (Wnt1) was found to be reduced in P19 cells treated with PCBs, whereas the expression of other potential predicted target genes (GSK3beta) was increased. Polychlorinated Biphenyls 106-110 glycogen synthase kinase 3 beta Mus musculus 178-186 22785175-2 2012 As glycogen synthase kinase-3beta (GSK3beta) is an important cellular regulator of survival and proliferation, we determined its role during injury and recovery of proximal tubules in a mercuric chloride-induced nephrotoxic model of acute kidney injury. Chlorides 195-203 glycogen synthase kinase 3 beta Mus musculus 3-33 22922870-13 2012 Furthermore, the ERK1/2, p38 MAPK and Akt/GSK3beta signalling pathways were found to be involved in the effects of gastrodin. gastrodin 115-124 glycogen synthase kinase 3 beta Mus musculus 42-50 22785175-2 2012 As glycogen synthase kinase-3beta (GSK3beta) is an important cellular regulator of survival and proliferation, we determined its role during injury and recovery of proximal tubules in a mercuric chloride-induced nephrotoxic model of acute kidney injury. Chlorides 195-203 glycogen synthase kinase 3 beta Mus musculus 35-43 22785175-3 2012 Renal proximal tubule-specific GSK3beta knockout mice exposed to mercuric chloride had improved survival and renal function compared to wild-type mice. Mercuric Chloride 65-82 glycogen synthase kinase 3 beta Mus musculus 31-39 22785175-6 2012 This enhanced repair, evidenced by increased Ki-67 and BRDU staining, along with increased cyclin D1 and c-myc levels, was recapitulated by treatment of wild-type mice with the small-molecule GSK3 inhibitor TDZD-8 following injury. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 207-213 glycogen synthase kinase 3 beta Mus musculus 192-196 22847803-2 2012 Inhibition of glycogen synthase kinase 3beta (GSK3beta) in innate cells leads to suppression of Toll-like receptor (TLR)-initiated proinflammatory cytokines under nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) p65 transcriptional control and promotion of cyclic adenosine monophosphate response element-binding (CREB)-dependent gene activation. Cyclic AMP 283-313 glycogen synthase kinase 3 beta Mus musculus 14-44 22847803-2 2012 Inhibition of glycogen synthase kinase 3beta (GSK3beta) in innate cells leads to suppression of Toll-like receptor (TLR)-initiated proinflammatory cytokines under nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) p65 transcriptional control and promotion of cyclic adenosine monophosphate response element-binding (CREB)-dependent gene activation. Cyclic AMP 283-313 glycogen synthase kinase 3 beta Mus musculus 46-54 22847803-3 2012 Therefore, we hypothesized that the cell permeable GSK3-specific inhibitor, SB216763, would protect against alveolar bone loss induced by the key periodontal pathogen, Porphyromonas gingivalis (P. gingivalis), in a murine model. SB 216763 76-84 glycogen synthase kinase 3 beta Mus musculus 51-55 22936801-10 2012 Taken together, these results suggest that ASPP 049 from C. comosa induced osteoblastic cell proliferation and differentiation through ERalpha-, Akt-, and GSK-3beta-dependent activation of beta-catenin signaling. aspp 43-47 glycogen synthase kinase 3 beta Mus musculus 155-164 22588329-7 2012 Meanwhile, pretreatment with propofol inhibited LPS-induced augmentation of toll-like receptor 4 (TLR4) expression at both mRNA and protein levels and further upregulated LPS-induced inactivation of glycogen synthase kinase-3beta (GSK-3beta) in BV-2 microglia cells. Propofol 29-37 glycogen synthase kinase 3 beta Mus musculus 199-229 22936801-0 2012 A phytoestrogen diarylheptanoid mediates estrogen receptor/Akt/glycogen synthase kinase 3beta protein-dependent activation of the Wnt/beta-catenin signaling pathway. Diarylheptanoids 16-31 glycogen synthase kinase 3 beta Mus musculus 63-93 22936801-7 2012 In addition, ASPP 049 induced phosphorylations at serine 473 of Akt and serine 9 of GSK-3beta. aspp 13-17 glycogen synthase kinase 3 beta Mus musculus 84-93 22936801-7 2012 In addition, ASPP 049 induced phosphorylations at serine 473 of Akt and serine 9 of GSK-3beta. Serine 72-78 glycogen synthase kinase 3 beta Mus musculus 84-93 22884995-10 2012 Moreover, there was a marked induction of AKT, GSK-3beta, beta-catenin, and carcinogenic markers in tumor tissues formed in mice after injection with cadmium-stimulated cells. Cadmium 150-157 glycogen synthase kinase 3 beta Mus musculus 47-56 22849606-0 2012 Hypothalamic glycogen synthase kinase 3beta has a central role in the regulation of food intake and glucose metabolism. Glucose 100-107 glycogen synthase kinase 3 beta Mus musculus 13-43 22849606-2 2012 In the present study, we provide the first evidence of increased hypothalamic signalling via GSK3beta in leptin-deficient Lep(ob/ob) mice and show that intracerebroventricular injection of a GSK3beta inhibitor acutely improves glucose tolerance in these mice. Glucose 227-234 glycogen synthase kinase 3 beta Mus musculus 191-199 22849606-5 2012 These results demonstrate that increased hypothalamic GSK3beta signalling contributes to deleterious effects of leptin deficiency and exacerbates high-fat diet-induced weight gain and glucose intolerance. Glucose 184-191 glycogen synthase kinase 3 beta Mus musculus 54-62 22749848-0 2012 Glycogen synthase kinase-3beta regulates anti-inflammatory property of fluoxetine. Fluoxetine 71-81 glycogen synthase kinase 3 beta Mus musculus 0-30 23035082-6 2012 At the molecular level, GLP-1(9-36)(amide) reduced elevated levels of mitochondrial-derived reactive oxygen species and restored dysregulated Akt-glycogen synthase kinase-3beta signaling in the hippocampus of APP/PS1 mice. Amides 36-41 glycogen synthase kinase 3 beta Mus musculus 146-176 22749848-7 2012 Upon LPS stimulation, fluoxetine caused a delay but increased in the phosphorylated levels of GSK-3beta (ser9), whereas it did not affect LPS-induced activation of mitogen-activated protein kinase (MAPK) and generation of reactive oxygen species (ROS). Fluoxetine 22-32 glycogen synthase kinase 3 beta Mus musculus 94-103 22749848-3 2012 How fluoxetine interferes with inflammation via a GSK-3beta-dependent pathway remains unclear. Fluoxetine 4-14 glycogen synthase kinase 3 beta Mus musculus 50-59 22588329-7 2012 Meanwhile, pretreatment with propofol inhibited LPS-induced augmentation of toll-like receptor 4 (TLR4) expression at both mRNA and protein levels and further upregulated LPS-induced inactivation of glycogen synthase kinase-3beta (GSK-3beta) in BV-2 microglia cells. Propofol 29-37 glycogen synthase kinase 3 beta Mus musculus 231-240 22749848-10 2012 GSK-3beta knockdown blocked the inhibitory effects of fluoxetine on LPS-induced iNOS/NO release and COX-2/PGE2 production. Fluoxetine 54-64 glycogen synthase kinase 3 beta Mus musculus 0-9 22714712-0 2012 Flurbiprofen, a cyclooxygenase inhibitor, protects mice from hepatic ischemia/reperfusion injury by inhibiting GSK-3beta signaling and mitochondrial permeability transition. Flurbiprofen 0-12 glycogen synthase kinase 3 beta Mus musculus 111-120 22749848-10 2012 GSK-3beta knockdown blocked the inhibitory effects of fluoxetine on LPS-induced iNOS/NO release and COX-2/PGE2 production. Dinoprostone 106-110 glycogen synthase kinase 3 beta Mus musculus 0-9 22749848-11 2012 These results indicated that GSK-3beta regulated anti-inflammatory property of fluoxetine. Fluoxetine 79-89 glycogen synthase kinase 3 beta Mus musculus 29-38 22773863-0 2012 Inhibiting glycogen synthase kinase-3 decreases 12-O-tetradecanoylphorbol-13-acetate-induced interferon-gamma-mediated skin inflammation. Tetradecanoylphorbol Acetate 48-84 glycogen synthase kinase 3 beta Mus musculus 11-37 22773863-2 2012 Because IFN-gamma is involved in inflammatory skin diseases, such as psoriasis, the aim of this study was to investigate the pathogenic role of GSK-3 in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced IFN-gamma-mediated ear skin inflammation. Tetradecanoylphorbol Acetate 153-189 glycogen synthase kinase 3 beta Mus musculus 144-149 22773863-2 2012 Because IFN-gamma is involved in inflammatory skin diseases, such as psoriasis, the aim of this study was to investigate the pathogenic role of GSK-3 in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced IFN-gamma-mediated ear skin inflammation. Tetradecanoylphorbol Acetate 191-194 glycogen synthase kinase 3 beta Mus musculus 144-149 22773863-4 2012 TPA/IFN-gamma induced GSK-3 activation, which in turn activated signal transducer and activator of transcription 1. Tetradecanoylphorbol Acetate 0-3 glycogen synthase kinase 3 beta Mus musculus 22-27 22773863-5 2012 Inhibiting GSK-3 pharmacologically, by administering 6-bromoindirubin-3"-oxime (1.5 mug per ear), and genetically, with lentiviral-based short-hairpin RNA, reduced TPA-induced acute skin inflammation but not T-cell infiltration. 6-bromoindirubin-3'-oxime 53-78 glycogen synthase kinase 3 beta Mus musculus 11-16 22773863-5 2012 Inhibiting GSK-3 pharmacologically, by administering 6-bromoindirubin-3"-oxime (1.5 mug per ear), and genetically, with lentiviral-based short-hairpin RNA, reduced TPA-induced acute skin inflammation but not T-cell infiltration. Tetradecanoylphorbol Acetate 164-167 glycogen synthase kinase 3 beta Mus musculus 11-16 22773863-6 2012 It is noteworthy that inhibiting GSK-3 decreased TPA-induced IFN-gamma production and the nuclear translocation of T-box transcription factor Tbx21, a transcription factor of IFN-gamma, in CD3-positive T cells. Tetradecanoylphorbol Acetate 49-52 glycogen synthase kinase 3 beta Mus musculus 33-38 22773863-7 2012 In chronic TPA-induced skin inflammation, inhibiting GSK-3 attenuated epidermis hyperproliferation and dermis angiogenesis. Tetradecanoylphorbol Acetate 11-14 glycogen synthase kinase 3 beta Mus musculus 53-58 22773863-8 2012 These results demonstrate the dual role of GSK-3 in TPA-induced skin inflammation that is not only to facilitate IFN-gamma signaling but also to regulate IFN-gamma production. Tetradecanoylphorbol Acetate 52-55 glycogen synthase kinase 3 beta Mus musculus 43-48 22484461-4 2012 Lithium chloride (LiCl), a GSK-3beta inhibitor, increased GSK-3beta phosphorylation in MC3T3-E1 and MG-63 cells. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 27-36 22484461-4 2012 Lithium chloride (LiCl), a GSK-3beta inhibitor, increased GSK-3beta phosphorylation in MC3T3-E1 and MG-63 cells. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 58-67 22484461-4 2012 Lithium chloride (LiCl), a GSK-3beta inhibitor, increased GSK-3beta phosphorylation in MC3T3-E1 and MG-63 cells. Lithium Chloride 18-22 glycogen synthase kinase 3 beta Mus musculus 27-36 22484461-4 2012 Lithium chloride (LiCl), a GSK-3beta inhibitor, increased GSK-3beta phosphorylation in MC3T3-E1 and MG-63 cells. Lithium Chloride 18-22 glycogen synthase kinase 3 beta Mus musculus 58-67 22484461-8 2012 A PKR inhibitor, 2-aminopurine, also induced GSK-3beta phosphorylation in MC3T3-E1 and MG-63 cells. 2-Aminopurine 17-30 glycogen synthase kinase 3 beta Mus musculus 45-54 22714712-6 2012 Mechanistic studies revealed that flurbiprofen markedly inhibited glycogen synthase kinase (GSK)-3beta activity and increased phosphorylation of GSK-3beta at Ser9, which, consequently, could modulate the adenine nucleotide translocase (ANT)-cyclophilin D (CyP-D) complex and the susceptibility to MPT induction. Flurbiprofen 34-46 glycogen synthase kinase 3 beta Mus musculus 145-154 22714712-7 2012 Therefore, administration of flurbiprofen prior to hepatic I/R ameliorates mitochondrial and hepatocellular damage through inhibition of MPT and inactivation of GSK-3beta, and provides experimental evidence for clinical use of flurbiprofen to protect liver function in surgical settings in addition to its conventional use for pain relief. Flurbiprofen 29-41 glycogen synthase kinase 3 beta Mus musculus 161-170 22714712-7 2012 Therefore, administration of flurbiprofen prior to hepatic I/R ameliorates mitochondrial and hepatocellular damage through inhibition of MPT and inactivation of GSK-3beta, and provides experimental evidence for clinical use of flurbiprofen to protect liver function in surgical settings in addition to its conventional use for pain relief. Flurbiprofen 227-239 glycogen synthase kinase 3 beta Mus musculus 161-170 22581840-0 2012 Chemopreventive sphingadienes downregulate Wnt signaling via a PP2A/Akt/GSK3beta pathway in colon cancer. sphingadienes 16-29 glycogen synthase kinase 3 beta Mus musculus 72-80 22825337-0 2012 Perifosine enhances mTORC1-targeted cancer therapy by activation of GSK3beta in NSCLC cells. perifosine 0-10 glycogen synthase kinase 3 beta Mus musculus 68-76 22825337-5 2012 Moreover, we show that perifosine, as an Akt inhibitor, decreases rapamycin-induced phosphorylation of GSK3beta and elevated p-GSK3beta levels in rapamycin-resistant cell lines. perifosine 23-33 glycogen synthase kinase 3 beta Mus musculus 103-111 22825337-5 2012 Moreover, we show that perifosine, as an Akt inhibitor, decreases rapamycin-induced phosphorylation of GSK3beta and elevated p-GSK3beta levels in rapamycin-resistant cell lines. perifosine 23-33 glycogen synthase kinase 3 beta Mus musculus 127-135 22825337-5 2012 Moreover, we show that perifosine, as an Akt inhibitor, decreases rapamycin-induced phosphorylation of GSK3beta and elevated p-GSK3beta levels in rapamycin-resistant cell lines. Sirolimus 66-75 glycogen synthase kinase 3 beta Mus musculus 103-111 22825337-5 2012 Moreover, we show that perifosine, as an Akt inhibitor, decreases rapamycin-induced phosphorylation of GSK3beta and elevated p-GSK3beta levels in rapamycin-resistant cell lines. Sirolimus 66-75 glycogen synthase kinase 3 beta Mus musculus 127-135 22825337-8 2012 However, inhibition of GSK3beta by a selective inhibitor- LiCl, or downregulation of GSK3beta expression by siRNA, reverses the growth inhibitory effects of perifosine on rapamycin resistant cells, suggesting the important role of GSK3beta activation in enhancing mTORC1 inhibitors efficacy by perifosine. perifosine 157-167 glycogen synthase kinase 3 beta Mus musculus 23-31 22825337-8 2012 However, inhibition of GSK3beta by a selective inhibitor- LiCl, or downregulation of GSK3beta expression by siRNA, reverses the growth inhibitory effects of perifosine on rapamycin resistant cells, suggesting the important role of GSK3beta activation in enhancing mTORC1 inhibitors efficacy by perifosine. perifosine 157-167 glycogen synthase kinase 3 beta Mus musculus 85-93 22825337-8 2012 However, inhibition of GSK3beta by a selective inhibitor- LiCl, or downregulation of GSK3beta expression by siRNA, reverses the growth inhibitory effects of perifosine on rapamycin resistant cells, suggesting the important role of GSK3beta activation in enhancing mTORC1 inhibitors efficacy by perifosine. perifosine 157-167 glycogen synthase kinase 3 beta Mus musculus 85-93 22631612-8 2012 The reduction of beta-gamma bursts by amyloid beta is blocked by inhibiting GSK-3 either with lithium or with SB 216763. Lithium 94-101 glycogen synthase kinase 3 beta Mus musculus 76-81 22631612-8 2012 The reduction of beta-gamma bursts by amyloid beta is blocked by inhibiting GSK-3 either with lithium or with SB 216763. SB 216763 110-119 glycogen synthase kinase 3 beta Mus musculus 76-81 22826345-0 2012 Selective deletion of forebrain glycogen synthase kinase 3beta reveals a central role in serotonin-sensitive anxiety and social behaviour. Serotonin 89-98 glycogen synthase kinase 3 beta Mus musculus 32-62 22581840-11 2012 Our cumulative findings indicate that SDs inhibit Wnt signaling through a protein phosphatase 2A/Akt/GSK3beta-dependent mechanism that may contribute to their chemopreventive effects in intestinal tumorigenesis. sds 38-41 glycogen synthase kinase 3 beta Mus musculus 101-109 22581840-6 2012 Further, we observed a decrease in phosphorylated (inactive) GSK3beta in SD-treated mice and colon cancer cells. SD 0006 73-75 glycogen synthase kinase 3 beta Mus musculus 61-69 22581840-7 2012 Expression of constitutively active myristoylated-Akt or inactivation of GSK3beta using LiCl attenuated SD-mediated inhibition of Wnt transcriptional activity and active-beta-catenin levels. Lithium Chloride 88-92 glycogen synthase kinase 3 beta Mus musculus 73-81 22581840-7 2012 Expression of constitutively active myristoylated-Akt or inactivation of GSK3beta using LiCl attenuated SD-mediated inhibition of Wnt transcriptional activity and active-beta-catenin levels. SD 0006 104-106 glycogen synthase kinase 3 beta Mus musculus 73-81 22751928-3 2012 Here, two-dimensional (2D) gel electrophoresis and site-directed mutagenesis allowed us to identify two serines of Nrf2 that are phosphorylated by glycogen synthase kinase 3beta (GSK-3beta) in the sequence DSGISL. Serine 104-111 glycogen synthase kinase 3 beta Mus musculus 147-177 22897579-3 2012 In this study, we showed that high-fat diet (HFD) feeding significantly increased incidence of UD in wild type (WT) C57BL/6 mice, as did lithium-mediated inhibition of GSK3-beta, which is a key negative regulator of IRS1. Lithium 137-144 glycogen synthase kinase 3 beta Mus musculus 168-177 22583494-4 2012 Lithium is known to be neuroprotective in various models of neurodegenerative disease, and can reduce Abeta generation by modulating glycogen synthase kinase-3 (GSK-3) activity. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 133-159 22583494-4 2012 Lithium is known to be neuroprotective in various models of neurodegenerative disease, and can reduce Abeta generation by modulating glycogen synthase kinase-3 (GSK-3) activity. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 161-166 22583494-4 2012 Lithium is known to be neuroprotective in various models of neurodegenerative disease, and can reduce Abeta generation by modulating glycogen synthase kinase-3 (GSK-3) activity. UNII-042A8N37WH 102-107 glycogen synthase kinase 3 beta Mus musculus 133-159 22583494-4 2012 Lithium is known to be neuroprotective in various models of neurodegenerative disease, and can reduce Abeta generation by modulating glycogen synthase kinase-3 (GSK-3) activity. UNII-042A8N37WH 102-107 glycogen synthase kinase 3 beta Mus musculus 161-166 22751928-3 2012 Here, two-dimensional (2D) gel electrophoresis and site-directed mutagenesis allowed us to identify two serines of Nrf2 that are phosphorylated by glycogen synthase kinase 3beta (GSK-3beta) in the sequence DSGISL. Serine 104-111 glycogen synthase kinase 3 beta Mus musculus 179-188 22751928-6 2012 Intraperitoneal injection of the GSK-3 inhibitor SB216763 led to increased Nrf2 and heme oxygenase-1 levels in liver and hippocampus. SB 216763 49-57 glycogen synthase kinase 3 beta Mus musculus 33-38 22751928-7 2012 Moreover, mice with hippocampal absence of GSK-3beta exhibited increased levels of Nrf2 and phase 2 gene products, reduced glutathione, and decreased levels of carbonylated proteins and malondialdehyde. Glutathione 123-134 glycogen synthase kinase 3 beta Mus musculus 43-52 22751928-7 2012 Moreover, mice with hippocampal absence of GSK-3beta exhibited increased levels of Nrf2 and phase 2 gene products, reduced glutathione, and decreased levels of carbonylated proteins and malondialdehyde. Malondialdehyde 186-201 glycogen synthase kinase 3 beta Mus musculus 43-52 22814108-3 2012 Lithium, a known unspecific GSK3 inhibitor protects against experimental autoimmune encephalomyelitis. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 28-32 22339667-9 2012 The induced activation of GSK3 and p53, via the inhibition of proteins responsible for their inactivation (PKA via H-89 and SIRT-1 via nicotinamide, respectively), blocked the insulin"s effect on the epiblast.From our findings, we conclude that insulin increases epiblast cell number via the activation of PI3K, which ultimately inactivates GSK3 and p53. Niacinamide 135-147 glycogen synthase kinase 3 beta Mus musculus 26-30 22761446-6 2012 Among several phosphorylation residues in RelA, Thr-254 was identified as the critical phosphorylation site for GSK-3 that modulated chondrocyte differentiation. Threonine 48-51 glycogen synthase kinase 3 beta Mus musculus 112-117 22761446-7 2012 In conclusion, redundant functions of GSK-3alpha and GSK-3beta through phosphorylation of RelA at Thr-254 play a crucial role in early stages of chondrocyte differentiation. Threonine 98-101 glycogen synthase kinase 3 beta Mus musculus 53-62 22420773-9 2012 PGE2 also inactivated GSK-3beta and stimulated active-beta-catenin. Dinoprostone 0-4 glycogen synthase kinase 3 beta Mus musculus 22-31 22683604-8 2012 Treatment of differentiated 3T3-L1 adipocytes with glycogen synthase kinase-3beta (GSK-3beta) inhibitor, LiCl, led to 1.9-fold increase in NQO1 protein. Lithium Chloride 105-109 glycogen synthase kinase 3 beta Mus musculus 51-81 22683604-8 2012 Treatment of differentiated 3T3-L1 adipocytes with glycogen synthase kinase-3beta (GSK-3beta) inhibitor, LiCl, led to 1.9-fold increase in NQO1 protein. Lithium Chloride 105-109 glycogen synthase kinase 3 beta Mus musculus 83-92 22422579-5 2012 Cilostazol significantly increased the levels of GSK-3beta phosphorylation at Ser9 and beta-catenin phosphorylation at Ser675 in the cytosol and nucleus. Cilostazol 0-10 glycogen synthase kinase 3 beta Mus musculus 49-58 22422579-7 2012 Likewise, Abeta-stimulated GSK-3beta phosphorylation at Tyr 216 was decreased by cilostazol in the control but not in the CK2alpha siRNA-transfected cells. Tyrosine 56-59 glycogen synthase kinase 3 beta Mus musculus 27-36 22422579-7 2012 Likewise, Abeta-stimulated GSK-3beta phosphorylation at Tyr 216 was decreased by cilostazol in the control but not in the CK2alpha siRNA-transfected cells. Cilostazol 81-91 glycogen synthase kinase 3 beta Mus musculus 27-36 22422579-9 2012 In conclusion, increased cAMP-dependent protein kinase-linked CK2alpha activation underlies the pharmacological effects of cilostazol in downregulating p53 phosphorylation at Ser15 and upregulating GSK-3beta phosphorylation at Ser9/beta-catenin phosphorylation at Ser675, thereby suppressing Abeta(1-40)-induced neurotoxicity and improving neurite elongation. Cyclic AMP 25-29 glycogen synthase kinase 3 beta Mus musculus 198-207 22422579-9 2012 In conclusion, increased cAMP-dependent protein kinase-linked CK2alpha activation underlies the pharmacological effects of cilostazol in downregulating p53 phosphorylation at Ser15 and upregulating GSK-3beta phosphorylation at Ser9/beta-catenin phosphorylation at Ser675, thereby suppressing Abeta(1-40)-induced neurotoxicity and improving neurite elongation. Cilostazol 123-133 glycogen synthase kinase 3 beta Mus musculus 198-207 22580404-3 2012 In the present study, we showed that treatment with SB216763, a highly specific GSK-3beta inhibitor, resulted in a dose-dependent decrease in the mRNA and protein expression of CD40, as well as production of pro-inflammatory cytokines IL-6, TNF-alpha and IL-1beta, in the Porphyromonas gingivalis-lipopolysaccharide (LPS)-stimulated murine osteoblastic-like MC3T3-E1 cells. SB 216763 52-60 glycogen synthase kinase 3 beta Mus musculus 80-89 22580404-3 2012 In the present study, we showed that treatment with SB216763, a highly specific GSK-3beta inhibitor, resulted in a dose-dependent decrease in the mRNA and protein expression of CD40, as well as production of pro-inflammatory cytokines IL-6, TNF-alpha and IL-1beta, in the Porphyromonas gingivalis-lipopolysaccharide (LPS)-stimulated murine osteoblastic-like MC3T3-E1 cells. gingivalis-lipopolysaccharide 286-315 glycogen synthase kinase 3 beta Mus musculus 80-89 22580404-3 2012 In the present study, we showed that treatment with SB216763, a highly specific GSK-3beta inhibitor, resulted in a dose-dependent decrease in the mRNA and protein expression of CD40, as well as production of pro-inflammatory cytokines IL-6, TNF-alpha and IL-1beta, in the Porphyromonas gingivalis-lipopolysaccharide (LPS)-stimulated murine osteoblastic-like MC3T3-E1 cells. lps 317-320 glycogen synthase kinase 3 beta Mus musculus 80-89 22580404-4 2012 Furthermore, inhibition of GSK-3beta remarkably represses the LPS-induced activation of the nuclear factor kappa B (NF-kappaB) signaling pathway by suppressing IkappaBalpha phosphorylation, NF-kappaBp65 nuclear translocation, and NF-kappaBp65 DNA binding activity. lps 62-65 glycogen synthase kinase 3 beta Mus musculus 27-36 22580404-6 2012 The negative regulation effect of GSK-3beta inhibitor on CD40 expression is mediated through beta-catenin, for siRNA of beta-catenin attenuated the GSK-3beta inhibitor-induced repression of NF-kappaB activation and, consequently, the expression of CD40 and production of pro-inflammatory cytokines in LPS-stimulated MC3T3-E1 cells. lps 301-304 glycogen synthase kinase 3 beta Mus musculus 34-43 22580404-6 2012 The negative regulation effect of GSK-3beta inhibitor on CD40 expression is mediated through beta-catenin, for siRNA of beta-catenin attenuated the GSK-3beta inhibitor-induced repression of NF-kappaB activation and, consequently, the expression of CD40 and production of pro-inflammatory cytokines in LPS-stimulated MC3T3-E1 cells. lps 301-304 glycogen synthase kinase 3 beta Mus musculus 148-157 22580404-7 2012 Thus our results elucidate the molecular mechanisms whereby GSK-3beta inhibitor prevents the LPS-induced CD40 expression on osteoblasts and provide supportive evidence of the potential role of GSK-3beta inhibitors in suppressing the immune function of osteoblasts in inflammatory bone diseases. lps 93-96 glycogen synthase kinase 3 beta Mus musculus 60-69 22580404-7 2012 Thus our results elucidate the molecular mechanisms whereby GSK-3beta inhibitor prevents the LPS-induced CD40 expression on osteoblasts and provide supportive evidence of the potential role of GSK-3beta inhibitors in suppressing the immune function of osteoblasts in inflammatory bone diseases. lps 93-96 glycogen synthase kinase 3 beta Mus musculus 193-202 22000581-4 2012 Western blotting assay revealed that Akt-mediated glucose metabolism signaling was down-regulated in the diabetic testis and was further decreased in diabetic mice with Zn deficiency, reflected by reduced phosphorylation of both Akt and GSK-3beta and increased phosphorylation of glycogen synthase along with a disarrangement of fatty acid metabolism (increased expression of PPAR-alpha and decreased adenosine-monophosphate-activated protein kinase phosphorylation). Glucose 50-57 glycogen synthase kinase 3 beta Mus musculus 237-246 22674573-5 2012 Binding of E-LPs to the low density lipoprotein receptor-related protein 1 recruited the N-methyl-d-aspartate receptor, blocked intracellular Ca(2+) elevation, and inactivated glycogen synthase kinase 3beta, thereby inhibiting apoptosis. e-lps 11-16 glycogen synthase kinase 3 beta Mus musculus 176-206 22420773-0 2012 Prostaglandin E2 maintains mouse ESC undifferentiated state through regulation of connexin31, connexin43 and connexin45 expression: involvement of glycogen synthase kinase 3beta/beta-catenin. Dinoprostone 0-16 glycogen synthase kinase 3 beta Mus musculus 147-177 22420773-12 2012 CONCLUSIONS: PGE2 stimulates Cx isoforms via GSK-3beta/beta-catenin via EP2-receptor-dependent cAMP/PKA and PI3K/Akt in mouse ESCs, thereby partially contributing to the maintenance of their undifferentiated state. Dinoprostone 13-17 glycogen synthase kinase 3 beta Mus musculus 45-54 22420773-12 2012 CONCLUSIONS: PGE2 stimulates Cx isoforms via GSK-3beta/beta-catenin via EP2-receptor-dependent cAMP/PKA and PI3K/Akt in mouse ESCs, thereby partially contributing to the maintenance of their undifferentiated state. Cyclic AMP 95-99 glycogen synthase kinase 3 beta Mus musculus 45-54 22434044-1 2012 Acute amphetamine administration activates glycogen synthase kinase-3 (GSK3) by reducing its inhibitory serine-phosphorylation in mouse striatum and cerebral cortex. Amphetamine 6-17 glycogen synthase kinase 3 beta Mus musculus 43-69 22672803-0 2012 Design, synthesis and biological evaluation of novel imidazopyridines as potential antidiabetic GSK3beta inhibitors. imidazopyridine 53-69 glycogen synthase kinase 3 beta Mus musculus 96-104 22672803-1 2012 Design, synthesis and biological evaluation of the imidazopyridine analogs as novel GSK3beta inhibitors for treatment of type 2 diabetes mellitus are described. imidazopyridine 51-66 glycogen synthase kinase 3 beta Mus musculus 84-92 22672803-3 2012 The structure-activity relationship (SAR) of the imidazopyridine analogs and the binding mode of analog 23 in the catalytic domain of GSK3beta, based on our X-ray crystallography study, are described. imidazopyridine 49-64 glycogen synthase kinase 3 beta Mus musculus 134-142 22434044-1 2012 Acute amphetamine administration activates glycogen synthase kinase-3 (GSK3) by reducing its inhibitory serine-phosphorylation in mouse striatum and cerebral cortex. Amphetamine 6-17 glycogen synthase kinase 3 beta Mus musculus 71-75 22434044-1 2012 Acute amphetamine administration activates glycogen synthase kinase-3 (GSK3) by reducing its inhibitory serine-phosphorylation in mouse striatum and cerebral cortex. Serine 104-110 glycogen synthase kinase 3 beta Mus musculus 43-69 22434044-1 2012 Acute amphetamine administration activates glycogen synthase kinase-3 (GSK3) by reducing its inhibitory serine-phosphorylation in mouse striatum and cerebral cortex. Serine 104-110 glycogen synthase kinase 3 beta Mus musculus 71-75 22434044-3 2012 Here we tested if regulation of Akt and GSK3 was similarly affected by longer-term administration of amphetamine, as well as of methylphenidate, since each of these is administered chronically in patients with attention deficit hyperactivity disorder (ADHD). Amphetamine 101-112 glycogen synthase kinase 3 beta Mus musculus 40-44 22434044-5 2012 After eight days of amphetamine or methylphenidate treatment, striatal Akt and GSK3 were dephosphorylated similar to reported changes after acute amphetamine treatment. Amphetamine 20-31 glycogen synthase kinase 3 beta Mus musculus 79-83 22434044-5 2012 After eight days of amphetamine or methylphenidate treatment, striatal Akt and GSK3 were dephosphorylated similar to reported changes after acute amphetamine treatment. Methylphenidate 35-50 glycogen synthase kinase 3 beta Mus musculus 79-83 22434044-5 2012 After eight days of amphetamine or methylphenidate treatment, striatal Akt and GSK3 were dephosphorylated similar to reported changes after acute amphetamine treatment. Amphetamine 146-157 glycogen synthase kinase 3 beta Mus musculus 79-83 22434044-6 2012 Oppositely, in the cerebral cortex and hippocampus Akt and GSK3 phosphorylation increased after eight days of amphetamine or methylphenidate treatment. Amphetamine 110-121 glycogen synthase kinase 3 beta Mus musculus 59-63 22434044-6 2012 Oppositely, in the cerebral cortex and hippocampus Akt and GSK3 phosphorylation increased after eight days of amphetamine or methylphenidate treatment. Methylphenidate 125-140 glycogen synthase kinase 3 beta Mus musculus 59-63 22434044-7 2012 These opposite brain region changes in Akt and GSK3 phosphorylation matched opposite changes in the association of Akt with beta-arrestin and GSK3, which after eight days of amphetamine treatment were increased in the striatum and decreased in the cerebral cortex. Amphetamine 174-185 glycogen synthase kinase 3 beta Mus musculus 47-51 22434044-7 2012 These opposite brain region changes in Akt and GSK3 phosphorylation matched opposite changes in the association of Akt with beta-arrestin and GSK3, which after eight days of amphetamine treatment were increased in the striatum and decreased in the cerebral cortex. Amphetamine 174-185 glycogen synthase kinase 3 beta Mus musculus 142-146 22434044-8 2012 Thus, whereas the acute dephosphorylating effect of stimulants on Akt and GSK3 in the striatum was maintained, the response switched in the cerebral cortex after eight days of amphetamine or methylphenidate treatment to cause increased phosphorylation of Akt and GSK3. Amphetamine 176-187 glycogen synthase kinase 3 beta Mus musculus 263-267 22434044-8 2012 Thus, whereas the acute dephosphorylating effect of stimulants on Akt and GSK3 in the striatum was maintained, the response switched in the cerebral cortex after eight days of amphetamine or methylphenidate treatment to cause increased phosphorylation of Akt and GSK3. Methylphenidate 191-206 glycogen synthase kinase 3 beta Mus musculus 74-78 22434044-8 2012 Thus, whereas the acute dephosphorylating effect of stimulants on Akt and GSK3 in the striatum was maintained, the response switched in the cerebral cortex after eight days of amphetamine or methylphenidate treatment to cause increased phosphorylation of Akt and GSK3. Methylphenidate 191-206 glycogen synthase kinase 3 beta Mus musculus 263-267 22459179-6 2012 The phosphorylation of Akt and glycogen synthase kinase-3beta (GSK-3beta) was significantly increased in mice treated with ethanol (5 g/kg bw), while the protein levels of PI3K-p85 were significantly reduced. Ethanol 123-130 glycogen synthase kinase 3 beta Mus musculus 31-61 22459179-6 2012 The phosphorylation of Akt and glycogen synthase kinase-3beta (GSK-3beta) was significantly increased in mice treated with ethanol (5 g/kg bw), while the protein levels of PI3K-p85 were significantly reduced. Ethanol 123-130 glycogen synthase kinase 3 beta Mus musculus 63-72 22547702-4 2012 Mechanistic data indicate that ROS deficiency in both cells and mice results in decreased production of IL-10 in response to treatment with LPS, at least in part, through attenuation of the Akt-GSK3-beta signal pathway and that it can be reversed by the administration of rIL-10. Reactive Oxygen Species 31-34 glycogen synthase kinase 3 beta Mus musculus 194-203 22484506-14 2012 Besides, pressure overload-induced increase of alpha-SMA and phosphorylation of ERK, AKT and GSK3beta were significantly reduced by chronic oral treatment with KS370G. ks370 160-165 glycogen synthase kinase 3 beta Mus musculus 93-101 22649795-0 2012 Inhibition of GSK3 attenuates amphetamine-induced hyperactivity and sensitization in the mouse. Amphetamine 30-41 glycogen synthase kinase 3 beta Mus musculus 14-18 22536778-0 2012 Nicotinic acid hydroxamate downregulated the melanin synthesis and tyrosinase activity through activating the MEK/ERK and AKT/GSK3beta signaling pathways. nicotinohydroxamic acid 0-26 glycogen synthase kinase 3 beta Mus musculus 126-134 22447251-4 2012 Western blotting revealed that SNX-2112 lead to the degradation of Hsp90 client proteins including Akt, IKKalpha, NF-kappaB, B-Raf and GSK3beta. SNX 2112 31-39 glycogen synthase kinase 3 beta Mus musculus 159-167 22649795-1 2012 Glycogen synthase kinase 3 (GSK3) is implicated in mediating dopamine-dependent behaviors. Dopamine 61-69 glycogen synthase kinase 3 beta Mus musculus 0-26 22536778-0 2012 Nicotinic acid hydroxamate downregulated the melanin synthesis and tyrosinase activity through activating the MEK/ERK and AKT/GSK3beta signaling pathways. Melanins 45-52 glycogen synthase kinase 3 beta Mus musculus 126-134 22649795-1 2012 Glycogen synthase kinase 3 (GSK3) is implicated in mediating dopamine-dependent behaviors. Dopamine 61-69 glycogen synthase kinase 3 beta Mus musculus 28-32 22536778-4 2012 NAH-mediated increases in the phosphorylation of mitogen-activated protein kinase kinase (MEK)/ERK and AKT/glycogen synthase kinase-3beta (GSK3beta) were also found, which in turn led to the inhibition of MITF expression and then downregulated tyrosinase and tyrosinase-related protein (TRP)-1 expressions. Niacin 0-3 glycogen synthase kinase 3 beta Mus musculus 139-147 22649795-2 2012 Previous studies have demonstrated the ability of amphetamine, which increases extracellular dopamine levels and influences behavior, to regulate the activity of GSK3. Amphetamine 50-61 glycogen synthase kinase 3 beta Mus musculus 162-166 22649795-2 2012 Previous studies have demonstrated the ability of amphetamine, which increases extracellular dopamine levels and influences behavior, to regulate the activity of GSK3. Dopamine 93-101 glycogen synthase kinase 3 beta Mus musculus 162-166 22649795-3 2012 This study used valproic acid and the selective GSK3 inhibitor, SB 216763, to examine the role of GSK3 in amphetamine-induced hyperactivity and the development of sensitized stereotypic behavior. SB 216763 64-73 glycogen synthase kinase 3 beta Mus musculus 48-52 22649795-12 2012 These data support a role for GSK3 in acute amphetamine-induced hyperactivity and the development of sensitization to amphetamine-induced stereotypy. Amphetamine 118-129 glycogen synthase kinase 3 beta Mus musculus 30-34 22649795-3 2012 This study used valproic acid and the selective GSK3 inhibitor, SB 216763, to examine the role of GSK3 in amphetamine-induced hyperactivity and the development of sensitized stereotypic behavior. Amphetamine 106-117 glycogen synthase kinase 3 beta Mus musculus 98-102 22649795-11 2012 Analysis of the levels of phospho-GSK3alpha and beta by immunoblot indicated that valproate increased phosphorylation of ser21-GSK3alpha in the frontal cortex, as well as ser9-GSK3beta in the frontal cortex and caudate putamen of amphetamine-injected mice. Valproic Acid 82-91 glycogen synthase kinase 3 beta Mus musculus 176-184 22649795-12 2012 These data support a role for GSK3 in acute amphetamine-induced hyperactivity and the development of sensitization to amphetamine-induced stereotypy. Amphetamine 44-55 glycogen synthase kinase 3 beta Mus musculus 30-34 22037925-0 2012 Involvement of PI3K, GSK-3beta and PPARgamma in the antidepressant-like effect of folic acid in the forced swimming test in mice. Folic Acid 82-92 glycogen synthase kinase 3 beta Mus musculus 21-30 22356228-5 2012 In addition, both K(v)7 channel openers dose-dependently increased phospho-serine-9 levels of GSK3beta in the prefrontal cortex and hippocampus, a common molecular mechanism shared by anti-manic drugs. Serine 75-81 glycogen synthase kinase 3 beta Mus musculus 94-102 22127439-10 2012 GTP also increases the expression of three genes involved in myogenesis, Pp3ca, Gsk3b, and Pax7. Guanosine Triphosphate 0-3 glycogen synthase kinase 3 beta Mus musculus 80-85 22037925-10 2012 These results indicate that the antidepressant-like effect of folic acid in the FST might be dependent on inhibition of GSK-3beta and activation of PPARgamma, reinforcing the notion that these are important targets for antidepressant activity. Folic Acid 62-72 glycogen synthase kinase 3 beta Mus musculus 120-129 22539723-2 2012 We found that glycogen synthase kinase-3 (GSK3), when deinhibited by default in cells deprived of growth factors, activates acetyltransferase TIP60 through phosphorylating TIP60-Ser(86), which directly acetylates and stimulates the protein kinase ULK1, which is required for autophagy. Serine 178-181 glycogen synthase kinase 3 beta Mus musculus 14-40 22539723-2 2012 We found that glycogen synthase kinase-3 (GSK3), when deinhibited by default in cells deprived of growth factors, activates acetyltransferase TIP60 through phosphorylating TIP60-Ser(86), which directly acetylates and stimulates the protein kinase ULK1, which is required for autophagy. Serine 178-181 glycogen synthase kinase 3 beta Mus musculus 42-46 22524197-8 2012 In vitro data revealed that the ALDH2 activator Alda-1 and glycogen synthase kinase-3beta inhibition protected against high glucose-induced mitochondrial and mechanical anomalies, the effect of which was cancelled by mitochondrial uncoupling. Glucose 124-131 glycogen synthase kinase 3 beta Mus musculus 48-89 22471389-8 2012 Interestingly, CAF diminished the insulin-stimulated serine phosphorylation of Akt (Ser473) and GSK3beta (Ser9), which may reduce glucose uptake in response to insulin and lipid accumulation. cafestol palmitate 15-18 glycogen synthase kinase 3 beta Mus musculus 96-104 22524197-7 2012 Intriguingly, ALDH2 attenuated or ablated streptozotocin-induced echocardiographic, mitochondrial, apoptotic and myocardial contractile and intracellular Ca2+ anomalies as well as changes in the phosphorylation of Akt, glycogen synthase kinase-3beta, Foxo3a and phosphatase and tensin homologue on chromosome ten, despite persistent hyperglycemia and a low respiratory exchange ratio. Streptozocin 42-56 glycogen synthase kinase 3 beta Mus musculus 219-249 22471389-8 2012 Interestingly, CAF diminished the insulin-stimulated serine phosphorylation of Akt (Ser473) and GSK3beta (Ser9), which may reduce glucose uptake in response to insulin and lipid accumulation. Glucose 130-137 glycogen synthase kinase 3 beta Mus musculus 96-104 22471389-12 2012 The anti-adipogenic activity of CAF was mediated by the inhibition of Akt activation and GSK3beta phosphorylation, which induced the down-regulation of lipid accumulation and lipid metabolizing genes, ultimately inhibiting adipocyte differentiation. cafestol palmitate 32-35 glycogen synthase kinase 3 beta Mus musculus 89-97 21978520-5 2012 Noticeably, FoxO3a formed a protein complex with GSK3beta in the cerebral cortex, and the interaction between the two proteins was stronger in IES-treated mice. indoleacetic acid 143-146 glycogen synthase kinase 3 beta Mus musculus 49-57 21978520-6 2012 Inhibition of glycogen synthase kinase-3 was able to abolish IES-induced LH behavior, disrupt IES-induced GSK3beta-FoxO3a interaction, and reduce nuclear FoxO3a accumulation. indoleacetic acid 94-97 glycogen synthase kinase 3 beta Mus musculus 106-114 21978520-9 2012 CONCLUSIONS: FoxO3a is activated in response to IES by interacting with GSK3beta, and inhibition of GSK3beta or reducing FoxO3a expression promotes resistance to stress-induced behavioral disturbance by disrupting this signaling mechanism. indoleacetic acid 48-51 glycogen synthase kinase 3 beta Mus musculus 72-80 22442497-10 2012 The GSK3beta inhibitor SB216763 ablated cold stress-induced cardiac contractile (but not remodeling) changes and ET-1-induced TRPV1 downregulation. SB 216763 23-31 glycogen synthase kinase 3 beta Mus musculus 4-12 22249311-5 2012 The Gsk3beta inhibitor, 1-azakenpaullone (1-AKP), was administered to c-Kit(Wv/+) and c-Kit(+/+) mice for 2 weeks, whereby alterations in glucose metabolism were examined and morphometric analyses were performed. kenpaullone 24-40 glycogen synthase kinase 3 beta Mus musculus 4-12 22249311-10 2012 Inhibition of Gsk3beta could prevent the onset of diabetes by improving glucose tolerance and beta-cell function. Glucose 72-79 glycogen synthase kinase 3 beta Mus musculus 14-22 22355115-1 2012 Glycogen synthase kinase 3beta (GSK3beta) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or anti-inflammatory agents. Lithium Chloride 85-101 glycogen synthase kinase 3 beta Mus musculus 0-30 22218715-8 2012 While the inactivation of Akt by LY294002 suppressed TLR2-mediated MCP-1 induction, the inactivation of GSK3beta by LiCl potentiated TLR2-mediated MCP-1 induction. Lithium Chloride 116-120 glycogen synthase kinase 3 beta Mus musculus 104-112 22258319-2 2012 In mice with DCLF-induced nephrotoxicity, TDZD-8, a selective glycogen synthase kinase (GSK)3beta inhibitor, improved acute kidney dysfunction and ameliorated tubular necrosis and apoptosis associated with induced cortical expression of cyclooxygenase-2 (COX-2) and prostaglandin E2. Diclofenac 13-17 glycogen synthase kinase 3 beta Mus musculus 88-97 22258319-2 2012 In mice with DCLF-induced nephrotoxicity, TDZD-8, a selective glycogen synthase kinase (GSK)3beta inhibitor, improved acute kidney dysfunction and ameliorated tubular necrosis and apoptosis associated with induced cortical expression of cyclooxygenase-2 (COX-2) and prostaglandin E2. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 42-48 glycogen synthase kinase 3 beta Mus musculus 88-97 22258319-6 2012 DCLF elicited oxidative stress, enhanced the activity of the redox-sensitive GSK3beta, and promoted a mitochondrial permeability transition by interacting with cyclophilin D, a key component of the mitochondrial permeability transition pore. Diclofenac 0-4 glycogen synthase kinase 3 beta Mus musculus 77-85 22258319-8 2012 Conversely, ectopic expression of a constitutively active GSK3beta abolished the effects of TDZD-8. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 92-98 glycogen synthase kinase 3 beta Mus musculus 58-66 22355115-1 2012 Glycogen synthase kinase 3beta (GSK3beta) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or anti-inflammatory agents. Lithium Chloride 85-101 glycogen synthase kinase 3 beta Mus musculus 32-40 22355115-8 2012 Taken together, our findings open perspectives in the treatment of nerve demyelination by administering GSK3beta inhibitors such as lithium. Lithium 132-139 glycogen synthase kinase 3 beta Mus musculus 104-112 21960132-11 2012 The protective capacity of GSK-3beta suppression was observed in WT mice by inhibiting it with the specific inhibitor SB216763. SB 216763 118-126 glycogen synthase kinase 3 beta Mus musculus 27-36 21546125-5 2012 Interestingly, sildenafil also phosphorylated Akt, which was associated with an increase of glycogen synthase kinase-3beta phosphorylation, providing a plausible explanation for the reductions in tau hyperphosphorylation (AT8 and PHF-1 epitopes) and attenuation of cognitive deficits shown by 9-month-old SAMP8 mice. Sildenafil Citrate 15-25 glycogen synthase kinase 3 beta Mus musculus 92-122 22266363-8 2012 Moreover, hesperetin stimulated the activation of mitogen-activated protein kinases (MAPKs), phosphorylation of cAMP-responsive element binding protein (CREB) and glycogen synthase kinase-3beta (GSK3beta), and subsequently induced the accumulation of beta-catenin. hesperetin 10-20 glycogen synthase kinase 3 beta Mus musculus 163-193 22266363-8 2012 Moreover, hesperetin stimulated the activation of mitogen-activated protein kinases (MAPKs), phosphorylation of cAMP-responsive element binding protein (CREB) and glycogen synthase kinase-3beta (GSK3beta), and subsequently induced the accumulation of beta-catenin. hesperetin 10-20 glycogen synthase kinase 3 beta Mus musculus 195-203 21315744-5 2012 In naive mice, we assessed METH-induced conditioned place preference (CPP), dopamine (DA) D2 receptor density and the basal and METH-induced activity of DISC1 partners, AKT and GSK-3beta in the ventral striatum. Methamphetamine 128-132 glycogen synthase kinase 3 beta Mus musculus 177-186 21315744-6 2012 In ED-treated mice, 4 weeks after METH treatment, we evaluated fear conditioning, depression-like responses in forced swim test, and the basal and METH-induced activity of AKT and GSK-3beta in the ventral striatum. Methamphetamine 147-151 glycogen synthase kinase 3 beta Mus musculus 180-189 21315744-7 2012 We found impairment in METH-induced CPP, decreased DA D2 receptor density and altered METH-induced phosphorylation of AKT and GSK-3beta in naive DISC1 female mice. Methamphetamine 86-90 glycogen synthase kinase 3 beta Mus musculus 126-135 21376063-5 2012 The purpose of the present study was to assess whether rolipram (PDE4 inhibitor) might synergize with TDZD-8 (GSK-3 blocker) to produce antipsychotic effects at low doses on the DISC1-L100P genetic model. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 102-108 glycogen synthase kinase 3 beta Mus musculus 110-115 21376063-7 2012 We have suggested that rolipram-induced increase of cAMP level might influence GSK-3 function and, hence the efficacy of TDZD-8. Rolipram 23-31 glycogen synthase kinase 3 beta Mus musculus 79-84 21376063-7 2012 We have suggested that rolipram-induced increase of cAMP level might influence GSK-3 function and, hence the efficacy of TDZD-8. Cyclic AMP 52-56 glycogen synthase kinase 3 beta Mus musculus 79-84 21376063-8 2012 Our second goal was to estimate how DISC1-Q31L with reduced PDE4B activity, and therefore mimicking rolipram-induced conditions, could alter pharmacological response to TDZD-8, GSK-3 activity and its interaction with DISC1. Rolipram 100-108 glycogen synthase kinase 3 beta Mus musculus 177-182 21960132-12 2012 Overall, our findings demonstrate that the TLR-2/GSK-3beta and TLR-9 signalling pathways play a central role in the development of intestinal mucositis and we suggest a new therapeutic strategy for limiting doxorubicin-induced intestinal inflammation. Doxorubicin 207-218 glycogen synthase kinase 3 beta Mus musculus 49-58 22048960-3 2012 Since FMRP is known to play an important role in adult hippocampal neurogenesis and hippocampus-dependent learning and FMRP regulates the adult neural stem cell fate through the translational regulation of glycogen synthase kinase 3beta (GSK3beta), we investigated the effects of a GSK3beta inhibitor, SB216763, on Fmr1 knockout mice (Fmr1 KO). SB 216763 302-310 glycogen synthase kinase 3 beta Mus musculus 238-246 22207510-10 2012 Furthermore, PHA-543613 treatment increased p-Akt and decreased p-GSK-3beta and CC3 expressions in the ipsilateral hemisphere (P<0.05, respectively), which was reversed by MLA and wortmannin. methyllycaconitine 175-178 glycogen synthase kinase 3 beta Mus musculus 66-75 22207510-10 2012 Furthermore, PHA-543613 treatment increased p-Akt and decreased p-GSK-3beta and CC3 expressions in the ipsilateral hemisphere (P<0.05, respectively), which was reversed by MLA and wortmannin. Wortmannin 183-193 glycogen synthase kinase 3 beta Mus musculus 66-75 22261023-0 2012 Quinolone derivatives containing strained spirocycle as orally active glycogen synthase kinase 3beta (GSK-3beta) inhibitors for type 2 diabetics. Quinolones 0-9 glycogen synthase kinase 3 beta Mus musculus 70-100 22261023-0 2012 Quinolone derivatives containing strained spirocycle as orally active glycogen synthase kinase 3beta (GSK-3beta) inhibitors for type 2 diabetics. Quinolones 0-9 glycogen synthase kinase 3 beta Mus musculus 102-111 22261023-0 2012 Quinolone derivatives containing strained spirocycle as orally active glycogen synthase kinase 3beta (GSK-3beta) inhibitors for type 2 diabetics. spirocycle 42-52 glycogen synthase kinase 3 beta Mus musculus 70-100 22261023-0 2012 Quinolone derivatives containing strained spirocycle as orally active glycogen synthase kinase 3beta (GSK-3beta) inhibitors for type 2 diabetics. spirocycle 42-52 glycogen synthase kinase 3 beta Mus musculus 102-111 22261023-1 2012 The design, synthesis, and evaluation of 6-6-7 tricyclic quinolones containing the strained spirocycle moiety aiming at the GSK-3beta inhibitor were described. 6-6-7 tricyclic quinolones 41-67 glycogen synthase kinase 3 beta Mus musculus 124-133 22261023-2 2012 Among the synthesized compounds, 44, having a cyclobutane ring on a spirocycle, showed excellent GSK-3beta inhibitory activity in both cell-free and cell-based assays (IC(50) = 36nM, EC(50) = 3.2muM, respectively). Cyclobutanes 46-57 glycogen synthase kinase 3 beta Mus musculus 97-106 21952928-0 2012 The phosphatidyl inositol 3 kinase-glycogen synthase kinase 3beta pathway mediates bilobalide-induced reduction in amyloid beta-peptide. bilobalide 83-93 glycogen synthase kinase 3 beta Mus musculus 35-65 21952928-7 2012 Similarly, inhibition of GSK3beta did not affect BACE-1 activity but decreased cathepsin B activity, suggesting that the PI3K-GSK3beta pathway was probably involved in BB-induced Abeta reduction. bilobalide 168-170 glycogen synthase kinase 3 beta Mus musculus 25-33 21952928-5 2012 Additionally, glycogen synthase kinase 3beta (GSK3beta) signaling might be involved in BB-induced Abeta reduction as a downstream target of the activated PI3K pathway. bilobalide 87-89 glycogen synthase kinase 3 beta Mus musculus 14-44 21952928-5 2012 Additionally, glycogen synthase kinase 3beta (GSK3beta) signaling might be involved in BB-induced Abeta reduction as a downstream target of the activated PI3K pathway. bilobalide 87-89 glycogen synthase kinase 3 beta Mus musculus 46-54 22236144-8 2012 CR counteracted age-related changes in p70S6K, increased Akt levels, and reduced p38-MAPK (albeit increasing preischemic phosphorylation), and paradoxically reduced postischemic GSK3beta phosphorylation. Chromium 0-2 glycogen synthase kinase 3 beta Mus musculus 178-186 22158133-2 2012 The mood stabilizer, lithium, is an inhibitor of glycogen synthase kinase-3beta (GSK-3beta), which is a modulator of the circadian clock system. Lithium 21-28 glycogen synthase kinase 3 beta Mus musculus 49-79 22238425-2 2012 By patch-clamping the inner membrane of murine cardiac mitochondria, we found that inhibition of GSK3beta activated mitoK(ATP). Adenosine Triphosphate 122-125 glycogen synthase kinase 3 beta Mus musculus 97-105 22158133-2 2012 The mood stabilizer, lithium, is an inhibitor of glycogen synthase kinase-3beta (GSK-3beta), which is a modulator of the circadian clock system. Lithium 21-28 glycogen synthase kinase 3 beta Mus musculus 81-90 22158133-4 2012 CR stress elevated GSK-3beta phosphorylation and blunted the rhythmic expression of PERIOD2 (PER2) in the brain. Chromium 0-2 glycogen synthase kinase 3 beta Mus musculus 19-28 22158133-5 2012 Moreover, lithium, when administered to the stress-imposed mice, reduced GSK-3beta phosphorylation and restored PER2 expression in the suprachiasmatic nucleus in a nighttime-specific manner. Lithium 10-17 glycogen synthase kinase 3 beta Mus musculus 73-82 22158133-6 2012 These data suggest that CR stress altered the circadian behavioral rhythm through a change in circadian gene expression of PER2 and GSK-3beta phosphorylation in the suprachiasmatic nucleus. Chromium 24-26 glycogen synthase kinase 3 beta Mus musculus 132-141 22155090-5 2012 We also identified GSK3, MMPs and PKC pathways as potential targets to prevent CsA damage. Cyclosporine 79-82 glycogen synthase kinase 3 beta Mus musculus 19-23 21895523-10 2012 Lithium robustly increased serine phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), suggesting that the underlying mechanisms responsible for lithium"s protective effects are triggered by increasing phosphorylation of this kinase and thereby inhibiting its activity. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 53-83 21895523-10 2012 Lithium robustly increased serine phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), suggesting that the underlying mechanisms responsible for lithium"s protective effects are triggered by increasing phosphorylation of this kinase and thereby inhibiting its activity. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 85-94 21895523-10 2012 Lithium robustly increased serine phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), suggesting that the underlying mechanisms responsible for lithium"s protective effects are triggered by increasing phosphorylation of this kinase and thereby inhibiting its activity. Serine 27-33 glycogen synthase kinase 3 beta Mus musculus 53-83 21895523-10 2012 Lithium robustly increased serine phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), suggesting that the underlying mechanisms responsible for lithium"s protective effects are triggered by increasing phosphorylation of this kinase and thereby inhibiting its activity. Serine 27-33 glycogen synthase kinase 3 beta Mus musculus 85-94 21895523-10 2012 Lithium robustly increased serine phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), suggesting that the underlying mechanisms responsible for lithium"s protective effects are triggered by increasing phosphorylation of this kinase and thereby inhibiting its activity. Lithium 155-162 glycogen synthase kinase 3 beta Mus musculus 53-83 21895523-10 2012 Lithium robustly increased serine phosphorylation of glycogen synthase kinase-3beta (GSK-3beta), suggesting that the underlying mechanisms responsible for lithium"s protective effects are triggered by increasing phosphorylation of this kinase and thereby inhibiting its activity. Lithium 155-162 glycogen synthase kinase 3 beta Mus musculus 85-94 22348181-0 2012 Identification of a Maleimide-Based Glycogen Synthase Kinase-3 (GSK-3) Inhibitor, BIP-135, that Prolongs the Median Survival Time of Delta7 SMA KO Mouse Model of Spinal Muscular Atrophy. maleimide 20-29 glycogen synthase kinase 3 beta Mus musculus 36-62 22348181-0 2012 Identification of a Maleimide-Based Glycogen Synthase Kinase-3 (GSK-3) Inhibitor, BIP-135, that Prolongs the Median Survival Time of Delta7 SMA KO Mouse Model of Spinal Muscular Atrophy. maleimide 20-29 glycogen synthase kinase 3 beta Mus musculus 64-69 21881002-7 2012 In these cells, lithium application reduced AQP2 abundance, which coincided with Gsk3beta inactivation and increased COX-2 expression. Lithium 16-23 glycogen synthase kinase 3 beta Mus musculus 81-89 22451318-3 2012 However, ACEA reduces the cytotoxic effect of Abeta42 oligomers in primary cultures of cortical neurons, and reverses Abeta-induced dephosphorylation of glycogen synthase kinase-3beta (GSK3beta) in vitro and in vivo. arachidonyl-2-chloroethylamide 9-13 glycogen synthase kinase 3 beta Mus musculus 153-183 22419037-3 2012 We find that the basally-induced decrease in this phosphoprotein is the result of recruitment of the striatal dopamine D2 pathway, as evidenced by enhanced levels of D2 receptor (D2R) mRNA expression and D2R function as examined using the D2R antagonist, eticlopride, as well as alterations in the phosphorylation status of several downstream molecular targets of D2R"s, including CREB, DARPP-32, Akt and GSK3beta. Dopamine 110-118 glycogen synthase kinase 3 beta Mus musculus 405-413 22298956-3 2012 In this study, we revealed that 6-bromoindirubin 3"-oxime (BIO), a specific GSK-3beta inhibitor, promoted N2A cells-derived neurons to become tumor-like neuroblasts. 6-bromoindirubin-3'-oxime 32-57 glycogen synthase kinase 3 beta Mus musculus 76-85 22233765-6 2012 Additionally, the expressions of cyclin-dependent kinase and glycogen synthase kinase 3beta, the most important kinases involved in tau phosphorylation, were markedly decreased by L-NBP treatment. l-nbp 180-185 glycogen synthase kinase 3 beta Mus musculus 61-91 21998135-3 2012 A subset of mice from each group was supplemented with sodium valproate (625 mg/kg), a compound with GSK3 inhibitory activity. Valproic Acid 55-71 glycogen synthase kinase 3 beta Mus musculus 101-105 21998135-7 2012 Valproate supplementation blocked GSK3beta activation and attenuated the development of atherosclerosis and the accumulation of hepatic lipids in each of the models examined. Valproic Acid 0-9 glycogen synthase kinase 3 beta Mus musculus 34-42 21998135-8 2012 The mechanism by which GSK3beta activity is regulated in these models likely involves alterations in phosphorylation at serine 9 and tyrosine 216. Serine 120-126 glycogen synthase kinase 3 beta Mus musculus 23-31 21998135-8 2012 The mechanism by which GSK3beta activity is regulated in these models likely involves alterations in phosphorylation at serine 9 and tyrosine 216. Tyrosine 133-141 glycogen synthase kinase 3 beta Mus musculus 23-31 21964322-7 2012 Treatment of confluent MC3T3E1 cells with an N-cadherin junction inhibitor-EGTA and a PI3K inhibitor LY294002 resulted in reduction of phosphorylation levels of AKT and GSK3 and expression of Osterix, Osteomodulin and Osteoglycin. Egtazic Acid 75-79 glycogen synthase kinase 3 beta Mus musculus 169-173 21964322-7 2012 Treatment of confluent MC3T3E1 cells with an N-cadherin junction inhibitor-EGTA and a PI3K inhibitor LY294002 resulted in reduction of phosphorylation levels of AKT and GSK3 and expression of Osterix, Osteomodulin and Osteoglycin. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 101-109 glycogen synthase kinase 3 beta Mus musculus 169-173 21946431-0 2012 Functional significance of glycogen synthase kinase-3 regulation by serotonin. Serotonin 68-77 glycogen synthase kinase 3 beta Mus musculus 27-53 21946431-2 2012 Enhancing brain serotonin has been found to regulate glycogen synthase Kinase-3 (GSK3), but the signaling mechanism and functional significance of this regulation remain to be determined. Serotonin 16-25 glycogen synthase kinase 3 beta Mus musculus 53-79 21946431-2 2012 Enhancing brain serotonin has been found to regulate glycogen synthase Kinase-3 (GSK3), but the signaling mechanism and functional significance of this regulation remain to be determined. Serotonin 16-25 glycogen synthase kinase 3 beta Mus musculus 81-85 21946431-5 2012 The results showed that activation of 5-HT1A receptors by 8-hydroxy-N,N-dipropyl-2-aminotetralin (8-OH-DPAT) increased phosphorylation of the N-terminal serine of both GSK3alpha and GSK3beta in several areas of the hippocampus. 8-Hydroxy-2-(di-n-propylamino)tetralin 58-96 glycogen synthase kinase 3 beta Mus musculus 182-190 21946431-5 2012 The results showed that activation of 5-HT1A receptors by 8-hydroxy-N,N-dipropyl-2-aminotetralin (8-OH-DPAT) increased phosphorylation of the N-terminal serine of both GSK3alpha and GSK3beta in several areas of the hippocampus. 8-Hydroxy-2-(di-n-propylamino)tetralin 98-107 glycogen synthase kinase 3 beta Mus musculus 182-190 21946431-5 2012 The results showed that activation of 5-HT1A receptors by 8-hydroxy-N,N-dipropyl-2-aminotetralin (8-OH-DPAT) increased phosphorylation of the N-terminal serine of both GSK3alpha and GSK3beta in several areas of the hippocampus. Serine 153-159 glycogen synthase kinase 3 beta Mus musculus 182-190 21946431-8 2012 Furthermore, acute fluoxetine treatment up-regulated both phospho-Ser21-GSK3alpha and phospho-Ser9-GSK3beta in the hippocampus. Fluoxetine 19-29 glycogen synthase kinase 3 beta Mus musculus 99-107 21946431-9 2012 Blocking phosphorylation of GSK3alpha and GSK3beta diminished the anti-immobility effect of fluoxetine treatment in the forced swim test, wherein the effect of GSK3beta was more prominent. Fluoxetine 92-102 glycogen synthase kinase 3 beta Mus musculus 42-50 21946431-9 2012 Blocking phosphorylation of GSK3alpha and GSK3beta diminished the anti-immobility effect of fluoxetine treatment in the forced swim test, wherein the effect of GSK3beta was more prominent. Fluoxetine 92-102 glycogen synthase kinase 3 beta Mus musculus 160-168 21946431-10 2012 These results together suggest that PI3K/Akt is a signaling mechanism mediating the GSK3-regulating effect of 5-HT1A receptors in the hippocampus, and regulation of GSK3 is an important intermediate signaling process in the behavioral functions of 5-HT1A receptors and fluoxetine. Fluoxetine 269-279 glycogen synthase kinase 3 beta Mus musculus 165-169 22531419-6 2012 While total tau protein levels were unaltered between the two groups, we found that dexamethasone significantly reduced tau phosphorylation at specific sites that were mediated by decreases in glycogen synthase kinase-3beta protein level activity. Dexamethasone 84-97 glycogen synthase kinase 3 beta Mus musculus 193-223 22064483-2 2012 In murine embryonic stem cells (mESCs), Gsk3beta is inhibited by multiple mechanisms, including its inhibitory phosphorylation on serine 9 by protein kinase B (Akt), a major effector of the canonical phosphatidylinositol 3-kinase (PI3K) pathway. Serine 130-136 glycogen synthase kinase 3 beta Mus musculus 40-48 22687999-7 2012 Additionally, phosphorylation of glycogen synthase kinase-3beta and mitogen-activated protein kinase kinase 4, which are upstream kinases of JNK in APAP-induced hepatotoxicity, were also suppressed in Gstm1-null mice. Acetaminophen 148-152 glycogen synthase kinase 3 beta Mus musculus 33-109 23251339-8 2012 Diabetes/TPEN group also showed a significant decrease in nuclear factor-erythroid 2-related factor 2 (Nrf2) expression and transcription action along with significant increases in Akt negative regulators, decrease in Akt and GSK-3beta phosphorylation, and increase in nuclear accumulation of Fyn (a Nrf2 negative regulator). N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine 9-13 glycogen synthase kinase 3 beta Mus musculus 226-235 22745733-0 2012 Glycogen synthase kinase 3 (GSK3) inhibitor, SB-216763, promotes pluripotency in mouse embryonic stem cells. SB 216763 45-54 glycogen synthase kinase 3 beta Mus musculus 28-32 23082110-5 2012 Though Akt activation improved to control levels after chloroquine treatment in PbA-infected mice, the addition of lithium chloride, a compound which inhibits GSK3beta activity and stimulates Akt activation, induced a modest, but significant activation of Akt in the brains of infected mice when compared to uninfected controls treated with chloroquine with and without lithium. Lithium Chloride 115-131 glycogen synthase kinase 3 beta Mus musculus 159-167 23082110-5 2012 Though Akt activation improved to control levels after chloroquine treatment in PbA-infected mice, the addition of lithium chloride, a compound which inhibits GSK3beta activity and stimulates Akt activation, induced a modest, but significant activation of Akt in the brains of infected mice when compared to uninfected controls treated with chloroquine with and without lithium. Lithium 115-122 glycogen synthase kinase 3 beta Mus musculus 159-167 22912839-0 2012 The effects of glycogen synthase kinase-3beta in serotonin neurons. Serotonin 49-58 glycogen synthase kinase 3 beta Mus musculus 15-45 22912839-2 2012 Increasing evidence has shown that GSK3 acts as a modulator in the serotonin neurotransmission system, including direct interaction with serotonin 1B (5-HT1B) receptors in a highly selective manner and prominent modulating effect on 5-HT1B receptor activity. Serotonin 67-76 glycogen synthase kinase 3 beta Mus musculus 35-39 22912839-6 2012 However, the expression of GSK3beta in snGSK3beta-KO mice was diminished in TpH2-expressing serotonin neurons. Serotonin 92-101 glycogen synthase kinase 3 beta Mus musculus 27-35 22912839-8 2012 The effect of anpirtoline on the horizontal, center, and vertical activities in the open field test was differentially affected by GSK3beta depletion in serotonin neurons, wherein vertical activity, but not horizontal activity, was significantly altered in snGSK3beta-KO mice. anpirtoline 14-25 glycogen synthase kinase 3 beta Mus musculus 131-139 22912839-8 2012 The effect of anpirtoline on the horizontal, center, and vertical activities in the open field test was differentially affected by GSK3beta depletion in serotonin neurons, wherein vertical activity, but not horizontal activity, was significantly altered in snGSK3beta-KO mice. Serotonin 153-162 glycogen synthase kinase 3 beta Mus musculus 131-139 22912839-10 2012 Therefore, results of this study demonstrated a serotonin neuron-targeting function of GSK3beta by regulating 5-HT1B autoreceptors, which impacts serotonergic neuron firing, serotonin release, and serotonin-regulated behaviors. Serotonin 48-57 glycogen synthase kinase 3 beta Mus musculus 87-95 22912839-10 2012 Therefore, results of this study demonstrated a serotonin neuron-targeting function of GSK3beta by regulating 5-HT1B autoreceptors, which impacts serotonergic neuron firing, serotonin release, and serotonin-regulated behaviors. Serotonin 174-183 glycogen synthase kinase 3 beta Mus musculus 87-95 22912839-10 2012 Therefore, results of this study demonstrated a serotonin neuron-targeting function of GSK3beta by regulating 5-HT1B autoreceptors, which impacts serotonergic neuron firing, serotonin release, and serotonin-regulated behaviors. Serotonin 174-183 glycogen synthase kinase 3 beta Mus musculus 87-95 22745733-6 2012 To our knowledge, SB-216763 is the first GSK3 inhibitor that can promote self-renewal of mESC co-cultured with MEFs for more than two months. SB 216763 18-27 glycogen synthase kinase 3 beta Mus musculus 41-45 23082110-7 2012 GSK3beta inhibition was significantly increased after chloroquine treatment, both in lithium and non-lithium treated PbA-infected mice. Chloroquine 54-65 glycogen synthase kinase 3 beta Mus musculus 0-8 23082110-7 2012 GSK3beta inhibition was significantly increased after chloroquine treatment, both in lithium and non-lithium treated PbA-infected mice. Lithium 85-92 glycogen synthase kinase 3 beta Mus musculus 0-8 23082110-7 2012 GSK3beta inhibition was significantly increased after chloroquine treatment, both in lithium and non-lithium treated PbA-infected mice. Lithium 101-108 glycogen synthase kinase 3 beta Mus musculus 0-8 23082110-9 2012 Regulation of Akt/GSK3beta with lithium reduces neuronal degeneration and may have neuroprotective effects in ECM. Lithium 32-39 glycogen synthase kinase 3 beta Mus musculus 18-26 23028846-3 2012 METHODOLOGY: In a murine ALF model induced by D-GalN(700 mg/kg)/LPS(10 microg/kg), we analyzed GSK3beta mechanisms using a specific chemical inhibitor, SB216763, and detected the role of endoplasmic reticulum stress (ERS). SB 216763 152-160 glycogen synthase kinase 3 beta Mus musculus 95-103 22745733-2 2012 Here, we show that SB-216763, a glycogen synthase kinase-3 (GSK3) inhibitor, can maintain mouse embryonic stem cells (mESCs) in a pluripotent state in the absence of exogenous leukemia inhibitory factor (LIF) when cultured on mouse embryonic fibroblasts (MEFs). SB 216763 19-28 glycogen synthase kinase 3 beta Mus musculus 32-58 22745733-2 2012 Here, we show that SB-216763, a glycogen synthase kinase-3 (GSK3) inhibitor, can maintain mouse embryonic stem cells (mESCs) in a pluripotent state in the absence of exogenous leukemia inhibitory factor (LIF) when cultured on mouse embryonic fibroblasts (MEFs). SB 216763 19-28 glycogen synthase kinase 3 beta Mus musculus 60-64 22540008-5 2012 METHODOLOGY/PRINCIPAL FINDINGS: We found that CHIR99021, a GSK-3 specific inhibitor, promotes self-renewal of ES cells from recalcitrant C57BL/6 (B6) and BALB/c mouse strains through stabilization of beta-catenin and c-Myc protein levels. Einsteinium 110-112 glycogen synthase kinase 3 beta Mus musculus 59-64 22536363-8 2012 Investigation of the major tau kinases showed that acute delivery of a high dose of thiamet-G into the brain also led to a marked activation of glycogen synthase kinase-3beta (GSK-3beta), possibly as a consequence of down-regulation of its upstream regulating kinase, AKT. thiamet 84-91 glycogen synthase kinase 3 beta Mus musculus 144-174 22536363-8 2012 Investigation of the major tau kinases showed that acute delivery of a high dose of thiamet-G into the brain also led to a marked activation of glycogen synthase kinase-3beta (GSK-3beta), possibly as a consequence of down-regulation of its upstream regulating kinase, AKT. thiamet 84-91 glycogen synthase kinase 3 beta Mus musculus 176-185 22347510-1 2012 Lithium is an anti-psychotic that has been shown to prevent the hyperphosphorylation of tau protein through the inhibition of glycogen-synthase kinase 3-beta (GSK3beta). Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 126-157 22428012-8 2012 Collectively, our data have identified a novel amplitude-enhancing effect of lithium on the PER2 protein rhythms in the central and peripheral circadian clockwork, which may involve a GSK3-mediated signalling pathway. Lithium 77-84 glycogen synthase kinase 3 beta Mus musculus 184-188 22511924-7 2012 Several of the most densely interconnected network hubs, including Kcnma1 and Gsk3beta, are known to influence behavioral or physiological responses to ethanol, validating our overall approach. Ethanol 152-159 glycogen synthase kinase 3 beta Mus musculus 78-86 21965663-4 2011 Dyrk1A-mediated phosphorylation of RCAN1 at Ser(112) primes the protein for the GSK3beta-mediated phosphorylation of Ser(108). Serine 44-47 glycogen synthase kinase 3 beta Mus musculus 80-88 21873331-8 2011 Inhibition of GSK-3 aggravated experimental fibrosis in bleomycin-challenged mice and in tsk-1 mice. Bleomycin 56-65 glycogen synthase kinase 3 beta Mus musculus 14-19 21985244-4 2011 In this in vitro study, we found that: (a) alpha-SN directly stimulates the phosphorylation of tau by glycogen synthase kinase-3beta (GSK-3beta), (b) alpha-SN forms a heterotrimeric complex with tau and GSK-3beta, and (c) the nonamyloid beta component (NAC) domain and an acidic region of alpha-SN are responsible for the stimulation of GSK-3beta-mediated tau phosphorylation. nac 253-256 glycogen synthase kinase 3 beta Mus musculus 134-143 21887819-6 2011 In addition, both dietary CUR and THC significantly decreased AOM-induced Wnt-1 and beta-catenin protein expression, as well as the phosphorylation of GSK-3beta in colonic tissue. tetrahydrocurcumin 34-37 glycogen synthase kinase 3 beta Mus musculus 151-160 21992552-0 2011 A novel glycogen synthase kinase-3 inhibitor 2-methyl-5-(3-{4-[(S )-methylsulfinyl]phenyl}-1-benzofuran-5-yl)-1,3,4-oxadiazole decreases tau phosphorylation and ameliorates cognitive deficits in a transgenic model of Alzheimer"s disease. 2-methyl-5-(3-{4-[(s )-methylsulfinyl]phenyl}-1-benzofuran-5-yl)-1,3,4-oxadiazole 45-126 glycogen synthase kinase 3 beta Mus musculus 8-34 21992552-5 2011 In this study, we report the pharmacological effects of a novel GSK-3 inhibitor, 2-methyl-5-(3-{4-[(S)-methylsulfinyl]phenyl}-1-benzofuran-5-yl)-1,3,4-oxadiazole (MMBO), which displays high selectivity for GSK-3 and brain penetration following oral administration. (S)-2-Methyl-5-[3-[4-(Methylsulfinyl)phenyl]benzofuran-5-yl]-1,3,4-oxadiazole 81-161 glycogen synthase kinase 3 beta Mus musculus 64-69 21992552-5 2011 In this study, we report the pharmacological effects of a novel GSK-3 inhibitor, 2-methyl-5-(3-{4-[(S)-methylsulfinyl]phenyl}-1-benzofuran-5-yl)-1,3,4-oxadiazole (MMBO), which displays high selectivity for GSK-3 and brain penetration following oral administration. (S)-2-Methyl-5-[3-[4-(Methylsulfinyl)phenyl]benzofuran-5-yl]-1,3,4-oxadiazole 81-161 glycogen synthase kinase 3 beta Mus musculus 206-211 21992552-5 2011 In this study, we report the pharmacological effects of a novel GSK-3 inhibitor, 2-methyl-5-(3-{4-[(S)-methylsulfinyl]phenyl}-1-benzofuran-5-yl)-1,3,4-oxadiazole (MMBO), which displays high selectivity for GSK-3 and brain penetration following oral administration. TCS 2002 163-167 glycogen synthase kinase 3 beta Mus musculus 64-69 21922189-0 2011 Enhanced catecholamine release in mice expressing PKB/SGK-resistant GSK3. Catecholamines 9-22 glycogen synthase kinase 3 beta Mus musculus 68-72 21922189-3 2011 PI3/PKB/Akt/SGK-dependent inhibition of GSK3 is disrupted in gene-targeted knockin mice with mutated and thus PKB/SGK-resistant GSK3alpha,ss (gsk3 ( KI )) where the serine of the PKB/SGK phosphorylation site has been replaced by alanine. Serine 240-246 glycogen synthase kinase 3 beta Mus musculus 40-44 21922189-3 2011 PI3/PKB/Akt/SGK-dependent inhibition of GSK3 is disrupted in gene-targeted knockin mice with mutated and thus PKB/SGK-resistant GSK3alpha,ss (gsk3 ( KI )) where the serine of the PKB/SGK phosphorylation site has been replaced by alanine. Alanine 304-311 glycogen synthase kinase 3 beta Mus musculus 40-44 21922189-14 2011 The observations reveal a completely novel function of PKB/Akt/SGK-dependent GSK3 signaling, i.e., regulation of catecholamine release. Catecholamines 113-126 glycogen synthase kinase 3 beta Mus musculus 77-81 21965663-4 2011 Dyrk1A-mediated phosphorylation of RCAN1 at Ser(112) primes the protein for the GSK3beta-mediated phosphorylation of Ser(108). Serine 117-120 glycogen synthase kinase 3 beta Mus musculus 80-88 21949120-1 2011 Glycogen synthase kinase-3beta (GSK-3beta) is a serine/threonine kinase originally identified as a regulator of glycogen deposition. Glycogen 112-120 glycogen synthase kinase 3 beta Mus musculus 0-30 22110426-7 2011 The clinical application of a classical GSK-3 inhibitor, lithium, is limited by its toxic consequences, including motor side effects. Lithium 57-64 glycogen synthase kinase 3 beta Mus musculus 40-45 21802267-6 2011 We also observed an increase in the intracellular accumulation of beta-catenin as well as the phosphorylation of glycogen synthase kinase-3beta (GSK3beta) protein after treatment with naringenin. naringenin 184-194 glycogen synthase kinase 3 beta Mus musculus 113-143 21802267-6 2011 We also observed an increase in the intracellular accumulation of beta-catenin as well as the phosphorylation of glycogen synthase kinase-3beta (GSK3beta) protein after treatment with naringenin. naringenin 184-194 glycogen synthase kinase 3 beta Mus musculus 145-153 21949120-1 2011 Glycogen synthase kinase-3beta (GSK-3beta) is a serine/threonine kinase originally identified as a regulator of glycogen deposition. Glycogen 112-120 glycogen synthase kinase 3 beta Mus musculus 32-41 21898827-2 2011 Here, we observed stimulation of in vitro astrocyte migration by the new potent glycogen synthase kinase-3 (GSK-3) inhibitor Ro3303544 and investigated the effect of Ro3303544 administration for 5 days following SCI in mice. ro3303544 125-134 glycogen synthase kinase 3 beta Mus musculus 80-106 22019984-8 2011 In contrast, pretreatment with SB216763, a specific inhibitor of GSK-3beta, resulted in an amelioration of neurite outgrowth by Nogo-66, compared with the Nogo-66 alone group (P<0.05). SB 216763 31-39 glycogen synthase kinase 3 beta Mus musculus 65-74 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin 15-26 glycogen synthase kinase 3 beta Mus musculus 79-109 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin 15-26 glycogen synthase kinase 3 beta Mus musculus 111-119 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin 15-26 glycogen synthase kinase 3 beta Mus musculus 147-155 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. ursodoxicoltaurine 214-219 glycogen synthase kinase 3 beta Mus musculus 79-109 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. ursodoxicoltaurine 214-219 glycogen synthase kinase 3 beta Mus musculus 111-119 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. ursodoxicoltaurine 214-219 glycogen synthase kinase 3 beta Mus musculus 147-155 21898827-2 2011 Here, we observed stimulation of in vitro astrocyte migration by the new potent glycogen synthase kinase-3 (GSK-3) inhibitor Ro3303544 and investigated the effect of Ro3303544 administration for 5 days following SCI in mice. ro3303544 125-134 glycogen synthase kinase 3 beta Mus musculus 108-113 21796107-1 2011 Emerging evidence suggests that the mood stabilizers lithium and valproate (VPA) have broad neuroprotective and neurotrophic properties, and that these occur via inhibition of glycogen synthase kinase 3 (GSK-3) and histone deacetylases (HDACs), respectively. Lithium 53-60 glycogen synthase kinase 3 beta Mus musculus 176-202 22053151-11 2011 Taken together, these findings indicate that lithium and other inhibitors of GSK3 are promising candidate therapeutic agents for treating FXS. Lithium 45-52 glycogen synthase kinase 3 beta Mus musculus 77-81 21796107-1 2011 Emerging evidence suggests that the mood stabilizers lithium and valproate (VPA) have broad neuroprotective and neurotrophic properties, and that these occur via inhibition of glycogen synthase kinase 3 (GSK-3) and histone deacetylases (HDACs), respectively. Lithium 53-60 glycogen synthase kinase 3 beta Mus musculus 204-209 21796107-1 2011 Emerging evidence suggests that the mood stabilizers lithium and valproate (VPA) have broad neuroprotective and neurotrophic properties, and that these occur via inhibition of glycogen synthase kinase 3 (GSK-3) and histone deacetylases (HDACs), respectively. Valproic Acid 65-74 glycogen synthase kinase 3 beta Mus musculus 176-202 21796107-1 2011 Emerging evidence suggests that the mood stabilizers lithium and valproate (VPA) have broad neuroprotective and neurotrophic properties, and that these occur via inhibition of glycogen synthase kinase 3 (GSK-3) and histone deacetylases (HDACs), respectively. Valproic Acid 65-74 glycogen synthase kinase 3 beta Mus musculus 204-209 21796107-1 2011 Emerging evidence suggests that the mood stabilizers lithium and valproate (VPA) have broad neuroprotective and neurotrophic properties, and that these occur via inhibition of glycogen synthase kinase 3 (GSK-3) and histone deacetylases (HDACs), respectively. Valproic Acid 76-79 glycogen synthase kinase 3 beta Mus musculus 176-202 21796107-1 2011 Emerging evidence suggests that the mood stabilizers lithium and valproate (VPA) have broad neuroprotective and neurotrophic properties, and that these occur via inhibition of glycogen synthase kinase 3 (GSK-3) and histone deacetylases (HDACs), respectively. Valproic Acid 76-79 glycogen synthase kinase 3 beta Mus musculus 204-209 21708147-4 2011 GSK-3 inhibition was achieved using ATP-competitive (6-bromoindirubin-3"-oxime and CHIR99021) or substrate-competitive (TAT-eIF2B) inhibitors to eliminate potential confounding effects on cell fate due to off-target kinase inhibition. Adenosine Triphosphate 36-39 glycogen synthase kinase 3 beta Mus musculus 0-5 21163265-1 2011 The GSK-3 family of serine/threonine kinases, which is comprised of two isoforms (alpha and beta), was initially identified as a negative regulator of glycogen synthase, the rate limiting enzyme of glycogen synthesis [1,2]. Glycogen 151-159 glycogen synthase kinase 3 beta Mus musculus 4-9 21671257-5 2011 Recent evidence indicates that glycogen synthase kinase 3beta (GSK3beta) is a potential mediator of ethanol-mediated neuronal death. Ethanol 100-107 glycogen synthase kinase 3 beta Mus musculus 31-61 21671257-5 2011 Recent evidence indicates that glycogen synthase kinase 3beta (GSK3beta) is a potential mediator of ethanol-mediated neuronal death. Ethanol 100-107 glycogen synthase kinase 3 beta Mus musculus 63-71 21671257-10 2011 C3G blocked ethanol-mediated GSK3beta activation by inducing phosphorylation at serine 9 while reducing the phosphorylation at tyrosine 216. Ethanol 12-19 glycogen synthase kinase 3 beta Mus musculus 29-37 21671257-10 2011 C3G blocked ethanol-mediated GSK3beta activation by inducing phosphorylation at serine 9 while reducing the phosphorylation at tyrosine 216. Serine 80-86 glycogen synthase kinase 3 beta Mus musculus 29-37 21708147-4 2011 GSK-3 inhibition was achieved using ATP-competitive (6-bromoindirubin-3"-oxime and CHIR99021) or substrate-competitive (TAT-eIF2B) inhibitors to eliminate potential confounding effects on cell fate due to off-target kinase inhibition. 6-bromoindirubin-3'-oxime 53-78 glycogen synthase kinase 3 beta Mus musculus 0-5 21660969-3 2011 aPKCepsilon relocates to the mitochondrion, inactivating glycogen synthase kinase 3beta (GSK3beta) to modulate glycogen metabolism, hypertrophy and HIF-1alpha. Glycogen 57-65 glycogen synthase kinase 3 beta Mus musculus 89-97 21724851-7 2011 Cultured differentiated pre-adipocyte cell lines exposed to the NO donors S-nitrosoglutathione (GSNO) or S-nitroso-N-acetylpenicillamine exhibited diminished insulin-stimulated phosphorylation of Akt but not of GSK3 nor of insulin-stimulated glucose uptake. S-Nitrosoglutathione 74-94 glycogen synthase kinase 3 beta Mus musculus 211-215 21724851-7 2011 Cultured differentiated pre-adipocyte cell lines exposed to the NO donors S-nitrosoglutathione (GSNO) or S-nitroso-N-acetylpenicillamine exhibited diminished insulin-stimulated phosphorylation of Akt but not of GSK3 nor of insulin-stimulated glucose uptake. S-Nitrosoglutathione 96-100 glycogen synthase kinase 3 beta Mus musculus 211-215 21575614-0 2011 alpha-Tocopherol impairs 7-ketocholesterol-induced caspase-3-dependent apoptosis involving GSK-3 activation and Mcl-1 degradation on 158N murine oligodendrocytes. alpha-Tocopherol 0-16 glycogen synthase kinase 3 beta Mus musculus 91-96 21575614-0 2011 alpha-Tocopherol impairs 7-ketocholesterol-induced caspase-3-dependent apoptosis involving GSK-3 activation and Mcl-1 degradation on 158N murine oligodendrocytes. 7-ketocholesterol 25-42 glycogen synthase kinase 3 beta Mus musculus 91-96 21575614-5 2011 With alpha-tocopherol (400 muM), which was capable of counteracting 7-ketocholesterol-induced apoptosis, Akt and GSK3beta dephosphorylation were inhibited as well as Mcl-1 degradation. alpha-Tocopherol 5-21 glycogen synthase kinase 3 beta Mus musculus 113-121 21575614-5 2011 With alpha-tocopherol (400 muM), which was capable of counteracting 7-ketocholesterol-induced apoptosis, Akt and GSK3beta dephosphorylation were inhibited as well as Mcl-1 degradation. 7-ketocholesterol 68-85 glycogen synthase kinase 3 beta Mus musculus 113-121 21575614-6 2011 These data underline that the potential protective effects of alpha-tocopherol against 7-ketocholesterol-induced apoptosis do not depend on the cell line considered, and that the cascade of events (Akt/GSK3beta/Mcl-1) constitutes a link between 7-ketocholesterol-induced cytoplasmic membrane dysfunctions and mitochondrial depolarisation leading to apoptosis. alpha-Tocopherol 62-78 glycogen synthase kinase 3 beta Mus musculus 202-210 21208504-4 2011 Since lithium has been shown to potentially act through glycogen synthase kinase-3 (GSK3) inhibition, we evaluated the efficacy of selective GSK3 inhibitors in this model. Lithium 6-13 glycogen synthase kinase 3 beta Mus musculus 56-82 21208504-4 2011 Since lithium has been shown to potentially act through glycogen synthase kinase-3 (GSK3) inhibition, we evaluated the efficacy of selective GSK3 inhibitors in this model. Lithium 6-13 glycogen synthase kinase 3 beta Mus musculus 84-88 21660969-14 2011 Moreover, we propose that preferential glucose utilization by PKCepsilon hearts is orchestrated by a p-GSK3beta/HIF-1alpha-mediated mechanism, playing a crucial role to sustain contractile function in response to chronic hypobaric hypoxia. Glucose 39-46 glycogen synthase kinase 3 beta Mus musculus 103-111 21821916-0 2011 Glycogen synthase kinase-3 is essential for beta-arrestin-2 complex formation and lithium-sensitive behaviors in mice. Lithium 82-89 glycogen synthase kinase 3 beta Mus musculus 0-26 21821916-5 2011 Here, we show what we believe to be a new link between GSK-3 and the beta-arrestin-2 complex in mice and propose an integrated mechanism that accounts for the effects of lithium on multiple behaviors. Lithium 170-177 glycogen synthase kinase 3 beta Mus musculus 55-60 21821916-6 2011 GSK-3beta (Gsk3b) overexpression reversed behavioral defects observed in lithium-treated mice and similar behaviors observed in Gsk3b+/- mice. Lithium 73-80 glycogen synthase kinase 3 beta Mus musculus 0-9 21821916-6 2011 GSK-3beta (Gsk3b) overexpression reversed behavioral defects observed in lithium-treated mice and similar behaviors observed in Gsk3b+/- mice. Lithium 73-80 glycogen synthase kinase 3 beta Mus musculus 11-16 21821916-7 2011 Furthermore, immunoprecipitation of striatial tissue from WT mice revealed that lithium disrupted the beta-arrestin-2/Akt/PP2A complex by directly inhibiting GSK-3. Lithium 80-87 glycogen synthase kinase 3 beta Mus musculus 158-163 21821916-8 2011 GSK-3 inhibitors or loss of one copy of the Gsk3b gene reduced beta-arrestin-2/Akt/PP2A complex formation in mice, while overexpression of Gsk3b restored complex formation in lithium-treated mice. Lithium 175-182 glycogen synthase kinase 3 beta Mus musculus 0-5 21821916-8 2011 GSK-3 inhibitors or loss of one copy of the Gsk3b gene reduced beta-arrestin-2/Akt/PP2A complex formation in mice, while overexpression of Gsk3b restored complex formation in lithium-treated mice. Lithium 175-182 glycogen synthase kinase 3 beta Mus musculus 44-49 21821916-8 2011 GSK-3 inhibitors or loss of one copy of the Gsk3b gene reduced beta-arrestin-2/Akt/PP2A complex formation in mice, while overexpression of Gsk3b restored complex formation in lithium-treated mice. Lithium 175-182 glycogen synthase kinase 3 beta Mus musculus 139-144 21821916-9 2011 Thus, GSK-3 regulates the stability of the beta-arrestin-2/Akt/PP2A complex, and lithium disrupts the complex through direct inhibition of GSK-3. Lithium 81-88 glycogen synthase kinase 3 beta Mus musculus 139-144 21821916-10 2011 We believe these findings reveal a new role for GSK-3 within the beta-arrestin complex and demonstrate that GSK-3 is a critical target of lithium in mammalian behaviors. Lithium 138-145 glycogen synthase kinase 3 beta Mus musculus 108-113 21470302-5 2011 Of note, melatonin activated Wnt 5 alpha/beta, beta-catenin and the phosphorylation of c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) in a time-dependent manner while it attenuated phosphorylation of glycogen synthase kinase 3 beta (GSK-3beta) in MC3T3-E1 cells. Melatonin 9-18 glycogen synthase kinase 3 beta Mus musculus 232-263 21470302-5 2011 Of note, melatonin activated Wnt 5 alpha/beta, beta-catenin and the phosphorylation of c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) in a time-dependent manner while it attenuated phosphorylation of glycogen synthase kinase 3 beta (GSK-3beta) in MC3T3-E1 cells. Melatonin 9-18 glycogen synthase kinase 3 beta Mus musculus 265-274 21470302-7 2011 Furthermore, Western blotting showed that Noggin reversed activation of beta-catenin and Wnt5 alpha/beta and suppression of GSK-3beta induced by melatonin in MC3T3-E1 cells, which was similarly induced by ERK inhibitor PD98059. Melatonin 145-154 glycogen synthase kinase 3 beta Mus musculus 124-133 21737790-6 2011 Rapamycin enhanced autophagy and, at the same time, abolished the effects of GSK-3beta inhibition on both prolonged ischemic injury and I/R injury. Sirolimus 0-9 glycogen synthase kinase 3 beta Mus musculus 77-86 21496192-2 2011 Cellular stimulation by Wnt or lithium chloride (LiCl) inactivates glycogen synthase kinase-3beta (GSK-3beta), causing nuclear accumulation of beta-catenin and transactivation of genes that transform cells. wnt 24-27 glycogen synthase kinase 3 beta Mus musculus 67-97 21039417-11 2011 In addition, it increased the inhibitory phosphorylation of glycogen synthase kinase-3beta (GSK3beta), derepressing Nrf2 activity, which was supported by the reversal of sauchinone"s activation of Nrf2 by an activated mutant of GSK3beta. sauchinone 170-180 glycogen synthase kinase 3 beta Mus musculus 60-90 21039417-11 2011 In addition, it increased the inhibitory phosphorylation of glycogen synthase kinase-3beta (GSK3beta), derepressing Nrf2 activity, which was supported by the reversal of sauchinone"s activation of Nrf2 by an activated mutant of GSK3beta. sauchinone 170-180 glycogen synthase kinase 3 beta Mus musculus 92-100 21039417-11 2011 In addition, it increased the inhibitory phosphorylation of glycogen synthase kinase-3beta (GSK3beta), derepressing Nrf2 activity, which was supported by the reversal of sauchinone"s activation of Nrf2 by an activated mutant of GSK3beta. sauchinone 170-180 glycogen synthase kinase 3 beta Mus musculus 228-236 21039417-12 2011 Moreover, phosphorylation of GSK3beta by sauchinone depended on PKCdelta activation. sauchinone 41-51 glycogen synthase kinase 3 beta Mus musculus 29-37 21039417-13 2011 CONCLUSION AND IMPLICATIONS Our results demonstrate that sauchinone protects the liver from APAP-induced toxicity by activating Nrf2, and this effect is mediated by PKCdelta activation, which induces inhibitory phosphorylation of GSK3beta. sauchinone 57-67 glycogen synthase kinase 3 beta Mus musculus 230-238 21567437-4 2011 The active Gsk3beta, however, was essential for the development of IRI pathology, as administration of its specific inhibitor, SB216763, ameliorated the hepatocellular damage, evidenced by reduced serum alanine aminotransferase (sALT) levels and well-preserved liver architecture compared with controls. SB 216763 127-135 glycogen synthase kinase 3 beta Mus musculus 11-19 21567437-7 2011 Gsk3beta inactivation by IR was a self-regulatory mechanism in liver homeostasis, critically dependent on phosphoinositide 3 (PI3)-kinase activation, as administration of a PI3 kinase inhibitor, wortmannin, reduced Gsk3 phosphorylation and augmented liver damage. Wortmannin 195-205 glycogen synthase kinase 3 beta Mus musculus 0-8 21567437-7 2011 Gsk3beta inactivation by IR was a self-regulatory mechanism in liver homeostasis, critically dependent on phosphoinositide 3 (PI3)-kinase activation, as administration of a PI3 kinase inhibitor, wortmannin, reduced Gsk3 phosphorylation and augmented liver damage. Wortmannin 195-205 glycogen synthase kinase 3 beta Mus musculus 0-4 21161565-5 2011 Using the specific GSK-3beta inhibitor SB415286, we demonstrate that GSK-3beta inhibition decreases the viability of Neuro-2A cells, as determined by cell proliferation assay and clonogenic survival. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 39-47 glycogen synthase kinase 3 beta Mus musculus 19-28 21161565-5 2011 Using the specific GSK-3beta inhibitor SB415286, we demonstrate that GSK-3beta inhibition decreases the viability of Neuro-2A cells, as determined by cell proliferation assay and clonogenic survival. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 39-47 glycogen synthase kinase 3 beta Mus musculus 69-78 21161565-6 2011 Moreover, we show that GSK-3beta inhibition induces apoptosis in neuroblastoma cells, as determined by Annexin V staining and confirmed with DAPI staining. DAPI 141-145 glycogen synthase kinase 3 beta Mus musculus 23-32 21718286-0 2011 A derivative of 2-aminothiazole inhibits melanogenesis in B16 mouse melanoma cells via glycogen synthase kinase 3beta phosphorylation. 2-aminothiazole 16-31 glycogen synthase kinase 3 beta Mus musculus 87-117 21718286-9 2011 CONCLUSIONS: We propose that KHG25855 showed hypopigmentary activity through tyrosinase downregulation via GSK3beta phosphorylation. khg25855 29-37 glycogen synthase kinase 3 beta Mus musculus 107-115 21697283-5 2011 In addition, indirubins blocked migration of endothelial cells, suggesting that anti-invasive glioma therapy with GSK-3 inhibitors in vivo not only inhibits invasion of tumor cells, but blocks migration of endothelial cells, which is also required for tumor angiogenesis. indirubin 13-23 glycogen synthase kinase 3 beta Mus musculus 114-119 21659643-7 2011 Moreover, the inhibitory phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) at Ser9 depends on Cdc42 and PKCiota, and expression of kinase-dead GSK-3beta in Cdc42-null EBs promotes the formation of linear endothelial segments without branches. ethylbenzene 179-182 glycogen synthase kinase 3 beta Mus musculus 44-74 21659643-7 2011 Moreover, the inhibitory phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) at Ser9 depends on Cdc42 and PKCiota, and expression of kinase-dead GSK-3beta in Cdc42-null EBs promotes the formation of linear endothelial segments without branches. ethylbenzene 179-182 glycogen synthase kinase 3 beta Mus musculus 76-85 21659643-7 2011 Moreover, the inhibitory phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) at Ser9 depends on Cdc42 and PKCiota, and expression of kinase-dead GSK-3beta in Cdc42-null EBs promotes the formation of linear endothelial segments without branches. ethylbenzene 179-182 glycogen synthase kinase 3 beta Mus musculus 155-164 21039417-0 2011 Nrf2-mediated liver protection by sauchinone, an antioxidant lignan, from acetaminophen toxicity through the PKCdelta-GSK3beta pathway. sauchinone 34-44 glycogen synthase kinase 3 beta Mus musculus 118-126 21576335-4 2011 In this work, we sought to determine if glycogen synthase kinase 3 (GSK-3) is important for ET-induced modulation of macrophage and DC function. et 92-94 glycogen synthase kinase 3 beta Mus musculus 68-73 21576335-6 2011 Additional studies reveal that the ET-induced expression of ANTXR in macrophages was decreased when GSK-3 activity was disrupted with chemical inhibitors or with small interfering RNA (siRNA) targeting GSK-3. et 35-37 glycogen synthase kinase 3 beta Mus musculus 100-105 21576335-6 2011 Additional studies reveal that the ET-induced expression of ANTXR in macrophages was decreased when GSK-3 activity was disrupted with chemical inhibitors or with small interfering RNA (siRNA) targeting GSK-3. et 35-37 glycogen synthase kinase 3 beta Mus musculus 202-207 21496192-2 2011 Cellular stimulation by Wnt or lithium chloride (LiCl) inactivates glycogen synthase kinase-3beta (GSK-3beta), causing nuclear accumulation of beta-catenin and transactivation of genes that transform cells. wnt 24-27 glycogen synthase kinase 3 beta Mus musculus 99-108 21496192-2 2011 Cellular stimulation by Wnt or lithium chloride (LiCl) inactivates glycogen synthase kinase-3beta (GSK-3beta), causing nuclear accumulation of beta-catenin and transactivation of genes that transform cells. Lithium Chloride 31-47 glycogen synthase kinase 3 beta Mus musculus 67-97 21496192-2 2011 Cellular stimulation by Wnt or lithium chloride (LiCl) inactivates glycogen synthase kinase-3beta (GSK-3beta), causing nuclear accumulation of beta-catenin and transactivation of genes that transform cells. Lithium Chloride 31-47 glycogen synthase kinase 3 beta Mus musculus 99-108 21496192-2 2011 Cellular stimulation by Wnt or lithium chloride (LiCl) inactivates glycogen synthase kinase-3beta (GSK-3beta), causing nuclear accumulation of beta-catenin and transactivation of genes that transform cells. Lithium Chloride 49-53 glycogen synthase kinase 3 beta Mus musculus 67-97 21496192-2 2011 Cellular stimulation by Wnt or lithium chloride (LiCl) inactivates glycogen synthase kinase-3beta (GSK-3beta), causing nuclear accumulation of beta-catenin and transactivation of genes that transform cells. Lithium Chloride 49-53 glycogen synthase kinase 3 beta Mus musculus 99-108 21430081-4 2011 DM-celecoxib as well as celecoxib administered daily for 4 weeks inhibited Akt and subsequent phosphorylation of glycogen synthase kinase-3beta and mammalian target of rapamycin. 2,5-dimethylcelecoxib 0-12 glycogen synthase kinase 3 beta Mus musculus 113-177 21236583-11 2011 Glycogen synthase kinase 3beta levels were reduced in male mice at both methamphetamine doses tested and in females receiving 40mg/kg. Methamphetamine 72-87 glycogen synthase kinase 3 beta Mus musculus 0-30 21593197-7 2011 Both CR and rapamycin decreased phosphorylation of mTOR, p70/S6K, and S6 ribosomal protein, but only CR decreased phosphorylation of Akt, GSK-3beta, extracellular signal regulated kinase/mitogen-activated protein kinase, and STAT3(TYR705). Chromium 101-103 glycogen synthase kinase 3 beta Mus musculus 138-147 21430081-4 2011 DM-celecoxib as well as celecoxib administered daily for 4 weeks inhibited Akt and subsequent phosphorylation of glycogen synthase kinase-3beta and mammalian target of rapamycin. Celecoxib 3-12 glycogen synthase kinase 3 beta Mus musculus 113-177 21540081-8 2011 We also investigated the signaling mechanism(s) that mediate PGRN-induced NPC proliferation and found that phosphorylation of serine 9 (S9) of glycogen synthase kinase 3-beta (GSK3beta), which was dependent on phosphatidylinositol 3-kinase (PI3K) activity, was induced by PGRN treatment. Serine 126-132 glycogen synthase kinase 3 beta Mus musculus 143-174 21531375-7 2011 During chronic inflammation, we found that inhibiting glycogen synthase kinase-3beta activity with lithium reduced tau phosphorylation and the accumulation of insoluble tau and reversed memory impairments. Lithium 99-106 glycogen synthase kinase 3 beta Mus musculus 54-84 21389981-4 2011 Here, we modeled lithium responsiveness using cellular assays of glycogen synthase kinase 3 (GSK-3) signaling and mood-related behavioral assays in inbred strains of mice that differ in their response to lithium. Lithium 17-24 glycogen synthase kinase 3 beta Mus musculus 65-91 21372171-2 2011 We found previously that GSK3beta selectively interacts with 5-hydroxytryptamine-1B receptors (5-HT1BR) that have important functions in serotonin neurotransmission and behavior. Serotonin 137-146 glycogen synthase kinase 3 beta Mus musculus 25-33 21372171-5 2011 Molecular ablation of GSK3beta and GSK3 inhibitors abolished serotonin-induced change of 5-HT1BR coupling to G(i)alpha(2) and associated signaling but had no effect on serotonin-induced recruitment of beta-arrestin2 to 5-HT1BR. Serotonin 61-70 glycogen synthase kinase 3 beta Mus musculus 22-30 21372171-5 2011 Molecular ablation of GSK3beta and GSK3 inhibitors abolished serotonin-induced change of 5-HT1BR coupling to G(i)alpha(2) and associated signaling but had no effect on serotonin-induced recruitment of beta-arrestin2 to 5-HT1BR. Serotonin 61-70 glycogen synthase kinase 3 beta Mus musculus 22-26 21372171-8 2011 GSK3 inhibitors also facilitated the 5-HT1BR agonist anpirtoline-induced behavioral effect in the tail suspension test but spared anpirtoline-induced locomotor activity. anpirtoline 53-64 glycogen synthase kinase 3 beta Mus musculus 0-4 21372171-8 2011 GSK3 inhibitors also facilitated the 5-HT1BR agonist anpirtoline-induced behavioral effect in the tail suspension test but spared anpirtoline-induced locomotor activity. anpirtoline 130-141 glycogen synthase kinase 3 beta Mus musculus 0-4 21399861-5 2011 Lithium chloride and SB216763, inhibitors of glycogen synthase kinase 3beta (GSK3beta), enhanced the FGF-2-stimulated VEGF release. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 45-75 21399861-5 2011 Lithium chloride and SB216763, inhibitors of glycogen synthase kinase 3beta (GSK3beta), enhanced the FGF-2-stimulated VEGF release. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 77-85 21399861-5 2011 Lithium chloride and SB216763, inhibitors of glycogen synthase kinase 3beta (GSK3beta), enhanced the FGF-2-stimulated VEGF release. SB 216763 21-29 glycogen synthase kinase 3 beta Mus musculus 45-75 21399861-5 2011 Lithium chloride and SB216763, inhibitors of glycogen synthase kinase 3beta (GSK3beta), enhanced the FGF-2-stimulated VEGF release. SB 216763 21-29 glycogen synthase kinase 3 beta Mus musculus 77-85 21389981-5 2011 We found that activating AKT through phosphosrylation of a key regulatory site (Thr308) was associated with lithium response-activation of signaling pathways downstream of GSK-3 in cells and attenuation of mood-related behaviors in mice-and this response was attenuated by selective and direct inhibition of AKT kinase activity. Lithium 108-115 glycogen synthase kinase 3 beta Mus musculus 172-177 21389981-7 2011 In contrast, selective and direct GSK-3 inhibition by the ATP-competitive inhibitor CHIR99021 bypassed the requirement for AKT activation and modulated behavior in both lithium-responsive and non-responsive mouse strains. Adenosine Triphosphate 58-61 glycogen synthase kinase 3 beta Mus musculus 34-39 21389981-7 2011 In contrast, selective and direct GSK-3 inhibition by the ATP-competitive inhibitor CHIR99021 bypassed the requirement for AKT activation and modulated behavior in both lithium-responsive and non-responsive mouse strains. Lithium 169-176 glycogen synthase kinase 3 beta Mus musculus 34-39 21389981-8 2011 These results distinguish the mechanism of action of lithium from direct GSK-3 inhibition both in vivo and in vitro, and highlight the therapeutic potential for selective GSK-3 inhibitors in BP treatment. Lithium 53-60 glycogen synthase kinase 3 beta Mus musculus 171-176 21389981-4 2011 Here, we modeled lithium responsiveness using cellular assays of glycogen synthase kinase 3 (GSK-3) signaling and mood-related behavioral assays in inbred strains of mice that differ in their response to lithium. Lithium 17-24 glycogen synthase kinase 3 beta Mus musculus 93-98 21456066-2 2011 We previously reported that suppression of GSK-3 activity with lithium chloride (LiCl) or small chemical inhibitors impaired cellular DNA synthesis and reduced cell proliferation in prostate cancer cells. Lithium Chloride 63-79 glycogen synthase kinase 3 beta Mus musculus 43-48 21456066-2 2011 We previously reported that suppression of GSK-3 activity with lithium chloride (LiCl) or small chemical inhibitors impaired cellular DNA synthesis and reduced cell proliferation in prostate cancer cells. Lithium Chloride 81-85 glycogen synthase kinase 3 beta Mus musculus 43-48 21456066-4 2011 METHODS: In this study, we used three GSK-3 inhibitors, LiCl, TDZD-8, and L803-mts, which are structurally unrelated and non-ATP competitive. Lithium Chloride 56-60 glycogen synthase kinase 3 beta Mus musculus 38-43 21456066-4 2011 METHODS: In this study, we used three GSK-3 inhibitors, LiCl, TDZD-8, and L803-mts, which are structurally unrelated and non-ATP competitive. Adenosine Triphosphate 125-128 glycogen synthase kinase 3 beta Mus musculus 38-43 21426409-5 2011 Additionally, 5,7-DMF increased cAMP levels, which activates a cascade of reactions, such as cAMP responsive element-binding protein and Akt/glycogen synthase kinase-3beta (GSK-3beta) signalling. 5,7-dimethoxyflavone 14-21 glycogen synthase kinase 3 beta Mus musculus 141-171 21143191-9 2011 In conclusion, we show for the first time that the myocardial protection afforded by rIPC is mediated via the PI3K/Akt/GSK3beta signalling pathway, activation of which is associated with nuclear accumulation of beta-catenin and the up-regulation of its downstream targets E-cadherin and PPARdelta involved in cell survival. ripc 85-89 glycogen synthase kinase 3 beta Mus musculus 119-127 21435383-5 2011 Meanwhile, VPA treatment markedly reduced the activities of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase 3beta (GSK3beta), two protein kinases involved in abnormal hyperphosphorylation of tau. Valproic Acid 11-14 glycogen synthase kinase 3 beta Mus musculus 97-127 21435383-5 2011 Meanwhile, VPA treatment markedly reduced the activities of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase 3beta (GSK3beta), two protein kinases involved in abnormal hyperphosphorylation of tau. Valproic Acid 11-14 glycogen synthase kinase 3 beta Mus musculus 129-137 21426409-5 2011 Additionally, 5,7-DMF increased cAMP levels, which activates a cascade of reactions, such as cAMP responsive element-binding protein and Akt/glycogen synthase kinase-3beta (GSK-3beta) signalling. 5,7-dimethoxyflavone 14-21 glycogen synthase kinase 3 beta Mus musculus 173-182 21426409-5 2011 Additionally, 5,7-DMF increased cAMP levels, which activates a cascade of reactions, such as cAMP responsive element-binding protein and Akt/glycogen synthase kinase-3beta (GSK-3beta) signalling. Cyclic AMP 32-36 glycogen synthase kinase 3 beta Mus musculus 141-171 21426409-5 2011 Additionally, 5,7-DMF increased cAMP levels, which activates a cascade of reactions, such as cAMP responsive element-binding protein and Akt/glycogen synthase kinase-3beta (GSK-3beta) signalling. Cyclic AMP 32-36 glycogen synthase kinase 3 beta Mus musculus 173-182 20567953-7 2011 Furthermore, pyrithiamine decreased the phosphorylation rates of glycogen synthase kinase (GSK)-3beta and raised its enzymatic activity, but had little influence on GSK-3alpha. Pyrithiamine 13-25 glycogen synthase kinase 3 beta Mus musculus 65-101 21493770-4 2011 PKB/SGK serine phosphorylation sites in GSK3 were mutated to alanine to create gsk3(KI) mice resistant to PKB/SGK inactivation. Serine 8-14 glycogen synthase kinase 3 beta Mus musculus 40-44 21493770-5 2011 Compared with wildtype animals, gsk3(KI) animals exhibited greater urinary phosphate and calcium clearances with higher excretion rates and lower plasma concentrations. Phosphates 75-84 glycogen synthase kinase 3 beta Mus musculus 32-36 21493770-5 2011 Compared with wildtype animals, gsk3(KI) animals exhibited greater urinary phosphate and calcium clearances with higher excretion rates and lower plasma concentrations. Calcium 89-96 glycogen synthase kinase 3 beta Mus musculus 32-36 21493770-6 2011 Isolated brush border membranes from gsk3(KI) mice showed less sodium-dependent phosphate transport and Na-phosphate co-transporter expression. Sodium 63-69 glycogen synthase kinase 3 beta Mus musculus 37-41 21493770-6 2011 Isolated brush border membranes from gsk3(KI) mice showed less sodium-dependent phosphate transport and Na-phosphate co-transporter expression. Phosphates 80-89 glycogen synthase kinase 3 beta Mus musculus 37-41 21493770-7 2011 Parathyroid hormone, 1,25-OH vitamin D levels, and bone mineral density were decreased in gsk3(KI) mice, suggesting a global dysregulation of bone mineral metabolism. 1,25-dihydroxyvitamin D 21-38 glycogen synthase kinase 3 beta Mus musculus 90-94 21493770-8 2011 Taken together, PKB/SGK phosphorylation of GSK3 increases phosphate transporter activity and reduces renal calcium and phosphate loss. Calcium 107-114 glycogen synthase kinase 3 beta Mus musculus 43-47 21493770-8 2011 Taken together, PKB/SGK phosphorylation of GSK3 increases phosphate transporter activity and reduces renal calcium and phosphate loss. Phosphates 58-67 glycogen synthase kinase 3 beta Mus musculus 43-47 21499833-0 2011 Lysophosphatidic acid induces neurite retraction in differentiated neuroblastoma cells via GSK-3beta activation. lysophosphatidic acid 0-21 glycogen synthase kinase 3 beta Mus musculus 91-100 21499833-6 2011 The LPA-induced neurite retraction and tau phosphorylation in differentiated Neuro2a cells were significantly abolished by the glycogen synthase kinase-3beta (GSK-3beta) inhibitor lithium chloride. lysophosphatidic acid 4-7 glycogen synthase kinase 3 beta Mus musculus 127-157 21499833-6 2011 The LPA-induced neurite retraction and tau phosphorylation in differentiated Neuro2a cells were significantly abolished by the glycogen synthase kinase-3beta (GSK-3beta) inhibitor lithium chloride. lysophosphatidic acid 4-7 glycogen synthase kinase 3 beta Mus musculus 159-168 21499833-6 2011 The LPA-induced neurite retraction and tau phosphorylation in differentiated Neuro2a cells were significantly abolished by the glycogen synthase kinase-3beta (GSK-3beta) inhibitor lithium chloride. Lithium Chloride 180-196 glycogen synthase kinase 3 beta Mus musculus 127-157 21499833-6 2011 The LPA-induced neurite retraction and tau phosphorylation in differentiated Neuro2a cells were significantly abolished by the glycogen synthase kinase-3beta (GSK-3beta) inhibitor lithium chloride. Lithium Chloride 180-196 glycogen synthase kinase 3 beta Mus musculus 159-168 21499833-9 2011 Taken together, these results suggest that GSK-3beta and PKA, rather than CREB, play important roles in tau phosphorylation and neurite retraction in LPA-stimulated differentiated Neuro2a cells. lysophosphatidic acid 150-153 glycogen synthase kinase 3 beta Mus musculus 43-52 21398658-6 2011 To confirm the effect of GSK3 activity on the efficacy of DSB repair, we further demonstrated that biochemical or genetic inhibition of GSK3 activity resulted in enhanced capacity in nonhomologous end-joining-mediated repair of DSBs in hippocampal neurons. 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione 58-61 glycogen synthase kinase 3 beta Mus musculus 25-29 21372039-6 2011 EGCG inhibited the phosphorylation of the IGF-1R, ERK (extracellular signal-regulated kinase), Akt, GSK-3beta (glycogen synthase kinase-3beta), Stat3, and JNK (c-Jun NH(2)-terminal kinase) proteins in the livers of experimental mice. epigallocatechin gallate 0-4 glycogen synthase kinase 3 beta Mus musculus 100-109 21398658-6 2011 To confirm the effect of GSK3 activity on the efficacy of DSB repair, we further demonstrated that biochemical or genetic inhibition of GSK3 activity resulted in enhanced capacity in nonhomologous end-joining-mediated repair of DSBs in hippocampal neurons. 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione 58-61 glycogen synthase kinase 3 beta Mus musculus 136-140 21398658-6 2011 To confirm the effect of GSK3 activity on the efficacy of DSB repair, we further demonstrated that biochemical or genetic inhibition of GSK3 activity resulted in enhanced capacity in nonhomologous end-joining-mediated repair of DSBs in hippocampal neurons. 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione 228-232 glycogen synthase kinase 3 beta Mus musculus 25-29 21398658-6 2011 To confirm the effect of GSK3 activity on the efficacy of DSB repair, we further demonstrated that biochemical or genetic inhibition of GSK3 activity resulted in enhanced capacity in nonhomologous end-joining-mediated repair of DSBs in hippocampal neurons. 1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione 228-232 glycogen synthase kinase 3 beta Mus musculus 136-140 21541314-0 2011 Glucose and fatty acids synergize to promote B-cell apoptosis through activation of glycogen synthase kinase 3beta independent of JNK activation. Glucose 0-7 glycogen synthase kinase 3 beta Mus musculus 84-114 21541314-0 2011 Glucose and fatty acids synergize to promote B-cell apoptosis through activation of glycogen synthase kinase 3beta independent of JNK activation. Fatty Acids 12-23 glycogen synthase kinase 3 beta Mus musculus 84-114 21541314-9 2011 CONCLUSIONS/SIGNIFICANCE: Glucose in the presence of FFA results in synergistic effects on ER stress, impaired insulin receptor substrate signaling and Gsk3beta activation. Glucose 26-33 glycogen synthase kinase 3 beta Mus musculus 152-160 21385899-4 2011 In RKTG-null mouse embryonic fibroblasts, lypophosphatidic acid (LPA), but not EGF (epidermal growth factor), could stimulate hyperphosphorylation of AKT and GSK3beta, accompanied by increases in phosphorylation of p53 at Ser15 and accumulation of p53, as well as its target genes p21 and p16. lypophosphatidic acid 42-63 glycogen synthase kinase 3 beta Mus musculus 158-166 21385899-4 2011 In RKTG-null mouse embryonic fibroblasts, lypophosphatidic acid (LPA), but not EGF (epidermal growth factor), could stimulate hyperphosphorylation of AKT and GSK3beta, accompanied by increases in phosphorylation of p53 at Ser15 and accumulation of p53, as well as its target genes p21 and p16. lpa 65-68 glycogen synthase kinase 3 beta Mus musculus 158-166 21385899-7 2011 In p53-mutated A431 epithelial carcinoma cells, knockdown of RKTG led to enhancement of LPA-stimulated AKT and GSK3beta phosphorylation, together with increased accumulation of beta-catenin and appearance of EMT features that were antagonized by p53 overexpression. lpa 88-91 glycogen synthase kinase 3 beta Mus musculus 111-119 21482799-7 2011 Rather, the activity of glycogen synthase kinase-3beta, a major tau kinase, was found increased, with decreased phosphorylation of Ser-9, a putative cyclin-dependent kinase 5 (CDK5) target. Serine 131-134 glycogen synthase kinase 3 beta Mus musculus 24-54 21233250-11 2011 CONCLUSIONS: We propose that the preconditioning signalling pathway involving an amplification loop results in a downregulation of GSK-3beta and a constant opening of mitoK(ATP) with ROS generation to activate the mTOR pathway and induce cardioprotection. Reactive Oxygen Species 183-186 glycogen synthase kinase 3 beta Mus musculus 131-140 21319221-3 2011 Our results show that a range of GSK3beta inhibitors (ARA-014418, lithium, indirubin, and L803-mt) increase OPs and OLs and promote myelination. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 54-64 glycogen synthase kinase 3 beta Mus musculus 33-41 21319221-3 2011 Our results show that a range of GSK3beta inhibitors (ARA-014418, lithium, indirubin, and L803-mt) increase OPs and OLs and promote myelination. Lithium 66-73 glycogen synthase kinase 3 beta Mus musculus 33-41 21319221-8 2011 We identify that two mechanisms of GSK3beta inhibition are to stimulate cAMP response element binding (CREB) and decrease Notch1 signaling, which positively and negatively regulate OL differentiation and myelination, respectively. Cyclic AMP 72-76 glycogen synthase kinase 3 beta Mus musculus 35-43 21372039-6 2011 EGCG inhibited the phosphorylation of the IGF-1R, ERK (extracellular signal-regulated kinase), Akt, GSK-3beta (glycogen synthase kinase-3beta), Stat3, and JNK (c-Jun NH(2)-terminal kinase) proteins in the livers of experimental mice. epigallocatechin gallate 0-4 glycogen synthase kinase 3 beta Mus musculus 111-141 21245377-3 2011 We now show that glycogen synthase kinase 3 (GSK-3) phosphorylates a group of Ser residues in the Neh6 domain of mouse Nrf2 that overlap with an SCF/beta-TrCP destruction motif (DSGIS, residues 334 to 338) and promotes its degradation in a Keap1-independent manner. Serine 78-81 glycogen synthase kinase 3 beta Mus musculus 17-43 21210815-0 2011 Glycogen synthase kinase-3 inhibition reduces ischemic cerebral damage, restores impaired mitochondrial biogenesis and prevents ROS production. Reactive Oxygen Species 128-131 glycogen synthase kinase 3 beta Mus musculus 0-26 21210815-3 2011 The glycogen synthase kinase-3 (GSK-3) inhibitor SB216763 activated an efficient mitochondrial biogenesis program in control cortical neurons and counteracted the OGD-mediated mitochondrial biogenesis impairment. SB 216763 49-57 glycogen synthase kinase 3 beta Mus musculus 4-30 21210815-3 2011 The glycogen synthase kinase-3 (GSK-3) inhibitor SB216763 activated an efficient mitochondrial biogenesis program in control cortical neurons and counteracted the OGD-mediated mitochondrial biogenesis impairment. SB 216763 49-57 glycogen synthase kinase 3 beta Mus musculus 32-37 21210815-5 2011 The in vitro effects of SB216763 were mimicked by two other structurally unrelated GSK-3 inhibitors. SB 216763 24-32 glycogen synthase kinase 3 beta Mus musculus 83-88 21210815-8 2011 We conclude that GSK-3 inhibition by SB216763 might pave the way of novel promising therapies aimed at stimulating the renewal of functional mitochondria and reducing reactive oxygen species-mediated damage in ischemic stroke. SB 216763 37-45 glycogen synthase kinase 3 beta Mus musculus 17-22 21210815-8 2011 We conclude that GSK-3 inhibition by SB216763 might pave the way of novel promising therapies aimed at stimulating the renewal of functional mitochondria and reducing reactive oxygen species-mediated damage in ischemic stroke. Reactive Oxygen Species 167-190 glycogen synthase kinase 3 beta Mus musculus 17-22 21245377-3 2011 We now show that glycogen synthase kinase 3 (GSK-3) phosphorylates a group of Ser residues in the Neh6 domain of mouse Nrf2 that overlap with an SCF/beta-TrCP destruction motif (DSGIS, residues 334 to 338) and promotes its degradation in a Keap1-independent manner. Serine 78-81 glycogen synthase kinase 3 beta Mus musculus 45-50 21175620-4 2011 Lithium, an inhibitor of GSK3 and IMPase, reduces the accumulation of mitochondrial ATP synthase subunit c and autofluorescence in CbCln3(Deltaex7/8/Deltaex7/8) cells, and mitigates the abnormal subcellular distribution of acidic vesicles in the cells. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 25-29 21123822-7 2011 Our primary goal of this study was to evaluate a GSK3beta inhibitor (6-bromoindirubin-3"-oxime BIO) for amelioration of bone destruction in a murine model of MBD. 6-bromoindirubin-3'-oxime 69-94 glycogen synthase kinase 3 beta Mus musculus 49-57 20932949-8 2011 Additionally, in MC3T3-E1 cells, lithium attenuates BMP-2-induced osteogenic differentiation through GSK3 inhibition; while in C2C12 cells, these negative effects of lithium ions on BMP-2 signaling do not rely on GSK3 inhibition or activation of canonical WNT signaling. Lithium 33-40 glycogen synthase kinase 3 beta Mus musculus 213-217 20932949-9 2011 Our work suggests the presence of a novel GSK3/WNT-independent mechanism of lithium action during the early stages of osteogenic differentiation. Lithium 76-83 glycogen synthase kinase 3 beta Mus musculus 42-46 20705523-1 2011 UNLABELLED: We investigated the antinociceptive effects of AR-A014418, a selective inhibitor of glycogen synthase kinase-3beta (GSK-3beta) in mice. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 59-69 glycogen synthase kinase 3 beta Mus musculus 96-126 20705523-1 2011 UNLABELLED: We investigated the antinociceptive effects of AR-A014418, a selective inhibitor of glycogen synthase kinase-3beta (GSK-3beta) in mice. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 59-69 glycogen synthase kinase 3 beta Mus musculus 128-137 20705523-7 2011 In addition, a 30-minute pretreatment with NP031115 (3 and 10 mg/kg, ip), a different GSK-3 beta inhibitor, also attenuated the late phase of formalin-induced nociception. np031115 43-51 glycogen synthase kinase 3 beta Mus musculus 86-96 20705523-7 2011 In addition, a 30-minute pretreatment with NP031115 (3 and 10 mg/kg, ip), a different GSK-3 beta inhibitor, also attenuated the late phase of formalin-induced nociception. Formaldehyde 142-150 glycogen synthase kinase 3 beta Mus musculus 86-96 20932949-0 2011 Lithium chloride attenuates BMP-2 signaling and inhibits osteogenic differentiation through a novel WNT/GSK3- independent mechanism. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 104-108 20932949-1 2011 Lithium inhibition of glycogen synthase kinase3 (GSK3) activity has been shown to mimic the canonical WNT signaling. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 22-47 20932949-1 2011 Lithium inhibition of glycogen synthase kinase3 (GSK3) activity has been shown to mimic the canonical WNT signaling. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 49-53 20932949-2 2011 Analogous to WNT, lithium prevents GSK3-mediated phosphorylation of cytosolic transcription factor beta-catenin and its subsequent degradation by the proteasome complex. Lithium 18-25 glycogen synthase kinase 3 beta Mus musculus 35-39 20932949-8 2011 Additionally, in MC3T3-E1 cells, lithium attenuates BMP-2-induced osteogenic differentiation through GSK3 inhibition; while in C2C12 cells, these negative effects of lithium ions on BMP-2 signaling do not rely on GSK3 inhibition or activation of canonical WNT signaling. Lithium 33-40 glycogen synthase kinase 3 beta Mus musculus 101-105 21601837-4 2011 Induction of DC maturation using GM-CSF, IL-4 and TNF-alpha resulted in GSK-3beta inhibition, as reflected by increased phosphorylation of Serine 9 on the kinase, and concomitant stabilization of its substrate, beta-catenin. Serine 139-145 glycogen synthase kinase 3 beta Mus musculus 72-81 21705841-7 2011 Berberine also depressed the increasing of phosphorylated GSK-3beta in diabetic mice. Berberine 0-9 glycogen synthase kinase 3 beta Mus musculus 58-67 22216166-4 2011 In an effort to uncouple the reorganizations, we have used taxol, nocodazole, and the specific GSK3-beta inhibitor DW12, to disrupt the dynamic microtubule network of differentiating cultures of the mouse skeletal muscle cell line C2. DW12 115-119 glycogen synthase kinase 3 beta Mus musculus 95-104 21321389-6 2011 Cotinine stimulated Akt signaling, including the inhibition of glycogen synthase kinase 3beta (GSK3beta), which promotes neuronal survival and the synaptic plasticity processes underlying learning and memory in the hippocampus and cortex of wild type and Tg6799 AD mice. Cotinine 0-8 glycogen synthase kinase 3 beta Mus musculus 63-93 20680007-2 2011 Aside from the long-recognized role in insulin signal transduction and glycogen biosynthesis, GSK3beta has been recently coined as a master control molecule in nuclear factor-kappaB activation and inflammatory kidney injury. Glycogen 71-79 glycogen synthase kinase 3 beta Mus musculus 94-102 20732383-5 2011 Lithium Chloride (LiCl), which is an inhibitor of GSK3beta, markedly reduced the TNF-alpha-stimulated IL-6 release, similar to the results with Wnt3a. Lithium Chloride 0-16 glycogen synthase kinase 3 beta Mus musculus 50-58 20732383-5 2011 Lithium Chloride (LiCl), which is an inhibitor of GSK3beta, markedly reduced the TNF-alpha-stimulated IL-6 release, similar to the results with Wnt3a. Lithium Chloride 18-22 glycogen synthase kinase 3 beta Mus musculus 50-58 21393344-3 2011 Use of lithium chloride in murine models suppressed carcinoid cell growth, reduced GSK-3beta levels, and reduced expression of chromogranin A. Lithium Chloride 7-23 glycogen synthase kinase 3 beta Mus musculus 83-92 22180358-3 2011 Here, we report that RSV stimulates glucose uptake and potentiates insulin signaling in Neuro-2A (N2A) cells, which is characterized by the increased phosphorylation of protein kinase B (Akt) and glycogen synthase kinase-3beta (GSK-3beta). Resveratrol 21-24 glycogen synthase kinase 3 beta Mus musculus 196-226 22180358-3 2011 Here, we report that RSV stimulates glucose uptake and potentiates insulin signaling in Neuro-2A (N2A) cells, which is characterized by the increased phosphorylation of protein kinase B (Akt) and glycogen synthase kinase-3beta (GSK-3beta). Resveratrol 21-24 glycogen synthase kinase 3 beta Mus musculus 228-237 22180358-4 2011 Furthermore, RSV activates AMPK in N2A cells, which can be prevented using a specific pharmacological inhibitor, Compound C. Compound C abrogates RSV-induced Akt and GSK-3beta phosphorylation and glucose uptake. Resveratrol 13-16 glycogen synthase kinase 3 beta Mus musculus 166-175 22180358-4 2011 Furthermore, RSV activates AMPK in N2A cells, which can be prevented using a specific pharmacological inhibitor, Compound C. Compound C abrogates RSV-induced Akt and GSK-3beta phosphorylation and glucose uptake. Resveratrol 146-149 glycogen synthase kinase 3 beta Mus musculus 166-175 22022450-5 2011 HDAC6 in particular was found to be critical for tolerance induction, as its deacetylation of acetyl-tubulin was increased during LPS tolerance, this was enhanced by inhibition of GSK3, and the HDAC6 inhibitor tubacin completely blocked tolerance and the promotion of tolerance by inhibition of GSK3. tubacin 210-217 glycogen synthase kinase 3 beta Mus musculus 180-184 21966423-6 2011 Interventions affecting the NF-kappaB pathway are promising clinical therapeutics, thus we further examined the effect of IKK-2 inhibition by MLN120B and glycogen synthase kinase 3 beta inhibition by TDZD-8 on NF-kappaB activation. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 200-206 glycogen synthase kinase 3 beta Mus musculus 154-185 22022450-5 2011 HDAC6 in particular was found to be critical for tolerance induction, as its deacetylation of acetyl-tubulin was increased during LPS tolerance, this was enhanced by inhibition of GSK3, and the HDAC6 inhibitor tubacin completely blocked tolerance and the promotion of tolerance by inhibition of GSK3. tubacin 210-217 glycogen synthase kinase 3 beta Mus musculus 295-299 21047779-4 2010 Treatment of wild-type embryonic stem cells and neural stem cells with the Gsk-3 inhibitor, lithium, phenocopies the DNA hypomethylation at these imprinted loci. Lithium 92-99 glycogen synthase kinase 3 beta Mus musculus 75-80 21887357-4 2011 Inhibition occurs in a dose-dependent manner and is attenuated after treatment with the GSK3beta antagonist SB21673. 3-hydroxypyrazine-2-carboxylic acid 108-115 glycogen synthase kinase 3 beta Mus musculus 88-96 20940307-5 2010 Moreover, treatment of MEFs with LiCl, an inhibitor of GSK3beta and CK2, only partially suppresses the phosphorylation, suggesting Plk3 as an additional kinase that phosphorylates these sites in vivo. Lithium Chloride 33-37 glycogen synthase kinase 3 beta Mus musculus 55-63 20816918-14 2010 These results suggest that the modulation of GSK3beta activity by valproate may be useful and may play a role in the prevention of morphine tolerance. Morphine 131-139 glycogen synthase kinase 3 beta Mus musculus 45-53 20959465-9 2010 In addition to beta-arrestin1-dependent EGFR activation, butaprost increased PKA activation, as measured by phospho-GSK3beta (p-GSK3beta) and p-cAMP-response element-binding protein formation. butaprost 57-66 glycogen synthase kinase 3 beta Mus musculus 116-124 20959465-9 2010 In addition to beta-arrestin1-dependent EGFR activation, butaprost increased PKA activation, as measured by phospho-GSK3beta (p-GSK3beta) and p-cAMP-response element-binding protein formation. butaprost 57-66 glycogen synthase kinase 3 beta Mus musculus 128-136 20872791-0 2010 Glycogen synthase kinase-3beta indirectly facilitates interferon-gamma-induced nuclear factor-kappaB activation and nitric oxide biosynthesis. Nitric Oxide 116-128 glycogen synthase kinase 3 beta Mus musculus 0-30 21145457-2 2010 We now report that IP7 is a physiologic inhibitor of Akt, a serine/threonine kinase that regulates glucose homeostasis and protein translation, respectively, via the GSK3beta and mTOR pathways. ip7 19-22 glycogen synthase kinase 3 beta Mus musculus 166-174 21092141-4 2010 We recently reported that mouse c-Myb protein is controlled by ubiquitin-dependent degradation by SCF-Fbw7 E3 ligase via glycogen synthase kinase 3 (GSK3)-mediated phosphorylation of Thr-572 in a Cdc4 phosphodegron (CPD)-dependent manner. Threonine 183-186 glycogen synthase kinase 3 beta Mus musculus 121-147 21092141-4 2010 We recently reported that mouse c-Myb protein is controlled by ubiquitin-dependent degradation by SCF-Fbw7 E3 ligase via glycogen synthase kinase 3 (GSK3)-mediated phosphorylation of Thr-572 in a Cdc4 phosphodegron (CPD)-dependent manner. Threonine 183-186 glycogen synthase kinase 3 beta Mus musculus 149-153 21194439-12 2010 However, GSK-3beta inactivation inhibited transactivation activity of p65 by deacetylating p65 at lysine 310. Lysine 98-104 glycogen synthase kinase 3 beta Mus musculus 9-18 21189866-9 2010 The down-regulation of Gsk3beta in moderate selenium-deficiency observed in the previous paper provides a possible explanation for the activation of the Nrf2 pathway, because inhibition of GSK3beta results in the nuclear accumulation of Nrf2. Selenium 44-52 glycogen synthase kinase 3 beta Mus musculus 23-31 21189866-9 2010 The down-regulation of Gsk3beta in moderate selenium-deficiency observed in the previous paper provides a possible explanation for the activation of the Nrf2 pathway, because inhibition of GSK3beta results in the nuclear accumulation of Nrf2. Selenium 44-52 glycogen synthase kinase 3 beta Mus musculus 189-197 19818092-7 2010 The activation of glycogen synthase kinase 3b (GSK-3b) was associated with morphine tolerance, because an inhibitor of GSK-3beta prevented it. Morphine 75-83 glycogen synthase kinase 3 beta Mus musculus 18-45 19818092-7 2010 The activation of glycogen synthase kinase 3b (GSK-3b) was associated with morphine tolerance, because an inhibitor of GSK-3beta prevented it. Morphine 75-83 glycogen synthase kinase 3 beta Mus musculus 47-53 19818092-7 2010 The activation of glycogen synthase kinase 3b (GSK-3b) was associated with morphine tolerance, because an inhibitor of GSK-3beta prevented it. Morphine 75-83 glycogen synthase kinase 3 beta Mus musculus 119-128 20828853-10 2010 In addition, adiponectin, but not UCP2, promoted the activation of glycogen synthase kinase 3beta (GSK3beta), a key molecule involved in regulating glycogen homeostasis. Glycogen 67-75 glycogen synthase kinase 3 beta Mus musculus 99-107 20828853-11 2010 CONCLUSIONS: Rosiglitazone elicits its protective functions against NAFLD largely through the induction of adiponectin, which prevents mitochondria stresses by promoting GSK3beta activation and UCP2 upregulation, two pathways coordinating the glucose and lipid metabolism in liver. Rosiglitazone 13-26 glycogen synthase kinase 3 beta Mus musculus 170-178 20816918-6 2010 Chronic morphine treatment activates glycogen synthase kinase 3beta (GSK3beta), whose inhibition diminishes morphine tolerance. Morphine 8-16 glycogen synthase kinase 3 beta Mus musculus 37-67 20816918-6 2010 Chronic morphine treatment activates glycogen synthase kinase 3beta (GSK3beta), whose inhibition diminishes morphine tolerance. Morphine 8-16 glycogen synthase kinase 3 beta Mus musculus 69-77 20816918-6 2010 Chronic morphine treatment activates glycogen synthase kinase 3beta (GSK3beta), whose inhibition diminishes morphine tolerance. Morphine 108-116 glycogen synthase kinase 3 beta Mus musculus 37-67 20600866-4 2010 Therefore, we examined if the serine phosphorylation of GSK3 in Fmr1 knockout mice also was altered outside the brain and if administration of lithium ameliorated the macroorchidism phenotype. Serine 30-36 glycogen synthase kinase 3 beta Mus musculus 56-60 20816918-6 2010 Chronic morphine treatment activates glycogen synthase kinase 3beta (GSK3beta), whose inhibition diminishes morphine tolerance. Morphine 108-116 glycogen synthase kinase 3 beta Mus musculus 69-77 20816918-8 2010 Although the activation of GABAergic neurons may be responsible for the chief pharmacologic effect of valproate, recent studies have shown that valproate also suppresses GSK3beta activity. Valproic Acid 144-153 glycogen synthase kinase 3 beta Mus musculus 170-178 20816918-12 2010 While mice treated with morphine developed tolerance, co-administration of valproate attenuated the development of tolerance and impaired the activation of GSK3beta in mice brains. Valproic Acid 75-84 glycogen synthase kinase 3 beta Mus musculus 156-164 20816918-14 2010 These results suggest that the modulation of GSK3beta activity by valproate may be useful and may play a role in the prevention of morphine tolerance. Valproic Acid 66-75 glycogen synthase kinase 3 beta Mus musculus 45-53 21079728-1 2010 BACKGROUND: Thiadiazolidinones (TDZD) are small heterocyclic compounds first described as non-ATP competitive inhibitors of glycogen synthase kinase 3beta (GSK-3beta). thiadiazolidinones 12-30 glycogen synthase kinase 3 beta Mus musculus 124-154 21079728-1 2010 BACKGROUND: Thiadiazolidinones (TDZD) are small heterocyclic compounds first described as non-ATP competitive inhibitors of glycogen synthase kinase 3beta (GSK-3beta). thiadiazolidinones 12-30 glycogen synthase kinase 3 beta Mus musculus 156-165 21079728-1 2010 BACKGROUND: Thiadiazolidinones (TDZD) are small heterocyclic compounds first described as non-ATP competitive inhibitors of glycogen synthase kinase 3beta (GSK-3beta). tdzd 32-36 glycogen synthase kinase 3 beta Mus musculus 124-154 21079728-1 2010 BACKGROUND: Thiadiazolidinones (TDZD) are small heterocyclic compounds first described as non-ATP competitive inhibitors of glycogen synthase kinase 3beta (GSK-3beta). tdzd 32-36 glycogen synthase kinase 3 beta Mus musculus 156-165 21079728-1 2010 BACKGROUND: Thiadiazolidinones (TDZD) are small heterocyclic compounds first described as non-ATP competitive inhibitors of glycogen synthase kinase 3beta (GSK-3beta). Adenosine Triphosphate 94-97 glycogen synthase kinase 3 beta Mus musculus 124-154 21079728-1 2010 BACKGROUND: Thiadiazolidinones (TDZD) are small heterocyclic compounds first described as non-ATP competitive inhibitors of glycogen synthase kinase 3beta (GSK-3beta). Adenosine Triphosphate 94-97 glycogen synthase kinase 3 beta Mus musculus 156-165 21079728-5 2010 Also, we observed a sustained activation of the ERK pathway, a concomitant phosphorylation and activation of ribosomal S6 kinase (p90RSK) and an inactivation of GSK-3beta by phosphorylation at Ser 9. Serine 193-196 glycogen synthase kinase 3 beta Mus musculus 161-170 20600866-3 2010 The inhibitory serine phosphorylation of glycogen synthase kinase-3 (GSK3) is lower in brain regions of Fmr1 knockout mice than wild-type mice and the GSK3 inhibitor lithium rescues several behavioral impairments in Fmr1 knockout mice. Lithium 166-173 glycogen synthase kinase 3 beta Mus musculus 151-155 20600866-3 2010 The inhibitory serine phosphorylation of glycogen synthase kinase-3 (GSK3) is lower in brain regions of Fmr1 knockout mice than wild-type mice and the GSK3 inhibitor lithium rescues several behavioral impairments in Fmr1 knockout mice. Serine 15-21 glycogen synthase kinase 3 beta Mus musculus 41-67 20600866-3 2010 The inhibitory serine phosphorylation of glycogen synthase kinase-3 (GSK3) is lower in brain regions of Fmr1 knockout mice than wild-type mice and the GSK3 inhibitor lithium rescues several behavioral impairments in Fmr1 knockout mice. Serine 15-21 glycogen synthase kinase 3 beta Mus musculus 69-73 20600866-3 2010 The inhibitory serine phosphorylation of glycogen synthase kinase-3 (GSK3) is lower in brain regions of Fmr1 knockout mice than wild-type mice and the GSK3 inhibitor lithium rescues several behavioral impairments in Fmr1 knockout mice. Serine 15-21 glycogen synthase kinase 3 beta Mus musculus 151-155 20600866-3 2010 The inhibitory serine phosphorylation of glycogen synthase kinase-3 (GSK3) is lower in brain regions of Fmr1 knockout mice than wild-type mice and the GSK3 inhibitor lithium rescues several behavioral impairments in Fmr1 knockout mice. Lithium 166-173 glycogen synthase kinase 3 beta Mus musculus 41-67 20600866-3 2010 The inhibitory serine phosphorylation of glycogen synthase kinase-3 (GSK3) is lower in brain regions of Fmr1 knockout mice than wild-type mice and the GSK3 inhibitor lithium rescues several behavioral impairments in Fmr1 knockout mice. Lithium 166-173 glycogen synthase kinase 3 beta Mus musculus 69-73 20600866-6 2010 The inhibitory serine phosphorylation of GSK3 was significantly lower in the testis and liver of Fmr1 knockout mice than wild-type mice, and chronic lithium treatment reduced macroorchidism in Fmr1 knockout mice. Serine 15-21 glycogen synthase kinase 3 beta Mus musculus 41-45 20600866-6 2010 The inhibitory serine phosphorylation of GSK3 was significantly lower in the testis and liver of Fmr1 knockout mice than wild-type mice, and chronic lithium treatment reduced macroorchidism in Fmr1 knockout mice. Lithium 149-156 glycogen synthase kinase 3 beta Mus musculus 41-45 20600866-9 2010 These results provide further evidence of the involvement of dysregulated GSK3 in FXS, and demonstrate that lithium administration reduces macroorchidism and reactive astrocytes in Fmr1 knockout mice. Lithium 108-115 glycogen synthase kinase 3 beta Mus musculus 74-78 20807318-8 2010 Decrease in GSK3 activity demonstrated by increased phosphorylation of GSK3alpha and GSK3beta was detected 20 mins after an acute cocaine injection. Cocaine 130-137 glycogen synthase kinase 3 beta Mus musculus 12-16 20848477-11 2010 In vivo blockade of GSK3-beta resulted in a shift from NF-kappaB activity toward CREB activity in murine MLC and LPMC. lpmc 113-117 glycogen synthase kinase 3 beta Mus musculus 20-29 20807318-8 2010 Decrease in GSK3 activity demonstrated by increased phosphorylation of GSK3alpha and GSK3beta was detected 20 mins after an acute cocaine injection. Cocaine 130-137 glycogen synthase kinase 3 beta Mus musculus 85-93 20807318-10 2010 SB 222200 prior to repeated cocaine resulted in increased phosphorylation of GSK3alpha and GSK3beta akin to changes following acute cocaine. SB 222200 0-9 glycogen synthase kinase 3 beta Mus musculus 91-99 20976192-8 2010 CONCLUSIONS/SIGNIFICANCE: These findings suggest that DGKbeta KO mice exhibit lithium-sensitive behavioral abnormalities that are, at least in part, due to the impairment of Akt-GSK3beta signaling and cortical spine formation. Lithium 78-85 glycogen synthase kinase 3 beta Mus musculus 178-186 20600172-5 2010 Morphine decreased the levels of microglia phosphorylated Akt (p-Akt) and p-GSK-3beta (glycogen synthase kinase-3 beta) in an opioid-receptor dependent manner. Morphine 0-8 glycogen synthase kinase 3 beta Mus musculus 76-85 20600172-5 2010 Morphine decreased the levels of microglia phosphorylated Akt (p-Akt) and p-GSK-3beta (glycogen synthase kinase-3 beta) in an opioid-receptor dependent manner. Morphine 0-8 glycogen synthase kinase 3 beta Mus musculus 87-118 20600172-6 2010 More interestingly, GSK-3beta inhibitor SB216763 significantly increases morphine-induced apoptosis in both BV-2 microglia and mouse primary microglial cells. SB 216763 40-48 glycogen synthase kinase 3 beta Mus musculus 20-29 20600172-6 2010 More interestingly, GSK-3beta inhibitor SB216763 significantly increases morphine-induced apoptosis in both BV-2 microglia and mouse primary microglial cells. Morphine 73-81 glycogen synthase kinase 3 beta Mus musculus 20-29 20600172-9 2010 Taken together, our data clearly demonstrates that morphine-induced apoptosis in microglial cells, which is mediated via GSK-3beta and p38 MAPK pathways. Morphine 51-59 glycogen synthase kinase 3 beta Mus musculus 121-130 20888430-2 2010 Here we investigated whether lithium chloride (LiCl), an inhibitor of glycogen synthase kinase-3beta (GSK-3beta), could counteract atherosclerosis induced by a high-fat diet in ApoE-/- mice. Lithium Chloride 29-45 glycogen synthase kinase 3 beta Mus musculus 70-100 20888430-2 2010 Here we investigated whether lithium chloride (LiCl), an inhibitor of glycogen synthase kinase-3beta (GSK-3beta), could counteract atherosclerosis induced by a high-fat diet in ApoE-/- mice. Lithium Chloride 29-45 glycogen synthase kinase 3 beta Mus musculus 102-111 20888430-2 2010 Here we investigated whether lithium chloride (LiCl), an inhibitor of glycogen synthase kinase-3beta (GSK-3beta), could counteract atherosclerosis induced by a high-fat diet in ApoE-/- mice. Lithium Chloride 47-51 glycogen synthase kinase 3 beta Mus musculus 70-100 20888430-2 2010 Here we investigated whether lithium chloride (LiCl), an inhibitor of glycogen synthase kinase-3beta (GSK-3beta), could counteract atherosclerosis induced by a high-fat diet in ApoE-/- mice. Lithium Chloride 47-51 glycogen synthase kinase 3 beta Mus musculus 102-111 20724593-11 2010 These findings show that tPA induces Tyr(4507) phosphorylation of LDL receptor-related protein 1, which in turn leads to the downstream phosphorylation of Erk1/2, p90RSK, and GSK3beta, followed by the induction of cyclin D1 in murine interstitial fibroblasts. Tyrosine 37-40 glycogen synthase kinase 3 beta Mus musculus 175-183 20710043-3 2010 We found that MTA1s influences Wnt1 pathway through extracellular signal-regulated kinase (ERK) signaling as selective silencing of the endogenous MTA1s or ERK, or its target glycogen synthase kinase 3beta resulted in a substantial decrease in beta-catenin expression, leading to the inhibition of Wnt1 target genes. mta1s 14-19 glycogen synthase kinase 3 beta Mus musculus 175-205 20637838-8 2010 Sorafenib inhibited the activation of the MAP kinase p38 and its downstream target mitogen and stress activated protein kinase (MSK), and partially inhibited protein kinase B (AKT) and its subsequent inactivation of the downstream target glycogen synthase kinase 3-beta (GSK3-beta). Sorafenib 0-9 glycogen synthase kinase 3 beta Mus musculus 238-269 20637838-8 2010 Sorafenib inhibited the activation of the MAP kinase p38 and its downstream target mitogen and stress activated protein kinase (MSK), and partially inhibited protein kinase B (AKT) and its subsequent inactivation of the downstream target glycogen synthase kinase 3-beta (GSK3-beta). Sorafenib 0-9 glycogen synthase kinase 3 beta Mus musculus 271-280 20552232-7 2010 However, pH/min was significantly larger in gsk3 ( KI ) than in gsk3 ( WT ) mice and pH/min was virtually abolished by the H(+)/K(+)-ATPase inhibitor omeprazole (100 muM) in gastric glands from both gsk3 ( KI ) and gsk3 ( WT ). Omeprazole 152-162 glycogen synthase kinase 3 beta Mus musculus 45-49 20552232-7 2010 However, pH/min was significantly larger in gsk3 ( KI ) than in gsk3 ( WT ) mice and pH/min was virtually abolished by the H(+)/K(+)-ATPase inhibitor omeprazole (100 muM) in gastric glands from both gsk3 ( KI ) and gsk3 ( WT ). Omeprazole 152-162 glycogen synthase kinase 3 beta Mus musculus 65-69 20552232-7 2010 However, pH/min was significantly larger in gsk3 ( KI ) than in gsk3 ( WT ) mice and pH/min was virtually abolished by the H(+)/K(+)-ATPase inhibitor omeprazole (100 muM) in gastric glands from both gsk3 ( KI ) and gsk3 ( WT ). Omeprazole 152-162 glycogen synthase kinase 3 beta Mus musculus 65-69 20552232-7 2010 However, pH/min was significantly larger in gsk3 ( KI ) than in gsk3 ( WT ) mice and pH/min was virtually abolished by the H(+)/K(+)-ATPase inhibitor omeprazole (100 muM) in gastric glands from both gsk3 ( KI ) and gsk3 ( WT ). Omeprazole 152-162 glycogen synthase kinase 3 beta Mus musculus 65-69 20552232-10 2010 The protein kinase A (PKA) inhibitor H89 (150 nM) and the H(2)-receptor antagonist ranitidine (100 muM) decreased pH/min in gsk3 ( KI ) but not gsk3 ( WT ) and again abrogated the differences between the genotypes. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide 37-40 glycogen synthase kinase 3 beta Mus musculus 125-129 20552232-10 2010 The protein kinase A (PKA) inhibitor H89 (150 nM) and the H(2)-receptor antagonist ranitidine (100 muM) decreased pH/min in gsk3 ( KI ) but not gsk3 ( WT ) and again abrogated the differences between the genotypes. Ranitidine 83-93 glycogen synthase kinase 3 beta Mus musculus 125-129 20542495-6 2010 The induction of mitochondrial SOD2 by resveratrol was mediated through the activation of the PI3K/Akt and GSK-3beta/beta-catenin signaling pathways. Resveratrol 39-50 glycogen synthase kinase 3 beta Mus musculus 107-116 20626347-4 2010 RESULTS: Here, we address the effects of GSK3beta inhibitors BIO (6-bromoindirubin-3"-oxime) and CHIR99021 on mESCs (mouse ESCs), focusing on modulation of beta-catenin activities. 6-bromoindirubin-3'-oxime 66-91 glycogen synthase kinase 3 beta Mus musculus 41-49 20690801-4 2010 We provide evidence that cAMP/PKA signalling is involved affecting the GSK-3beta phosphorylation status at phospho-GSK-3beta (Ser9), thereby altering beta-catenin degradation downstream. Cyclic AMP 25-29 glycogen synthase kinase 3 beta Mus musculus 71-80 20690801-4 2010 We provide evidence that cAMP/PKA signalling is involved affecting the GSK-3beta phosphorylation status at phospho-GSK-3beta (Ser9), thereby altering beta-catenin degradation downstream. Cyclic AMP 25-29 glycogen synthase kinase 3 beta Mus musculus 115-124 20522596-6 2010 DIO mice treated with myriocin showed a complete reversal of glucose intolerance and insulin resistance which was associated with enhanced insulin-stimulated Akt and glycogen synthase kinase 3beta phosphorylation. thermozymocidin 22-30 glycogen synthase kinase 3 beta Mus musculus 166-196 20625330-0 2010 Kainic acid-induced seizures activate GSK-3beta in the hippocampus of D2R-/- mice. Kainic Acid 0-11 glycogen synthase kinase 3 beta Mus musculus 38-47 20506162-9 2010 The inhibition of IL-2 production by mAb 9D7 was counteracted by pretreating the cells with LiCl (a GSK-3 inhibitor). Lithium Chloride 92-96 glycogen synthase kinase 3 beta Mus musculus 100-105 20681671-6 2010 Moreover, administration of pterostilbene for 23 weeks significantly suppressed AOM-induced GSK3beta phosphorylation and Wnt/beta-catenin signaling. pterostilbene 28-41 glycogen synthase kinase 3 beta Mus musculus 92-100 20362583-10 2010 Ethanol treatment dampened phosphorylation of Akt and GSK-3beta associated with upregulated PP2A, which was accentuated by ALDH2 KO. Ethanol 0-7 glycogen synthase kinase 3 beta Mus musculus 54-63 20362052-7 2010 Interestingly, stretch and PGE(2) each significantly reduced H(2)O(2)-mediated AKT phosphorylation and was reversed by pretreatment with orthovanadate while stretch alone reduced GSK-3beta inhibitory phosphorylation at ser-9. Prostaglandins E 27-30 glycogen synthase kinase 3 beta Mus musculus 179-188 20362052-7 2010 Interestingly, stretch and PGE(2) each significantly reduced H(2)O(2)-mediated AKT phosphorylation and was reversed by pretreatment with orthovanadate while stretch alone reduced GSK-3beta inhibitory phosphorylation at ser-9. Vanadates 137-150 glycogen synthase kinase 3 beta Mus musculus 179-188 20299330-3 2010 We set out to characterize developmental growth and response to chronic isoproterenol (ISO) stress in knockin (KI) mice lacking the critical N-terminal serines, 21 of GSK-3alpha and 9 of GSK-3beta respectively, required for inactivation by upstream kinases. Isoproterenol 72-85 glycogen synthase kinase 3 beta Mus musculus 187-196 20530674-4 2010 Moreover, we found that Dex-induced destabilization of Nmyc is mediated by activation of glycogen synthase kinase 3beta, which targets Nmyc for proteasomal degradation. Dexamethasone 24-27 glycogen synthase kinase 3 beta Mus musculus 89-119 20661723-5 2010 RA treatment of F9 cells also led to a transient and parallel increase in both Akt and glycogen synthase kinase 3beta phosphorylations. Tretinoin 0-2 glycogen synthase kinase 3 beta Mus musculus 87-117 20530871-0 2010 NFAT/Fas signaling mediates the neuronal apoptosis and motor side effects of GSK-3 inhibition in a mouse model of lithium therapy. Lithium 114-121 glycogen synthase kinase 3 beta Mus musculus 77-82 20528914-8 2010 The GSK3beta inhibitor LiCl potentiated LPS-induced Nox1 expression in accordance with beta-catenin accumulation and nuclear translocation. Lithium Chloride 23-27 glycogen synthase kinase 3 beta Mus musculus 4-12 20530871-0 2010 NFAT/Fas signaling mediates the neuronal apoptosis and motor side effects of GSK-3 inhibition in a mouse model of lithium therapy. ammonium ferrous sulfate 5-8 glycogen synthase kinase 3 beta Mus musculus 77-82 20530871-4 2010 Lithium inhibits glycogen synthase kinase-3 (GSK-3) in vivo, and we recently reported neuronal apoptosis and motor deficits in dominant-negative GSK-3-transgenic mice. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 17-43 20530871-4 2010 Lithium inhibits glycogen synthase kinase-3 (GSK-3) in vivo, and we recently reported neuronal apoptosis and motor deficits in dominant-negative GSK-3-transgenic mice. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 45-50 20530871-4 2010 Lithium inhibits glycogen synthase kinase-3 (GSK-3) in vivo, and we recently reported neuronal apoptosis and motor deficits in dominant-negative GSK-3-transgenic mice. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 145-150 20530871-5 2010 We hypothesized that therapeutic levels of lithium could also induce neuronal loss through GSK-3 inhibition. Lithium 43-50 glycogen synthase kinase 3 beta Mus musculus 91-96 20143421-10 2010 These analyses showed that HSB-13 inhibits GSK3, p38 MAPK, and cyclin-dependent kinases (CDKs). 6-amino-2-(3',5'-dibromo-4'-hydroxybenzylidene)-2H-benzo(b)(1,4)oxazin-3-(4H)-one 27-33 glycogen synthase kinase 3 beta Mus musculus 43-47 20143421-11 2010 In comparison, another compound, called ASK-2a, that protects cerebellar granule neurons against low-potassium-induced death inhibits GSK3 and p38 MAPK but not CDKs. Potassium 101-110 glycogen synthase kinase 3 beta Mus musculus 134-138 20472447-4 2010 In this article, we disclose novel ITK inhibitors based on (4 or 5-aryl)pyrazolyl-indole scaffold that were also found to be selective for ITK over other kinases like IRK, CDK2, GSK3ss and PKA. (4 or 5-aryl)pyrazolyl-indole 59-88 glycogen synthase kinase 3 beta Mus musculus 178-182 20357757-2 2010 Because mood stabilizers, antipsychotics, antidepressants, and mood-regulating neuromodulators increase the inhibitory serine-phosphorylation of glycogen synthase kinase-3 (GSK3), we hypothesized that deficient GSK3 serine-phosphorylation may increase vulnerability to mood-related behavioral disturbances. Serine 119-125 glycogen synthase kinase 3 beta Mus musculus 145-171 20357757-2 2010 Because mood stabilizers, antipsychotics, antidepressants, and mood-regulating neuromodulators increase the inhibitory serine-phosphorylation of glycogen synthase kinase-3 (GSK3), we hypothesized that deficient GSK3 serine-phosphorylation may increase vulnerability to mood-related behavioral disturbances. Serine 119-125 glycogen synthase kinase 3 beta Mus musculus 173-177 20357757-2 2010 Because mood stabilizers, antipsychotics, antidepressants, and mood-regulating neuromodulators increase the inhibitory serine-phosphorylation of glycogen synthase kinase-3 (GSK3), we hypothesized that deficient GSK3 serine-phosphorylation may increase vulnerability to mood-related behavioral disturbances. Serine 119-125 glycogen synthase kinase 3 beta Mus musculus 211-215 20357757-2 2010 Because mood stabilizers, antipsychotics, antidepressants, and mood-regulating neuromodulators increase the inhibitory serine-phosphorylation of glycogen synthase kinase-3 (GSK3), we hypothesized that deficient GSK3 serine-phosphorylation may increase vulnerability to mood-related behavioral disturbances. Serine 216-222 glycogen synthase kinase 3 beta Mus musculus 145-171 20357757-2 2010 Because mood stabilizers, antipsychotics, antidepressants, and mood-regulating neuromodulators increase the inhibitory serine-phosphorylation of glycogen synthase kinase-3 (GSK3), we hypothesized that deficient GSK3 serine-phosphorylation may increase vulnerability to mood-related behavioral disturbances. Serine 216-222 glycogen synthase kinase 3 beta Mus musculus 173-177 20357757-4 2010 GSK3 knockin mice displayed increased susceptibility to amphetamine-induced hyperactivity and to stress-induced depressive-like behaviors. Amphetamine 56-67 glycogen synthase kinase 3 beta Mus musculus 0-4 20357757-5 2010 Furthermore, serine-phosphorylation of GSK3 was reduced during both mood-related behavioral responses in wild-type mouse brain and in blood cells from patients with bipolar disorder. Serine 13-19 glycogen synthase kinase 3 beta Mus musculus 39-43 20357757-6 2010 Therefore, proper control of GSK3 by serine-phosphorylation, which is targeted by agents therapeutic for bipolar disorder, is an important mechanism that regulates mood stabilization, and mice with disabled GSK3 serine-phosphorylation may provide a valuable model to study bipolar disorder. Serine 37-43 glycogen synthase kinase 3 beta Mus musculus 29-33 20357757-6 2010 Therefore, proper control of GSK3 by serine-phosphorylation, which is targeted by agents therapeutic for bipolar disorder, is an important mechanism that regulates mood stabilization, and mice with disabled GSK3 serine-phosphorylation may provide a valuable model to study bipolar disorder. Serine 37-43 glycogen synthase kinase 3 beta Mus musculus 207-211 20357757-6 2010 Therefore, proper control of GSK3 by serine-phosphorylation, which is targeted by agents therapeutic for bipolar disorder, is an important mechanism that regulates mood stabilization, and mice with disabled GSK3 serine-phosphorylation may provide a valuable model to study bipolar disorder. Serine 212-218 glycogen synthase kinase 3 beta Mus musculus 29-33 20357757-6 2010 Therefore, proper control of GSK3 by serine-phosphorylation, which is targeted by agents therapeutic for bipolar disorder, is an important mechanism that regulates mood stabilization, and mice with disabled GSK3 serine-phosphorylation may provide a valuable model to study bipolar disorder. Serine 212-218 glycogen synthase kinase 3 beta Mus musculus 207-211 20592205-6 2010 This PPP2R5delta reduction increases the phosphorylation of GSK3beta at serine 9, which inactivates GSK3beta, indicating that PPP2R5delta positively regulates GSK3beta activity in the brain. Serine 72-78 glycogen synthase kinase 3 beta Mus musculus 60-68 20592205-6 2010 This PPP2R5delta reduction increases the phosphorylation of GSK3beta at serine 9, which inactivates GSK3beta, indicating that PPP2R5delta positively regulates GSK3beta activity in the brain. Serine 72-78 glycogen synthase kinase 3 beta Mus musculus 100-108 20592205-6 2010 This PPP2R5delta reduction increases the phosphorylation of GSK3beta at serine 9, which inactivates GSK3beta, indicating that PPP2R5delta positively regulates GSK3beta activity in the brain. Serine 72-78 glycogen synthase kinase 3 beta Mus musculus 100-108 20592205-10 2010 Importantly, both the GSK3 inhibitor 3-(2,4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)1H-pyrrole-2,5-dione (SB216763) and linopirdine reduce PPI when directly infused into the medial prefrontal cortex (mPFC). SB 216763 37-106 glycogen synthase kinase 3 beta Mus musculus 22-26 20592205-10 2010 Importantly, both the GSK3 inhibitor 3-(2,4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)1H-pyrrole-2,5-dione (SB216763) and linopirdine reduce PPI when directly infused into the medial prefrontal cortex (mPFC). SB 216763 108-116 glycogen synthase kinase 3 beta Mus musculus 22-26 20592205-10 2010 Importantly, both the GSK3 inhibitor 3-(2,4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)1H-pyrrole-2,5-dione (SB216763) and linopirdine reduce PPI when directly infused into the medial prefrontal cortex (mPFC). linopirdine 122-133 glycogen synthase kinase 3 beta Mus musculus 22-26 20357757-0 2010 Deficiency in the inhibitory serine-phosphorylation of glycogen synthase kinase-3 increases sensitivity to mood disturbances. Serine 29-35 glycogen synthase kinase 3 beta Mus musculus 55-81 20534514-5 2010 Mice expressing RGS-insensitive G(alpha)i2 also exhibited increased cortical and hippocampal phosphorylation of glycogen synthase kinase-3beta, a constitutively active proapoptotic kinase that is inhibited through phosphorylation in response to serotonin, SSRIs, and 5-HT1 receptor agonists. Serotonin 245-254 glycogen synthase kinase 3 beta Mus musculus 112-142 20631880-1 2010 BACKGROUND: Glycogen synthase kinase 3beta (GSK3beta) is a ubiquitous serine/threonine kinase that is regulated by serine phosphorylation at 9. Serine 70-76 glycogen synthase kinase 3 beta Mus musculus 12-42 20631880-1 2010 BACKGROUND: Glycogen synthase kinase 3beta (GSK3beta) is a ubiquitous serine/threonine kinase that is regulated by serine phosphorylation at 9. Serine 70-76 glycogen synthase kinase 3 beta Mus musculus 44-52 20631880-3 2010 Since most of the GSK3beta inhibitors are targeted at the ATP-binding site, which is highly conserved among diverse protein kinases, the development of novel non-ATP competitive GSK3beta inhibitors is needed. Adenosine Triphosphate 58-61 glycogen synthase kinase 3 beta Mus musculus 18-26 20631880-3 2010 Since most of the GSK3beta inhibitors are targeted at the ATP-binding site, which is highly conserved among diverse protein kinases, the development of novel non-ATP competitive GSK3beta inhibitors is needed. Adenosine Triphosphate 58-61 glycogen synthase kinase 3 beta Mus musculus 178-186 20631880-3 2010 Since most of the GSK3beta inhibitors are targeted at the ATP-binding site, which is highly conserved among diverse protein kinases, the development of novel non-ATP competitive GSK3beta inhibitors is needed. Adenosine Triphosphate 162-165 glycogen synthase kinase 3 beta Mus musculus 18-26 20631880-3 2010 Since most of the GSK3beta inhibitors are targeted at the ATP-binding site, which is highly conserved among diverse protein kinases, the development of novel non-ATP competitive GSK3beta inhibitors is needed. Adenosine Triphosphate 162-165 glycogen synthase kinase 3 beta Mus musculus 178-186 20631880-4 2010 METHODS: Based on the unique phosphorylation motif of GSK3beta, we designed and generated a novel class of GSK3beta inhibitor (GSK3i) peptides. Peptides 134-142 glycogen synthase kinase 3 beta Mus musculus 54-62 20631880-4 2010 METHODS: Based on the unique phosphorylation motif of GSK3beta, we designed and generated a novel class of GSK3beta inhibitor (GSK3i) peptides. Peptides 134-142 glycogen synthase kinase 3 beta Mus musculus 107-115 20631880-11 2010 This peptide may serve as a novel template for the design of non-ATP competitive GSK3 inhibitors. Adenosine Triphosphate 65-68 glycogen synthase kinase 3 beta Mus musculus 81-85 20049527-1 2010 Previous studies indicated that ethanol-induced neurodegeneration in postnatal day 7 (P7) mice, widely used as a model for the fetal alcohol spectrum disorders, was accompanied by glycogen synthase kinase-3beta (GSK-3beta) and caspase-3 activation. Ethanol 32-39 glycogen synthase kinase 3 beta Mus musculus 212-221 20347018-6 2010 Inhibition of GSK3 via SB 216763 dose-dependently reduced ambulatory and stereotypic activity produced by SKF-82958. Antimony 23-25 glycogen synthase kinase 3 beta Mus musculus 14-18 20060080-10 2010 In contrast, glycogen synthase kinase-3[beta] (GSK-3[beta]) inhibition using lithium had anabolic effects improving in vivo gains in BMD via an increase in bone formation, while TCA-mediated inhibition of the norepinephrine transporter had minimal skeletal effect. Lithium 77-84 glycogen synthase kinase 3 beta Mus musculus 13-45 20060080-10 2010 In contrast, glycogen synthase kinase-3[beta] (GSK-3[beta]) inhibition using lithium had anabolic effects improving in vivo gains in BMD via an increase in bone formation, while TCA-mediated inhibition of the norepinephrine transporter had minimal skeletal effect. Lithium 77-84 glycogen synthase kinase 3 beta Mus musculus 47-58 20060080-12 2010 Likewise, the anabolic effect of GSK-3[beta] inhibition using lithium reconfirms the importance of Wnt/beta-catenin signaling in the skeleton and it"s targeting by recent drug discovery efforts. Lithium 62-69 glycogen synthase kinase 3 beta Mus musculus 33-43 20049527-1 2010 Previous studies indicated that ethanol-induced neurodegeneration in postnatal day 7 (P7) mice, widely used as a model for the fetal alcohol spectrum disorders, was accompanied by glycogen synthase kinase-3beta (GSK-3beta) and caspase-3 activation. Ethanol 32-39 glycogen synthase kinase 3 beta Mus musculus 180-210 20049527-8 2010 Lithium, a GSK-3beta inhibitor, blocked ethanol-induced caspase-3 activation, phosphorylated tau elevation, C-tau formation, and microglial activation. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 11-20 20049527-8 2010 Lithium, a GSK-3beta inhibitor, blocked ethanol-induced caspase-3 activation, phosphorylated tau elevation, C-tau formation, and microglial activation. Ethanol 40-47 glycogen synthase kinase 3 beta Mus musculus 11-20 20097210-9 2010 The phosphorylation level of GSK 3beta was also increased by isorhamnetin. 3-methylquercetin 61-73 glycogen synthase kinase 3 beta Mus musculus 29-38 20083607-7 2010 The pro-proliferative effect of cannabinoids in GCPs was mediated through the CB(1)/AKT/glycogen synthase kinase-3beta/beta-catenin pathway. Cannabinoids 32-44 glycogen synthase kinase 3 beta Mus musculus 88-118 20300527-3 2010 Glycogen synthase kinase-3 (GSK3) is hyperactive in brains of Fmr1 knockout mice, and inhibition of GSK3 by lithium administration ameliorates some behavioral impairment in these mice. Lithium 108-115 glycogen synthase kinase 3 beta Mus musculus 0-26 20300527-3 2010 Glycogen synthase kinase-3 (GSK3) is hyperactive in brains of Fmr1 knockout mice, and inhibition of GSK3 by lithium administration ameliorates some behavioral impairment in these mice. Lithium 108-115 glycogen synthase kinase 3 beta Mus musculus 100-104 20300527-8 2010 Fmr1 knockout mice displayed more anxiety-related behaviors during social interaction (grooming, rearing, and digging) than wild-type mice, which was ameliorated by inhibition of GSK3 with chronic lithium treatment. Lithium 197-204 glycogen synthase kinase 3 beta Mus musculus 179-183 20061376-0 2010 Silencing glycogen synthase kinase-3beta inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and myeloid cell leukemia sequence 1. Acetaminophen 50-63 glycogen synthase kinase 3 beta Mus musculus 10-40 20061376-0 2010 Silencing glycogen synthase kinase-3beta inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and myeloid cell leukemia sequence 1. glutamate cysteine 121-139 glycogen synthase kinase 3 beta Mus musculus 10-40 20061376-3 2010 APAP treatment to mice caused glycogen synthase kinase-3beta (GSK-3beta) activation and translocation to mitochondria during the initial phase of APAP-induced liver injury ( approximately 1 h). Acetaminophen 0-4 glycogen synthase kinase 3 beta Mus musculus 30-60 20061376-3 2010 APAP treatment to mice caused glycogen synthase kinase-3beta (GSK-3beta) activation and translocation to mitochondria during the initial phase of APAP-induced liver injury ( approximately 1 h). Acetaminophen 0-4 glycogen synthase kinase 3 beta Mus musculus 62-71 20061376-4 2010 The silencing of GSK-3beta, but not Akt-2 (protein kinase B) or glycogen synthase kinase-3alpha (GSK-3alpha), using antisense significantly protected mice from APAP-induced liver injury. Acetaminophen 160-164 glycogen synthase kinase 3 beta Mus musculus 17-26 20061376-5 2010 The silencing of GSK-3beta affected several key pathways important in conferring protection against APAP-induced liver injury. Acetaminophen 100-104 glycogen synthase kinase 3 beta Mus musculus 17-26 20061376-10 2010 The silencing of GSK-3beta reduced Mcl-1 degradation caused by APAP treatment. Acetaminophen 63-67 glycogen synthase kinase 3 beta Mus musculus 17-26 20056751-2 2010 Because lithium, a potent inhibitor of GSK3beta, causes nephrogenic diabetes insipidus, GSK3beta may play a crucial role in regulating water homeostasis. Lithium 8-15 glycogen synthase kinase 3 beta Mus musculus 39-47 20061376-11 2010 The silencing of GSK-3beta also resulted in an inhibition of the early phase (0-2 h), and blunted the late phase (after 4 h) of JNK activation and translocation to mitochondria in liver following APAP treatment. Acetaminophen 196-200 glycogen synthase kinase 3 beta Mus musculus 17-26 19939226-7 2010 In vitro studies show that homocysteine increases Abeta formation, reduces phosphorylated GSK3 levels, without changes in total APP and its metabolism, and these effects are prevented by selective GSK3 inhibition. Homocysteine 27-39 glycogen synthase kinase 3 beta Mus musculus 90-94 19939226-7 2010 In vitro studies show that homocysteine increases Abeta formation, reduces phosphorylated GSK3 levels, without changes in total APP and its metabolism, and these effects are prevented by selective GSK3 inhibition. Homocysteine 27-39 glycogen synthase kinase 3 beta Mus musculus 197-201 19997769-7 2010 Treatment of wild type cardiomyocytes with phenylephrine, which inactivates GSK3beta, redistributed emerin and beta-catenin. Phenylephrine 43-56 glycogen synthase kinase 3 beta Mus musculus 76-84 20056751-9 2010 In summary, GSK3beta inactivation or deletion reduces aquaporin 2 expression by modulating adenylate cyclase activity and cAMP generation, thereby impairing responses to vasopressin in the renal collecting duct. Cyclic AMP 122-126 glycogen synthase kinase 3 beta Mus musculus 12-20 19959748-2 2010 Because bleomycin (BLM) causes lung injury, which is characterized by an inflammatory response followed by a fibrotic degeneration, we postulated that blocking GSK-3 activity with a specific inhibitor could affect the inflammatory and profibrotic cytokine network generated in the BLM-induced process of pulmonary inflammation and fibrosis. Bleomycin 8-17 glycogen synthase kinase 3 beta Mus musculus 160-165 19959748-2 2010 Because bleomycin (BLM) causes lung injury, which is characterized by an inflammatory response followed by a fibrotic degeneration, we postulated that blocking GSK-3 activity with a specific inhibitor could affect the inflammatory and profibrotic cytokine network generated in the BLM-induced process of pulmonary inflammation and fibrosis. Bleomycin 19-22 glycogen synthase kinase 3 beta Mus musculus 160-165 20034560-6 2010 The first two derivatives were previously described indirubins with low nanomolar inhibitory activity against GSK-3 and CDKs. indirubin 52-62 glycogen synthase kinase 3 beta Mus musculus 110-115 20004245-6 2010 Thus, we suggest that the hyperphosphorylated tau mediates, at least in part, the pathology observed in the brain of GSK3 overexpressing mice. uridine triacetate 46-49 glycogen synthase kinase 3 beta Mus musculus 117-121 20117291-2 2010 We investigate the potential of developing small-molecule inhibitors of glycogen synthase kinase 3beta (GSK-3beta)-SB216763 or SB415286-as radioprotective agents to attenuate intestinal injury. SB 216763 115-123 glycogen synthase kinase 3 beta Mus musculus 72-102 20174568-8 2010 Moreover, administration of morphine and M. tuberculosis decreased the levels of phosphorylation of Akt and GSK3beta in the wild type mice, but not in TLR9 KO mice, suggesting an involvement of Akt/GSK3beta in morphine and M. tuberculosis-mediated TLR9 signaling. Morphine 28-36 glycogen synthase kinase 3 beta Mus musculus 108-116 20174568-8 2010 Moreover, administration of morphine and M. tuberculosis decreased the levels of phosphorylation of Akt and GSK3beta in the wild type mice, but not in TLR9 KO mice, suggesting an involvement of Akt/GSK3beta in morphine and M. tuberculosis-mediated TLR9 signaling. Morphine 28-36 glycogen synthase kinase 3 beta Mus musculus 198-206 20174568-8 2010 Moreover, administration of morphine and M. tuberculosis decreased the levels of phosphorylation of Akt and GSK3beta in the wild type mice, but not in TLR9 KO mice, suggesting an involvement of Akt/GSK3beta in morphine and M. tuberculosis-mediated TLR9 signaling. Morphine 210-218 glycogen synthase kinase 3 beta Mus musculus 198-206 19799873-0 2010 Lithium ameliorates altered glycogen synthase kinase-3 and behavior in a mouse model of fragile X syndrome. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 28-54 19799873-3 2010 Increased mGluR signaling may contribute to the pathology of FXS, and the mGluR5 antagonist MPEP increased inhibitory serine-phosphorylation of brain GSK3 selectively in Fmr1 knockout mice but not in wild-type mice. 6-methyl-2-(phenylethynyl)pyridine 92-96 glycogen synthase kinase 3 beta Mus musculus 150-154 19799873-3 2010 Increased mGluR signaling may contribute to the pathology of FXS, and the mGluR5 antagonist MPEP increased inhibitory serine-phosphorylation of brain GSK3 selectively in Fmr1 knockout mice but not in wild-type mice. Serine 118-124 glycogen synthase kinase 3 beta Mus musculus 150-154 19799873-4 2010 Inhibitory serine-phosphorylation of GSK3 was lower in Fmr1 knockout, than wild-type, mouse brain regions and was increased by acute or chronic lithium treatment, which also increased hippocampal brain-derived neurotrophic factor levels. Serine 11-17 glycogen synthase kinase 3 beta Mus musculus 37-41 19799873-4 2010 Inhibitory serine-phosphorylation of GSK3 was lower in Fmr1 knockout, than wild-type, mouse brain regions and was increased by acute or chronic lithium treatment, which also increased hippocampal brain-derived neurotrophic factor levels. Lithium 144-151 glycogen synthase kinase 3 beta Mus musculus 37-41 20117291-2 2010 We investigate the potential of developing small-molecule inhibitors of glycogen synthase kinase 3beta (GSK-3beta)-SB216763 or SB415286-as radioprotective agents to attenuate intestinal injury. SB 216763 115-123 glycogen synthase kinase 3 beta Mus musculus 104-113 19940121-4 2010 Thr(188) of C/EBPbeta is phosphorylated initially to prime the factor for subsequent phosphorylation at Ser(184) or Thr(179) by GSK3beta, which translocates into the nuclei during the G(1)/S transition. Threonine 0-3 glycogen synthase kinase 3 beta Mus musculus 128-136 19940121-4 2010 Thr(188) of C/EBPbeta is phosphorylated initially to prime the factor for subsequent phosphorylation at Ser(184) or Thr(179) by GSK3beta, which translocates into the nuclei during the G(1)/S transition. Serine 104-107 glycogen synthase kinase 3 beta Mus musculus 128-136 19940121-4 2010 Thr(188) of C/EBPbeta is phosphorylated initially to prime the factor for subsequent phosphorylation at Ser(184) or Thr(179) by GSK3beta, which translocates into the nuclei during the G(1)/S transition. Threonine 116-119 glycogen synthase kinase 3 beta Mus musculus 128-136 19962768-8 2010 Clozapine also reversed some of the sensitization-induced biochemical changes, including increased phosphorylation of GSK-3beta and CREB, in the frontal cortex. Clozapine 0-9 glycogen synthase kinase 3 beta Mus musculus 118-127 20005102-3 2010 Among these, the 4,7-diazaindazole compound 2c has improved drug-like properties and kinase selectivity than those of indazole 1, and displays greater than 80% inhibition of GSK3beta phosphorylation in a BT474 tumor xenograft model in mice. 4,7-diazaindazole 17-34 glycogen synthase kinase 3 beta Mus musculus 174-182 20111716-9 2010 Phosphorylation at serine-9 of GSK3beta (pSer9GSK3beta) reduces kinase activity. Serine 19-25 glycogen synthase kinase 3 beta Mus musculus 31-39 20111716-9 2010 Phosphorylation at serine-9 of GSK3beta (pSer9GSK3beta) reduces kinase activity. Serine 19-25 glycogen synthase kinase 3 beta Mus musculus 46-54 20005102-3 2010 Among these, the 4,7-diazaindazole compound 2c has improved drug-like properties and kinase selectivity than those of indazole 1, and displays greater than 80% inhibition of GSK3beta phosphorylation in a BT474 tumor xenograft model in mice. Indazoles 26-34 glycogen synthase kinase 3 beta Mus musculus 174-182 19855063-4 2010 Langendorff-perfused murine hearts were treated with the specific GSK-3 inhibitor AR-A014418 (GSK Inhib VIII) for 10 min or subjected to four cycles of 5-min ischemia-reperfusion (PC) before 20-min global ischemia and 120-min reperfusion. N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea 82-92 glycogen synthase kinase 3 beta Mus musculus 66-71 20017491-8 2010 Docking studies support that 2 binds to the ATP-noncompetitive pocket of glycogen synthesis kinase-3beta (GSK-3beta), which is a putative target of manzamines. Adenosine Triphosphate 44-47 glycogen synthase kinase 3 beta Mus musculus 106-115 20017491-8 2010 Docking studies support that 2 binds to the ATP-noncompetitive pocket of glycogen synthesis kinase-3beta (GSK-3beta), which is a putative target of manzamines. manzamine A 148-158 glycogen synthase kinase 3 beta Mus musculus 106-115 21063101-9 2010 The glucose-induced current was significantly larger in gsk3(KI) than in gsk3(WT) mice. Glucose 4-11 glycogen synthase kinase 3 beta Mus musculus 56-60 20511724-2 2010 Specifically, the well known antimanic and mood stabilizing medications lithium, valproate, olanzapine and clozapine have been shown to inhibit GSK-3 activity. Lithium 72-79 glycogen synthase kinase 3 beta Mus musculus 144-149 20511724-2 2010 Specifically, the well known antimanic and mood stabilizing medications lithium, valproate, olanzapine and clozapine have been shown to inhibit GSK-3 activity. Valproic Acid 81-90 glycogen synthase kinase 3 beta Mus musculus 144-149 20511724-2 2010 Specifically, the well known antimanic and mood stabilizing medications lithium, valproate, olanzapine and clozapine have been shown to inhibit GSK-3 activity. Olanzapine 92-102 glycogen synthase kinase 3 beta Mus musculus 144-149 20511724-2 2010 Specifically, the well known antimanic and mood stabilizing medications lithium, valproate, olanzapine and clozapine have been shown to inhibit GSK-3 activity. Clozapine 107-116 glycogen synthase kinase 3 beta Mus musculus 144-149 20462044-8 2010 Berberine reversed the alternations of T, A2 and 17-OHP levels, but did not influence the level of P. (3) RT-PCR showed that the mRNA expressions of cytochrome 17-hydroxylase (CYP17) and mini-chromosome maintenance protein-2 (MCM-2) elevated, but extracellular regulated protein-1 (ERK-1), protein kinase B (AKT-2) and glycogen synthase kinase-3 (GSK-3beta) lowered in the medium after Dex inducing. Berberine 0-9 glycogen synthase kinase 3 beta Mus musculus 347-356 21063101-1 2010 Glycogen synthase kinase 3 GSK3beta participates in a wide variety of functions including regulation of glucose metabolism. Glucose 104-111 glycogen synthase kinase 3 beta Mus musculus 27-35 21063101-4 2010 The present study thus explored whether GSK3beta influences the Na(+)-coupled transport of glucose. Glucose 91-98 glycogen synthase kinase 3 beta Mus musculus 40-48 21063101-9 2010 The glucose-induced current was significantly larger in gsk3(KI) than in gsk3(WT) mice. Glucose 4-11 glycogen synthase kinase 3 beta Mus musculus 73-77 21063101-10 2010 The present observations reveal a novel function of GSK3, i.e. the stimulation of Na(+)-coupled glucose transport. Glucose 96-103 glycogen synthase kinase 3 beta Mus musculus 52-56 20413892-9 2010 The phosphorylation level of p53 decreased upon tau overexpression, and a more profound reduction of the phosphorylated p53 was detected when the cells were treated with lithium and roscovitine, inhibitors of GSK-3 and cyclin-dependent kinase-5 (Cdk-5). Lithium 170-177 glycogen synthase kinase 3 beta Mus musculus 209-214 19858210-3 2009 5-Aza treatment caused significant up-regulation of glycogen synthase kinase (GSK)-3beta and down-regulation of beta-catenin, whereas it stimulated GSK-3alpha expression only modestly. Azacitidine 0-5 glycogen synthase kinase 3 beta Mus musculus 52-88 19858210-4 2009 The promoter region of GSK-3beta was heavily methylated in control MSCs, but was demethylated by 5-Aza. Azacitidine 97-102 glycogen synthase kinase 3 beta Mus musculus 23-32 19858210-6 2009 GSK-3 inhibitors, including LiCl, SB 216743, and BIO, abolished 5-Aza-induced up-regulation of CM-specific genes, suggesting that GSK-3 is necessary and sufficient for CM differentiation in MSCs. Lithium Chloride 28-32 glycogen synthase kinase 3 beta Mus musculus 0-5 19858210-6 2009 GSK-3 inhibitors, including LiCl, SB 216743, and BIO, abolished 5-Aza-induced up-regulation of CM-specific genes, suggesting that GSK-3 is necessary and sufficient for CM differentiation in MSCs. Lithium Chloride 28-32 glycogen synthase kinase 3 beta Mus musculus 130-135 19858210-6 2009 GSK-3 inhibitors, including LiCl, SB 216743, and BIO, abolished 5-Aza-induced up-regulation of CM-specific genes, suggesting that GSK-3 is necessary and sufficient for CM differentiation in MSCs. sb 216743 34-43 glycogen synthase kinase 3 beta Mus musculus 0-5 19858210-6 2009 GSK-3 inhibitors, including LiCl, SB 216743, and BIO, abolished 5-Aza-induced up-regulation of CM-specific genes, suggesting that GSK-3 is necessary and sufficient for CM differentiation in MSCs. sb 216743 34-43 glycogen synthase kinase 3 beta Mus musculus 130-135 19858210-6 2009 GSK-3 inhibitors, including LiCl, SB 216743, and BIO, abolished 5-Aza-induced up-regulation of CM-specific genes, suggesting that GSK-3 is necessary and sufficient for CM differentiation in MSCs. Azacitidine 64-69 glycogen synthase kinase 3 beta Mus musculus 0-5 19858210-6 2009 GSK-3 inhibitors, including LiCl, SB 216743, and BIO, abolished 5-Aza-induced up-regulation of CM-specific genes, suggesting that GSK-3 is necessary and sufficient for CM differentiation in MSCs. Azacitidine 64-69 glycogen synthase kinase 3 beta Mus musculus 130-135 19858210-7 2009 Although specific knockdown of endogenous GSK-3beta abolished 5-Aza-induced expression of cardiac specific genes, surprisingly, that of GSK-3alpha facilitated CM differentiation in MSCs. Azacitidine 62-67 glycogen synthase kinase 3 beta Mus musculus 42-51 19602048-4 2009 GB and IP significantly increased cell viability, expression of hypoxia-inducible factor-1 alpha (HIF-1alpha), erythropoietin (EPO), phosphorylated Bad at serine 136 (136p-Bad) and phosphorylated glycogen synthase kinase- 3beta at serine 9 (p-GSK-3beta), and decreased the percentage of apoptotic cells and the level of active caspase-3 in severely ischaemic neurons. ginkgolide B 0-2 glycogen synthase kinase 3 beta Mus musculus 243-252 20016849-8 2009 Phosphorylation of glycogen synthase kinase (GSK3)beta-serine 9 that promotes platelet function, was reduced in thrombin-stimulated PP1cgamma(-/-) platelets by an AKT independent mechanism. beta-serine 50-61 glycogen synthase kinase 3 beta Mus musculus 45-49 20016849-10 2009 CONCLUSIONS/SIGNIFICANCE: These studies illustrate a role for PP1cgamma in maintaining GSK3beta-serine9 phosphorylation downstream of thrombin signaling and promoting thrombus formation via fibrinogen binding and platelet aggregation. serine9 96-103 glycogen synthase kinase 3 beta Mus musculus 87-95 19959876-3 2009 Disruption of Gsk3 in BM transiently expanded phenotypic HSCs in a betta-catenin-dependent manner, consistent with a role for Wnt signaling in HSC homeostasis. betta-catenin 67-80 glycogen synthase kinase 3 beta Mus musculus 14-18 19959876-6 2009 Thus, GSK-3 regulated both Wnt and mTOR signaling in mouse HSCs, with these pathways promoting HSC self renewal and lineage commitment, respectively, such that inhibition of Gsk3 in the presence of rapamycin expanded the HSC pool in vivo. Sirolimus 198-207 glycogen synthase kinase 3 beta Mus musculus 6-11 19959876-7 2009 These findings identify unexpected functions for GSK-3 in mouse HSC homeostasis, suggest a therapeutic approach to expand HSCs in vivo using currently available medications that target GSK-3 and mTOR, and provide a compelling explanation for the clinically prevalent hematopoietic effects observed in individuals prescribed the GSK-3 inhibitor lithium. Lithium 344-351 glycogen synthase kinase 3 beta Mus musculus 49-54 19710241-8 2009 Inhibition of either the AKT or STAT3 pathway potentiated H2O2-induced cell death and increased GSK-3beta activity by dephosphorylation at serine 9. Serine 139-145 glycogen synthase kinase 3 beta Mus musculus 96-105 19710241-9 2009 Furthermore, treatment with GSK-3beta inhibitors reduced H2O2-induced apoptosis and abolished the death-promoting effect of AKT and STAT3 inhibition. Hydrogen Peroxide 57-61 glycogen synthase kinase 3 beta Mus musculus 28-37 19698704-0 2009 Efficacy of a novel, orally active GSK-3 inhibitor 6-Methyl-N-[3-[[3-(1-methylethoxy)propyl]carbamoyl]-1H-pyrazol-4-yl]pyridine-3-carboxamide in tau transgenic mice. 6-methyl-N-(3-((3-(1-methylethoxy)propyl)carbamoyl)-1H-pyrazol-4-yl)pyridine-3-carboxamide 51-141 glycogen synthase kinase 3 beta Mus musculus 35-40 19698704-3 2009 In the present study, we report the efficacy of a newly discovered small molecule GSK-3 inhibitor, 6-methyl-N-[3-[[3-(1-methylethoxy)propyl]carbamoyl]-1H-pyrazol-4-yl]pyridine-3-carboxamide (compound A), to inhibit tau phosphorylation and to reduce the amount of pathological aggregated tau in JNPL3 mice that overexpress a mutant form of human tau. 6-methyl-N-(3-((3-(1-methylethoxy)propyl)carbamoyl)-1H-pyrazol-4-yl)pyridine-3-carboxamide 99-189 glycogen synthase kinase 3 beta Mus musculus 82-87 19666099-0 2009 Selective GSK-3beta inhibitors attenuate the cisplatin-induced cytotoxicity of auditory cells. Cisplatin 45-54 glycogen synthase kinase 3 beta Mus musculus 10-19 19666099-3 2009 Here we examined whether the GSK-3-specific inhibitors, SB 216763 and LiCl, could protect against cisplatin-induced cytotoxicity of auditory cells. SB 216763 56-65 glycogen synthase kinase 3 beta Mus musculus 29-34 19666099-3 2009 Here we examined whether the GSK-3-specific inhibitors, SB 216763 and LiCl, could protect against cisplatin-induced cytotoxicity of auditory cells. Lithium Chloride 70-74 glycogen synthase kinase 3 beta Mus musculus 29-34 19666099-4 2009 GSK-3 was activated by cisplatin treatment of HEI-OC1 cells. Cisplatin 23-32 glycogen synthase kinase 3 beta Mus musculus 0-5 19666099-9 2009 Collectively, these results suggest that cisplatin-induced ototoxicity might be associated with modulation of GSK-3 activation. Cisplatin 41-50 glycogen synthase kinase 3 beta Mus musculus 110-115 19682597-3 2009 Further, basal phosphorylation of Akt (p-Akt (Ser-473)/total Akt) and GSK-3beta (GSK-3beta (Ser-9)/total GSK-3beta) are reduced 60-70% in primary myotubes from eNOS(-/-) mice. Serine 92-95 glycogen synthase kinase 3 beta Mus musculus 81-90 19682597-3 2009 Further, basal phosphorylation of Akt (p-Akt (Ser-473)/total Akt) and GSK-3beta (GSK-3beta (Ser-9)/total GSK-3beta) are reduced 60-70% in primary myotubes from eNOS(-/-) mice. Serine 92-95 glycogen synthase kinase 3 beta Mus musculus 81-90 19682597-4 2009 Treatment with the calcium ionophore, A23187 (0.4 microM, 1 h), increased phosphorylation of Akt and GSK-3beta by approximately 2-fold (P<0.05) in myotubes from WT mice, but had no effect on phosphorylation of these proteins in eNOS(-/-) myotubes. Calcium 19-26 glycogen synthase kinase 3 beta Mus musculus 101-110 19682597-4 2009 Treatment with the calcium ionophore, A23187 (0.4 microM, 1 h), increased phosphorylation of Akt and GSK-3beta by approximately 2-fold (P<0.05) in myotubes from WT mice, but had no effect on phosphorylation of these proteins in eNOS(-/-) myotubes. Calcimycin 38-44 glycogen synthase kinase 3 beta Mus musculus 101-110 19775160-0 2009 2-{3-[4-(Alkylsulfinyl)phenyl]-1-benzofuran-5-yl}-5-methyl-1,3,4-oxadiazole derivatives as novel inhibitors of glycogen synthase kinase-3beta with good brain permeability. 2-{3-[4-(alkylsulfinyl)phenyl]-1-benzofuran-5-yl}-5-methyl-1,3,4-oxadiazole 0-75 glycogen synthase kinase 3 beta Mus musculus 111-141 19817973-9 2009 Taken together, melatonin improves glucose intolerance and insulin resistance in high fat diet-induced diabetic mice and stimulates glycogen synthesis via a PKCzeta-Akt-GSK3beta pathway in HepG2 cells. Melatonin 16-25 glycogen synthase kinase 3 beta Mus musculus 169-177 19775160-2 2009 Previously we reported a series of 1,3,4-oxadiazole derivatives as potent and highly selective GSK-3beta inhibitors, however, the representative compounds 1a,b showed poor pharmacokinetic profiles. 1,3,4-oxadiazole 35-51 glycogen synthase kinase 3 beta Mus musculus 95-104 19754464-11 2009 These data support the role of inositol-related processes rather than GSK3beta in the mechanism of the therapeutic action of lithium. Lithium 125-132 glycogen synthase kinase 3 beta Mus musculus 70-78 19754466-0 2009 Validating GSK3 as an in vivo target of lithium action. Lithium 40-47 glycogen synthase kinase 3 beta Mus musculus 11-15 19754466-2 2009 Lithium directly inhibits GSK3 (glycogen synthase kinase 3), a critical regulator of multiple signal transduction pathways. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 32-58 19754466-2 2009 Lithium directly inhibits GSK3 (glycogen synthase kinase 3), a critical regulator of multiple signal transduction pathways. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 26-30 19754466-3 2009 Inhibition of GSK3 provides a compelling explanation for many of the known effects of lithium, including effects on early development and insulin signalling/glycogen synthesis. Lithium 86-93 glycogen synthase kinase 3 beta Mus musculus 14-18 19382207-6 2009 Ethanol induced dephosphorylation of GSK3beta at Ser9 and the activation of Bax as well as caspase-3 in the developing mouse brain. Ethanol 0-7 glycogen synthase kinase 3 beta Mus musculus 37-45 19754466-3 2009 Inhibition of GSK3 provides a compelling explanation for many of the known effects of lithium, including effects on early development and insulin signalling/glycogen synthesis. Glycogen 157-165 glycogen synthase kinase 3 beta Mus musculus 14-18 19754466-7 2009 In this context, we describe a set of simple behaviours in mice that are robustly affected by chronic lithium treatment and are similarly affected by structurally diverse GSK3 inhibitors and by removing one copy of the Gsk3b gene. Lithium 102-109 glycogen synthase kinase 3 beta Mus musculus 219-224 19754466-8 2009 These observations, from several independent laboratories, support a central role for GSK3 in mediating behavioural responses to lithium. Lithium 129-136 glycogen synthase kinase 3 beta Mus musculus 86-90 19520363-2 2009 Because these diseases might be associated with inadequately controlled glycogen synthase kinase-3 (GSK3), we tested whether blocked inhibitory serine-phosphorylation of GSK3 impairs neurogenesis. Serine 144-150 glycogen synthase kinase 3 beta Mus musculus 170-174 19520363-3 2009 METHODS: Neural precursor cell (NPC) proliferation was measured by dentate gyrus bromodeoxyuridine (BrdU) labeling in GSK3alpha/beta(21A/21A/9A/9A) knockin mice with serine-to-alanine mutations to block inhibitory serine-phosphorylation of GSK3 while it remains within the physiological range, because GSK3 is not overexpressed. gyrus bromodeoxyuridine 75-98 glycogen synthase kinase 3 beta Mus musculus 118-122 19520363-3 2009 METHODS: Neural precursor cell (NPC) proliferation was measured by dentate gyrus bromodeoxyuridine (BrdU) labeling in GSK3alpha/beta(21A/21A/9A/9A) knockin mice with serine-to-alanine mutations to block inhibitory serine-phosphorylation of GSK3 while it remains within the physiological range, because GSK3 is not overexpressed. Bromodeoxyuridine 100-104 glycogen synthase kinase 3 beta Mus musculus 118-122 19520363-8 2009 In vivo chronic co-administration of lithium and fluoxetine, which each increase inhibitory serine-phosphorylation of wild-type GSK3, increased NPC proliferation in wild-type but not GSK3 knockin mice. Lithium 37-44 glycogen synthase kinase 3 beta Mus musculus 128-132 19520363-8 2009 In vivo chronic co-administration of lithium and fluoxetine, which each increase inhibitory serine-phosphorylation of wild-type GSK3, increased NPC proliferation in wild-type but not GSK3 knockin mice. Fluoxetine 49-59 glycogen synthase kinase 3 beta Mus musculus 128-132 19520363-8 2009 In vivo chronic co-administration of lithium and fluoxetine, which each increase inhibitory serine-phosphorylation of wild-type GSK3, increased NPC proliferation in wild-type but not GSK3 knockin mice. Serine 92-98 glycogen synthase kinase 3 beta Mus musculus 128-132 19657059-8 2009 The GSK-3beta inhibitor, LiCl, dramatically enhanced IGF-I induction of the 1.3-kb type IIb MyHC promoter, and constitutively active GSK-3beta attenuated IGF-I-induced 1.3-kb type IIb MyHC promoter activity. Lithium Chloride 25-29 glycogen synthase kinase 3 beta Mus musculus 4-13 19448134-2 2009 3-(2,4-Dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione (SB216763), a potent inhibitor of glycogen synthase kinase 3beta (GSK3beta), is frequently used to activate beta-catenin signaling by mimicking the action of Wnt molecules. SB 216763 0-70 glycogen synthase kinase 3 beta Mus musculus 105-135 19175796-3 2009 Treatment with GSK-3 inhibitor significantly blocked LPS-induced nitric oxide (NO) production as well as inducible NO synthase (iNOS) expression in BV2 murine microglial cells and primary rat microglia-enriched cultures. Nitric Oxide 65-77 glycogen synthase kinase 3 beta Mus musculus 15-20 19175796-11 2009 Furthermore, inhibiting GSK-3 increased the nuclear translocation of transcription factors, that all important for IL-10 expression, including CCAAT/enhancer-binding protein beat (C/EBPbeta), C/EBPdelta, cAMP response binding element protein and NF-kappaB. Cyclic AMP 204-208 glycogen synthase kinase 3 beta Mus musculus 24-29 19693287-11 2009 In addition, imatinib inhibited PDGF-induced downstream phosphorylation of Akt, GSK-3beta, and p70S6kinase. Imatinib Mesylate 13-21 glycogen synthase kinase 3 beta Mus musculus 80-89 19712471-0 2009 Rho iso-alpha acids from hops inhibit the GSK-3/NF-kappaB pathway and reduce inflammatory markers associated with bone and cartilage degradation. rho iso-alpha acids 0-19 glycogen synthase kinase 3 beta Mus musculus 42-47 19508174-6 2009 Treatment with valproic acid decreases muscle myostatin levels and enhances both follistatin expression and the inactivating phosphorylation of GSK-3beta, while these parameters are not affected by trichostatin-A. Valproic Acid 15-28 glycogen synthase kinase 3 beta Mus musculus 144-153 19448134-2 2009 3-(2,4-Dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione (SB216763), a potent inhibitor of glycogen synthase kinase 3beta (GSK3beta), is frequently used to activate beta-catenin signaling by mimicking the action of Wnt molecules. SB 216763 0-70 glycogen synthase kinase 3 beta Mus musculus 137-145 19448134-2 2009 3-(2,4-Dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione (SB216763), a potent inhibitor of glycogen synthase kinase 3beta (GSK3beta), is frequently used to activate beta-catenin signaling by mimicking the action of Wnt molecules. SB 216763 72-80 glycogen synthase kinase 3 beta Mus musculus 105-135 19448134-2 2009 3-(2,4-Dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione (SB216763), a potent inhibitor of glycogen synthase kinase 3beta (GSK3beta), is frequently used to activate beta-catenin signaling by mimicking the action of Wnt molecules. SB 216763 72-80 glycogen synthase kinase 3 beta Mus musculus 137-145 19344727-9 2009 Phosphorylation of Akt, GSK-3beta and Foxo3a was reduced following alcohol intake, the effect of which was abrogated by ALDH2. Alcohols 67-74 glycogen synthase kinase 3 beta Mus musculus 24-33 19578793-6 2009 By contrast, EGCG markedly suppressed the phosphorylations of both Akt and glycogen synthase kinase-3beta stimulated by sphingosine 1-phosphate. epigallocatechin gallate 13-17 glycogen synthase kinase 3 beta Mus musculus 75-105 19578793-6 2009 By contrast, EGCG markedly suppressed the phosphorylations of both Akt and glycogen synthase kinase-3beta stimulated by sphingosine 1-phosphate. sphingosine 1-phosphate 120-143 glycogen synthase kinase 3 beta Mus musculus 75-105 19408126-0 2009 Glycogen synthase kinase-3beta regulates etoposide-induced apoptosis via Bcl-2 mediated caspase-3 activation in C3H10T1/2 cells. Etoposide 41-50 glycogen synthase kinase 3 beta Mus musculus 0-30 19379814-0 2009 GSK3beta, a centre-staged kinase in neuropsychiatric disorders, modulates long term memory by inhibitory phosphorylation at serine-9. Serine 124-130 glycogen synthase kinase 3 beta Mus musculus 0-8 19379814-3 2009 We here report increased phosphorylation of GSK3ss at Serine-9 following cognitive training in two different hippocampus dependent cognitive tasks, i.e. inhibitory avoidance and novel object recognition task. Serine 54-60 glycogen synthase kinase 3 beta Mus musculus 44-48 19379814-6 2009 Application of actinomycin, but not anisomycin, mimicked GSK3ss[S9A] induced defects in L-LTP, suggesting that transcriptional activation is affected. Dactinomycin 15-26 glycogen synthase kinase 3 beta Mus musculus 57-61 19379814-8 2009 The combined data demonstrate a role for GSK3ss in long term memory formation, by inhibitory phosphorylation at Serine-9. Serine 112-118 glycogen synthase kinase 3 beta Mus musculus 41-45 19508392-8 2009 KEY RESULTS: Mice treated with GSK-3 inhibitors showed decreased mortality, renal tubular dilatation, vacuolization and sloughing, blood urea nitrogen, creatinine and renal cell apoptosis in response to endotoxaemia. Urea 137-141 glycogen synthase kinase 3 beta Mus musculus 31-36 19508392-8 2009 KEY RESULTS: Mice treated with GSK-3 inhibitors showed decreased mortality, renal tubular dilatation, vacuolization and sloughing, blood urea nitrogen, creatinine and renal cell apoptosis in response to endotoxaemia. Nitrogen 142-150 glycogen synthase kinase 3 beta Mus musculus 31-36 19508392-8 2009 KEY RESULTS: Mice treated with GSK-3 inhibitors showed decreased mortality, renal tubular dilatation, vacuolization and sloughing, blood urea nitrogen, creatinine and renal cell apoptosis in response to endotoxaemia. Creatinine 152-162 glycogen synthase kinase 3 beta Mus musculus 31-36 19421138-0 2009 Fbw7 promotes ubiquitin-dependent degradation of c-Myb: involvement of GSK3-mediated phosphorylation of Thr-572 in mouse c-Myb. Threonine 104-107 glycogen synthase kinase 3 beta Mus musculus 71-75 19421138-9 2009 Fbw7 recognized the phosphorylation of Thr-572, which was mediated by glycogen synthase kinase 3 (GSK3). Threonine 39-42 glycogen synthase kinase 3 beta Mus musculus 70-96 19421138-9 2009 Fbw7 recognized the phosphorylation of Thr-572, which was mediated by glycogen synthase kinase 3 (GSK3). Threonine 39-42 glycogen synthase kinase 3 beta Mus musculus 98-102 19408126-3 2009 Genotoxic stress induced by etoposide promoted apoptotic signaling by GSK3beta activation in C3H10T1/2 cells, a mouse mesenchymal cell line. Etoposide 28-37 glycogen synthase kinase 3 beta Mus musculus 70-78 19408126-4 2009 Etoposide led to the time-dependent activation of GSK3beta and caspase-3, which resulted in PARP cleavage. Etoposide 0-9 glycogen synthase kinase 3 beta Mus musculus 50-58 19408126-5 2009 LiCl (a specific inhibitor) and siRNA (gene knock-down) of GSK3beta prevented the effects of etoposide on apoptosis. Etoposide 93-102 glycogen synthase kinase 3 beta Mus musculus 59-67 19238412-3 2009 We therefore investigated the influence of a GSK-3 inhibitor, (2"Z,3"E)-6-bromoindirubin-3"-oxime (BIO), on the growth of human DP cells and mouse vibrissa follicles in culture. (2"z,3"e)-6-bromoindirubin-3"-oxime 62-97 glycogen synthase kinase 3 beta Mus musculus 45-50 19408126-9 2009 In conclusion, etoposide-induced apoptosis in C3H10T1/2 cells is mediated by GSK3beta, which leads to caspase-3 activation via decrease in Bcl-2 expression. Etoposide 15-24 glycogen synthase kinase 3 beta Mus musculus 77-85 19240057-11 2009 CONCLUSIONS: Our results indicate that AS101 can significantly protect against Cy-induced testicular damage and sperm DNA damage, probably by acting through Akt/GSK-3beta phosphorylation. ammonium trichloro(dioxoethylene-O,O'-)tellurate 39-44 glycogen synthase kinase 3 beta Mus musculus 161-170 19252918-3 2009 We have previously shown that Cerebrolysin (CBL) reduces the synaptic and behavioral deficits in amyloid precursor protein (APP) transgenic (tg) mice by decreasing APP phosphorylation via modulation of glycogen synthase kinase-3beta (GSK3beta) and cyclin-dependent kinase-5 (CDK5) activity. cerebrolysin 30-42 glycogen synthase kinase 3 beta Mus musculus 202-232 19240057-11 2009 CONCLUSIONS: Our results indicate that AS101 can significantly protect against Cy-induced testicular damage and sperm DNA damage, probably by acting through Akt/GSK-3beta phosphorylation. Cyclophosphamide 79-81 glycogen synthase kinase 3 beta Mus musculus 161-170 19303025-0 2009 Caffeic acid phenethyl ester accumulates beta-catenin through GSK-3beta and participates in proliferation through mTOR in C2C12 cells. caffeic acid phenethyl ester 0-28 glycogen synthase kinase 3 beta Mus musculus 62-71 19391115-2 2009 We newly established serum- and feeder-free B6 ES cells with full developmental potential by using leukemia inhibitory factor (LIF) and 6-bromoindirubin-3"-oxime (BIO), a glycogen synthase kinase-3 (GSK3) inhibitor. 6-bromoindirubin-3'-oxime 136-161 glycogen synthase kinase 3 beta Mus musculus 171-197 18720192-1 2009 Curcumin was investigated as an inhibitor of glycogen synthase kinase-3beta (GSK-3beta) in an attempt to explain some of its interesting multiple pharmacological effects, such as its anti-diabetic, anti-inflammatory, anti-cancer, anti-malarial and anti-alzheimer"s properties. Curcumin 0-8 glycogen synthase kinase 3 beta Mus musculus 45-75 19356803-5 2009 Mechanistically, this PKC alpha/theta crosstalk primarily affects the NFAT transactivation pathway in T lymphocytes, as observed by decreased phosphorylation of Ser-9 on GSK3 beta, reduced nuclear translocation and DNA binding of NFAT in isolated PKC alpha(-/-)/theta(-/-) CD3(+) T cells. Serine 161-164 glycogen synthase kinase 3 beta Mus musculus 170-179 19328817-0 2009 Cocaine-induced hyperactivity and sensitization are dependent on GSK3. Cocaine 0-7 glycogen synthase kinase 3 beta Mus musculus 65-69 19328817-2 2009 The activity of GSK3 is regulated by several kinases, with inactivation occurring via phosphorylation of the inhibitory serine-21 (alpha-isoform) and serine-9 (beta-isoform) residues. Serine 120-126 glycogen synthase kinase 3 beta Mus musculus 16-20 19328817-2 2009 The activity of GSK3 is regulated by several kinases, with inactivation occurring via phosphorylation of the inhibitory serine-21 (alpha-isoform) and serine-9 (beta-isoform) residues. Serine 150-156 glycogen synthase kinase 3 beta Mus musculus 16-20 19328817-3 2009 Here, we investigated whether acute cocaine administration regulates GSK3 activity and if inhibition of GSK3 by valproate or the selective GSK3 inhibitor SB 216763 would attenuate cocaine-induced behaviors in mice. Valproic Acid 112-121 glycogen synthase kinase 3 beta Mus musculus 104-108 19328817-3 2009 Here, we investigated whether acute cocaine administration regulates GSK3 activity and if inhibition of GSK3 by valproate or the selective GSK3 inhibitor SB 216763 would attenuate cocaine-induced behaviors in mice. Valproic Acid 112-121 glycogen synthase kinase 3 beta Mus musculus 104-108 19328817-14 2009 These results indicate that cocaine activated GSK3beta in the caudate putamen and that pharmacological inhibition of GSK3 reduced both the acute behavioral responses to cocaine and the long-term neuroadaptations produced by repeated cocaine, therefore suggesting a role for GSK3 in the behavioral and neurochemical manifestations associated with cocaine exposure. Cocaine 28-35 glycogen synthase kinase 3 beta Mus musculus 46-54 19328817-14 2009 These results indicate that cocaine activated GSK3beta in the caudate putamen and that pharmacological inhibition of GSK3 reduced both the acute behavioral responses to cocaine and the long-term neuroadaptations produced by repeated cocaine, therefore suggesting a role for GSK3 in the behavioral and neurochemical manifestations associated with cocaine exposure. Cocaine 28-35 glycogen synthase kinase 3 beta Mus musculus 46-50 19328817-14 2009 These results indicate that cocaine activated GSK3beta in the caudate putamen and that pharmacological inhibition of GSK3 reduced both the acute behavioral responses to cocaine and the long-term neuroadaptations produced by repeated cocaine, therefore suggesting a role for GSK3 in the behavioral and neurochemical manifestations associated with cocaine exposure. Cocaine 28-35 glycogen synthase kinase 3 beta Mus musculus 117-121 19328817-14 2009 These results indicate that cocaine activated GSK3beta in the caudate putamen and that pharmacological inhibition of GSK3 reduced both the acute behavioral responses to cocaine and the long-term neuroadaptations produced by repeated cocaine, therefore suggesting a role for GSK3 in the behavioral and neurochemical manifestations associated with cocaine exposure. Cocaine 169-176 glycogen synthase kinase 3 beta Mus musculus 117-121 19328817-14 2009 These results indicate that cocaine activated GSK3beta in the caudate putamen and that pharmacological inhibition of GSK3 reduced both the acute behavioral responses to cocaine and the long-term neuroadaptations produced by repeated cocaine, therefore suggesting a role for GSK3 in the behavioral and neurochemical manifestations associated with cocaine exposure. Cocaine 169-176 glycogen synthase kinase 3 beta Mus musculus 117-121 19328817-14 2009 These results indicate that cocaine activated GSK3beta in the caudate putamen and that pharmacological inhibition of GSK3 reduced both the acute behavioral responses to cocaine and the long-term neuroadaptations produced by repeated cocaine, therefore suggesting a role for GSK3 in the behavioral and neurochemical manifestations associated with cocaine exposure. Cocaine 169-176 glycogen synthase kinase 3 beta Mus musculus 117-121 19303025-3 2009 KEY FINDINGS: We found that CAPE induces rapid and transient phosphorylation of glycogen synthase kinase (GSK)-3beta in a phosphoinositide 3-kinase (PI3K)-dependent manner. caffeic acid phenethyl ester 28-32 glycogen synthase kinase 3 beta Mus musculus 80-116 19303025-7 2009 SIGNIFICANCE: Our results suggest that CAPE may act through beta-catenin accumulation via stimulation of GSK-3beta and may also participate in cellular proliferation through the mTOR-ERK pathway. caffeic acid phenethyl ester 39-43 glycogen synthase kinase 3 beta Mus musculus 105-114 19332462-9 2009 In addition, the ALDH2 transgene significantly attenuated chronic alcohol intake-induced myocardial fibrosis, protein carbonyl formation, apoptosis, enhanced NADPH oxidase p47(phox) and calcineurin expression, as well as phosphorylation of ASK-1, GSK-3beta, GATA4, and CREB. Alcohols 66-73 glycogen synthase kinase 3 beta Mus musculus 247-256 19384566-0 2009 Cyanidin-3-glucoside reverses ethanol-induced inhibition of neurite outgrowth: role of glycogen synthase kinase 3 Beta. cyanidin-3-o-glucoside 0-20 glycogen synthase kinase 3 beta Mus musculus 87-118 19384566-0 2009 Cyanidin-3-glucoside reverses ethanol-induced inhibition of neurite outgrowth: role of glycogen synthase kinase 3 Beta. Ethanol 30-37 glycogen synthase kinase 3 beta Mus musculus 87-118 19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 170-183 glycogen synthase kinase 3 beta Mus musculus 0-30 19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 170-183 glycogen synthase kinase 3 beta Mus musculus 32-40 19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 170-183 glycogen synthase kinase 3 beta Mus musculus 149-157 19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 170-183 glycogen synthase kinase 3 beta Mus musculus 149-157 19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 185-187 glycogen synthase kinase 3 beta Mus musculus 0-30 19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Tretinoin 185-187 glycogen synthase kinase 3 beta Mus musculus 32-40 19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Lithium 193-200 glycogen synthase kinase 3 beta Mus musculus 0-30 19384566-5 2009 Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3beta mutant prevented neurite outgrowth. Lithium 193-200 glycogen synthase kinase 3 beta Mus musculus 32-40 19384566-6 2009 Ethanol inhibited neurite outgrowth by activating GSK3beta through the dephosphorylation of GSK3beta at serine 9. Ethanol 0-7 glycogen synthase kinase 3 beta Mus musculus 50-58 19384566-6 2009 Ethanol inhibited neurite outgrowth by activating GSK3beta through the dephosphorylation of GSK3beta at serine 9. Ethanol 0-7 glycogen synthase kinase 3 beta Mus musculus 92-100 19384566-6 2009 Ethanol inhibited neurite outgrowth by activating GSK3beta through the dephosphorylation of GSK3beta at serine 9. Serine 104-110 glycogen synthase kinase 3 beta Mus musculus 50-58 19384566-6 2009 Ethanol inhibited neurite outgrowth by activating GSK3beta through the dephosphorylation of GSK3beta at serine 9. Serine 104-110 glycogen synthase kinase 3 beta Mus musculus 92-100 19384566-7 2009 Cyanidin-3-glucoside (C3G), a member of the anthocyanin family rich in many edible berries and other pigmented fruits, enhanced neurite outgrowth by promoting p-GSK3beta(Ser9). Anthocyanins 44-55 glycogen synthase kinase 3 beta Mus musculus 161-169 19384566-8 2009 More importantly, C3G reversed ethanol-mediated activation of GSK3beta and inhibition of neurite outgrowth as well as the expression of NF proteins. Ethanol 31-38 glycogen synthase kinase 3 beta Mus musculus 62-70 19286961-9 2009 Western blots revealed that sildenafil significantly increased phosphorylation of ERK1/2 and GSK-3beta and induced iNOS, eNOS, Bcl-2, and PKG activity in the heart 24 h after treatment. Sildenafil Citrate 28-38 glycogen synthase kinase 3 beta Mus musculus 93-102 19286961-10 2009 PD98059 inhibited the enhanced expression of iNOS, eNOS, and Bcl-2 and the phosphorylation of GSK-3beta. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 0-7 glycogen synthase kinase 3 beta Mus musculus 94-103 19332462-10 2009 CONCLUSIONS: The present results suggest that transgenic overexpression of ALDH2 effectively antagonizes chronic alcohol intake-elicited myocardial hypertrophy and contractile defect through a mechanism that is associated, at least in part, with phosphorylation of ASK-1, GSK-3beta, GATA4, and CREB. Alcohols 113-120 glycogen synthase kinase 3 beta Mus musculus 272-281 19162061-3 2009 Furthermore, lithium (10mM) inhibits GSK-3beta activity by upregulating p-GSK-3beta (ser-9) and increases p-FOXO1 (Ser256) suggesting an effective anti-apoptotic effect. Lithium 13-20 glycogen synthase kinase 3 beta Mus musculus 37-46 19230830-0 2009 Selective alpha7 nicotinic acetylcholine receptor activation regulates glycogen synthase kinase3beta and decreases tau phosphorylation in vivo. Acetylcholine 27-40 glycogen synthase kinase 3 beta Mus musculus 71-100 19006085-9 2009 When human brain extracts were exposed to calcium, GSK-3 was truncated, generating two fragments of approximately 40 and 30 kDa, a proteolytic process that was inhibited by calpeptin, a specific calpain inhibitor. Calcium 42-49 glycogen synthase kinase 3 beta Mus musculus 51-56 19006085-10 2009 Thus, this is the first report of calcium-dependent truncation of human GSK-3. Calcium 34-41 glycogen synthase kinase 3 beta Mus musculus 72-77 19162061-3 2009 Furthermore, lithium (10mM) inhibits GSK-3beta activity by upregulating p-GSK-3beta (ser-9) and increases p-FOXO1 (Ser256) suggesting an effective anti-apoptotic effect. Serine 85-88 glycogen synthase kinase 3 beta Mus musculus 37-46 19162061-3 2009 Furthermore, lithium (10mM) inhibits GSK-3beta activity by upregulating p-GSK-3beta (ser-9) and increases p-FOXO1 (Ser256) suggesting an effective anti-apoptotic effect. Lithium 13-20 glycogen synthase kinase 3 beta Mus musculus 74-83 18690793-9 2009 This finding uncovers the requirement of active GSK3 in RARbeta-induced commitment of mES cells toward the adipocyte lineage. 2-(N-morpholino)ethanesulfonic acid 86-89 glycogen synthase kinase 3 beta Mus musculus 48-52 19223464-5 2009 When PI3K/AKT1 signaling declines following leukemia inhibitory factor withdrawal, active GSK3beta accumulates in the nucleus, where it targets c-myc through phosphorylation on threonine 58 (T58), promoting its degradation. Threonine 177-186 glycogen synthase kinase 3 beta Mus musculus 90-98 19135973-6 2009 Testosterone activation of AR induces GSK3beta and PTEN. Testosterone 0-12 glycogen synthase kinase 3 beta Mus musculus 38-46 19107119-4 2009 In TF-1 and mouse embryonic stem cells, the uptake of a novel detachable TAT-conjugated glycogen synthase kinase-3 (GSK-3) peptide inhibitor was enhanced by an order of magnitude without affecting the cell viability. Triethylenemelamine 73-76 glycogen synthase kinase 3 beta Mus musculus 88-114 19339873-0 2009 Lithium and genetic inhibition of GSK3beta enhance the effect of methamphetamine on circadian rhythms in the mouse. Methamphetamine 65-80 glycogen synthase kinase 3 beta Mus musculus 34-42 19339873-2 2009 Although the actions of lithium on the circadian system are thought to occur through inhibition of glycogen synthase kinase-3beta (GSK3beta), the mechanism by which methamphetamine alters circadian rhythms is unknown. Lithium 24-31 glycogen synthase kinase 3 beta Mus musculus 99-129 19339873-2 2009 Although the actions of lithium on the circadian system are thought to occur through inhibition of glycogen synthase kinase-3beta (GSK3beta), the mechanism by which methamphetamine alters circadian rhythms is unknown. Lithium 24-31 glycogen synthase kinase 3 beta Mus musculus 131-139 19107119-4 2009 In TF-1 and mouse embryonic stem cells, the uptake of a novel detachable TAT-conjugated glycogen synthase kinase-3 (GSK-3) peptide inhibitor was enhanced by an order of magnitude without affecting the cell viability. Triethylenemelamine 73-76 glycogen synthase kinase 3 beta Mus musculus 116-121 19193882-5 2009 In addition, cGMP activation in DRG neurons leads to phosphorylation of glycogen synthase kinase 3 (GSK3), a protein that normally suppresses branching. Cyclic GMP 13-17 glycogen synthase kinase 3 beta Mus musculus 72-98 19126599-0 2009 Cadmium toxicity toward autophagy through ROS-activated GSK-3beta in mesangial cells. Cadmium 0-7 glycogen synthase kinase 3 beta Mus musculus 56-65 19126599-0 2009 Cadmium toxicity toward autophagy through ROS-activated GSK-3beta in mesangial cells. Reactive Oxygen Species 42-45 glycogen synthase kinase 3 beta Mus musculus 56-65 19126599-4 2009 Use of the GSK-3beta inhibitor SB 216763 or the small interfering RNA technique to knockdown the expression of GSK-3beta resulted in a decrease of Cd-induced autophagy. Cadmium 147-149 glycogen synthase kinase 3 beta Mus musculus 11-20 19126599-4 2009 Use of the GSK-3beta inhibitor SB 216763 or the small interfering RNA technique to knockdown the expression of GSK-3beta resulted in a decrease of Cd-induced autophagy. Cadmium 147-149 glycogen synthase kinase 3 beta Mus musculus 111-120 19126599-5 2009 In contrast, overexpression of GSK-3beta by transient transfection potentiated Cd toxicity toward the mesangial cells, suggesting that GSK-3beta plays a crucial role in regulating Cd-induced autophagy. Cadmium 79-81 glycogen synthase kinase 3 beta Mus musculus 31-40 19126599-5 2009 In contrast, overexpression of GSK-3beta by transient transfection potentiated Cd toxicity toward the mesangial cells, suggesting that GSK-3beta plays a crucial role in regulating Cd-induced autophagy. Cadmium 79-81 glycogen synthase kinase 3 beta Mus musculus 135-144 19126599-5 2009 In contrast, overexpression of GSK-3beta by transient transfection potentiated Cd toxicity toward the mesangial cells, suggesting that GSK-3beta plays a crucial role in regulating Cd-induced autophagy. Cadmium 180-182 glycogen synthase kinase 3 beta Mus musculus 31-40 19126599-5 2009 In contrast, overexpression of GSK-3beta by transient transfection potentiated Cd toxicity toward the mesangial cells, suggesting that GSK-3beta plays a crucial role in regulating Cd-induced autophagy. Cadmium 180-182 glycogen synthase kinase 3 beta Mus musculus 135-144 19126599-6 2009 Moreover, a decrease of the phosphorylated level at Ser9 of GSK-3beta was observed by immunoblot after treatment with Cd, indicating GSK-3beta was activated by Cd. Cadmium 118-120 glycogen synthase kinase 3 beta Mus musculus 60-69 19126599-6 2009 Moreover, a decrease of the phosphorylated level at Ser9 of GSK-3beta was observed by immunoblot after treatment with Cd, indicating GSK-3beta was activated by Cd. Cadmium 118-120 glycogen synthase kinase 3 beta Mus musculus 133-142 19126599-6 2009 Moreover, a decrease of the phosphorylated level at Ser9 of GSK-3beta was observed by immunoblot after treatment with Cd, indicating GSK-3beta was activated by Cd. Cadmium 160-162 glycogen synthase kinase 3 beta Mus musculus 60-69 19126599-6 2009 Moreover, a decrease of the phosphorylated level at Ser9 of GSK-3beta was observed by immunoblot after treatment with Cd, indicating GSK-3beta was activated by Cd. Cadmium 160-162 glycogen synthase kinase 3 beta Mus musculus 133-142 19126599-7 2009 This phenomenon was reversed by the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC), demonstrated that ROS might activate GSK-3beta. Reactive Oxygen Species 36-59 glycogen synthase kinase 3 beta Mus musculus 137-146 19126599-7 2009 This phenomenon was reversed by the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC), demonstrated that ROS might activate GSK-3beta. Reactive Oxygen Species 61-64 glycogen synthase kinase 3 beta Mus musculus 137-146 19126599-7 2009 This phenomenon was reversed by the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC), demonstrated that ROS might activate GSK-3beta. Acetylcysteine 76-92 glycogen synthase kinase 3 beta Mus musculus 137-146 19126599-7 2009 This phenomenon was reversed by the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC), demonstrated that ROS might activate GSK-3beta. Acetylcysteine 94-97 glycogen synthase kinase 3 beta Mus musculus 137-146 19126599-7 2009 This phenomenon was reversed by the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC), demonstrated that ROS might activate GSK-3beta. Reactive Oxygen Species 118-121 glycogen synthase kinase 3 beta Mus musculus 137-146 19126599-10 2009 In summary, this study demonstrated that, in MES-13 mesangial cells, Cd-induced autophagy was mediated through the ROS-GSK-3beta signaling pathway. Cadmium 69-71 glycogen synthase kinase 3 beta Mus musculus 119-128 19126599-10 2009 In summary, this study demonstrated that, in MES-13 mesangial cells, Cd-induced autophagy was mediated through the ROS-GSK-3beta signaling pathway. Reactive Oxygen Species 115-118 glycogen synthase kinase 3 beta Mus musculus 119-128 19193882-5 2009 In addition, cGMP activation in DRG neurons leads to phosphorylation of glycogen synthase kinase 3 (GSK3), a protein that normally suppresses branching. Cyclic GMP 13-17 glycogen synthase kinase 3 beta Mus musculus 100-104 19193882-7 2009 More importantly, overexpression of a dominant active form of GSK3 suppresses cGMP-dependent branching in DRG neurons. Cyclic GMP 78-82 glycogen synthase kinase 3 beta Mus musculus 62-66 19193882-8 2009 Thus, our study establishes an intrinsic signaling cascade that links cGMP activation to GSK3 inhibition in controlling axon branching during sensory axon development. Cyclic GMP 70-74 glycogen synthase kinase 3 beta Mus musculus 89-93 19070648-3 2009 Additionally, MPTP increased the level of phospho-c-Jun, a known substrate of c-Jun N-terminal kinase (JNK) and caused a rapid activation of GSK-3beta, evidenced by the decrease in the level of phospho-Ser9 of GSK-3beta. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 14-18 glycogen synthase kinase 3 beta Mus musculus 141-150 18929413-8 2009 Inhibition of GSK3beta by lithium in vivo suppressed the inflammatory response in mice infected with F. tularensis LVS and conferred a survival advantage. Lithium 26-33 glycogen synthase kinase 3 beta Mus musculus 14-22 19171302-0 2009 Involvement of GSK-3 in regulation of murine embryonic stem cell self-renewal revealed by a series of bisindolylmaleimides. bisindolylmaleimide 102-122 glycogen synthase kinase 3 beta Mus musculus 15-20 19171302-4 2009 We synthesized a series of bisindolylmaleimides, a subset of which inhibit GSK-3 in murine ESCs and robustly enhance self-renewal in the presence of leukemia inhibitory factor (LIF) and serum, but not in the absence of LIF. bisindolylmaleimide 27-47 glycogen synthase kinase 3 beta Mus musculus 75-80 19070648-3 2009 Additionally, MPTP increased the level of phospho-c-Jun, a known substrate of c-Jun N-terminal kinase (JNK) and caused a rapid activation of GSK-3beta, evidenced by the decrease in the level of phospho-Ser9 of GSK-3beta. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 14-18 glycogen synthase kinase 3 beta Mus musculus 210-219 19070648-5 2009 (+/-)-Catechin attenuated the phosphorylation of c-Jun and recovered the phosphorylation of GSK-3beta (Ser9). Catechin 0-14 glycogen synthase kinase 3 beta Mus musculus 92-101 19070648-6 2009 These results suggested that the suppression of JNK and GSK-3beta signaling cascades might contribute to the neuroprotective effect of (+/-)-catechin against toxicity of MPTP. Catechin 135-149 glycogen synthase kinase 3 beta Mus musculus 56-65 19070648-6 2009 These results suggested that the suppression of JNK and GSK-3beta signaling cascades might contribute to the neuroprotective effect of (+/-)-catechin against toxicity of MPTP. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 170-174 glycogen synthase kinase 3 beta Mus musculus 56-65 18928402-2 2009 Independent lines of research involving biochemical and behavioral approaches in normal and/or genetically modified mice provide converging evidence for an involvement of the signaling molecules Akt and glycogen synthase kinase-3 (GSK3) in the regulation of behavior by dopamine and serotonin (5-HT). Dopamine 270-278 glycogen synthase kinase 3 beta Mus musculus 231-235 18987114-8 2009 Within 18 days, DOCA/salt treatment significantly increased fluid intake and urinary flow rate, urinary protein and albumin excretion, and blood pressure in both genotypes but the respective values were significantly higher in gsk3(KI) than in gsk3(WT) mice. Desoxycorticosterone Acetate 16-20 glycogen synthase kinase 3 beta Mus musculus 227-231 18987114-8 2009 Within 18 days, DOCA/salt treatment significantly increased fluid intake and urinary flow rate, urinary protein and albumin excretion, and blood pressure in both genotypes but the respective values were significantly higher in gsk3(KI) than in gsk3(WT) mice. Desoxycorticosterone Acetate 16-20 glycogen synthase kinase 3 beta Mus musculus 244-248 18987114-8 2009 Within 18 days, DOCA/salt treatment significantly increased fluid intake and urinary flow rate, urinary protein and albumin excretion, and blood pressure in both genotypes but the respective values were significantly higher in gsk3(KI) than in gsk3(WT) mice. Salts 21-25 glycogen synthase kinase 3 beta Mus musculus 227-231 18987114-8 2009 Within 18 days, DOCA/salt treatment significantly increased fluid intake and urinary flow rate, urinary protein and albumin excretion, and blood pressure in both genotypes but the respective values were significantly higher in gsk3(KI) than in gsk3(WT) mice. Salts 21-25 glycogen synthase kinase 3 beta Mus musculus 244-248 18987114-12 2009 After 18 days, DOCA/salt treatment renal glomerular sclerosis and tubulointerstitial damage were significantly more pronounced in gsk3(KI) than in gsk3(WT) mice. Desoxycorticosterone Acetate 15-19 glycogen synthase kinase 3 beta Mus musculus 130-134 18987114-12 2009 After 18 days, DOCA/salt treatment renal glomerular sclerosis and tubulointerstitial damage were significantly more pronounced in gsk3(KI) than in gsk3(WT) mice. Salts 20-24 glycogen synthase kinase 3 beta Mus musculus 130-134 18928402-2 2009 Independent lines of research involving biochemical and behavioral approaches in normal and/or genetically modified mice provide converging evidence for an involvement of the signaling molecules Akt and glycogen synthase kinase-3 (GSK3) in the regulation of behavior by dopamine and serotonin (5-HT). Dopamine 270-278 glycogen synthase kinase 3 beta Mus musculus 203-229 18996433-10 2009 These increased calcium levels increased the phosphorylation of tau via up-regulation of phospho-glycogen synthase kinase-3beta (GSK-3beta). Calcium 16-23 glycogen synthase kinase 3 beta Mus musculus 129-138 19095952-5 2009 Furthermore, GSK-3 inhibitors, including valproate, attenuate ER stress-induced unesterified cholesterol accumulation in wild-type mouse embryonic fibroblasts. Valproic Acid 41-50 glycogen synthase kinase 3 beta Mus musculus 13-18 19095952-5 2009 Furthermore, GSK-3 inhibitors, including valproate, attenuate ER stress-induced unesterified cholesterol accumulation in wild-type mouse embryonic fibroblasts. Cholesterol 93-104 glycogen synthase kinase 3 beta Mus musculus 13-18 19095952-9 2009 Significant reductions were observed in total hepatic lipids (>50.4%) and hepatic GSK-3beta activity (>55.8%) in mice fed the valproate diet. Valproic Acid 132-141 glycogen synthase kinase 3 beta Mus musculus 85-94 19095952-11 2009 The in vivo anti-atherogenic effects of valproate are consistent with its ability to inhibit GSK-3 and interfere with pro-atherogenic ER stress signaling pathways in vitro. Valproic Acid 40-49 glycogen synthase kinase 3 beta Mus musculus 93-98 18928402-2 2009 Independent lines of research involving biochemical and behavioral approaches in normal and/or genetically modified mice provide converging evidence for an involvement of the signaling molecules Akt and glycogen synthase kinase-3 (GSK3) in the regulation of behavior by dopamine and serotonin (5-HT). Serotonin 283-292 glycogen synthase kinase 3 beta Mus musculus 203-229 18928402-2 2009 Independent lines of research involving biochemical and behavioral approaches in normal and/or genetically modified mice provide converging evidence for an involvement of the signaling molecules Akt and glycogen synthase kinase-3 (GSK3) in the regulation of behavior by dopamine and serotonin (5-HT). Serotonin 283-292 glycogen synthase kinase 3 beta Mus musculus 231-235 18801732-3 2008 We initially found that injecting fasted mice with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) markedly increased Ser-9 phosphorylation of hepatic GSK3beta within 15 min. acadesine 51-96 glycogen synthase kinase 3 beta Mus musculus 157-165 19066717-6 2009 Dex activated both GSK3beta and p38-mitogen-activated protein kinase (MAPK). Dexamethasone 0-3 glycogen synthase kinase 3 beta Mus musculus 19-27 19066717-9 2009 These results suggest that Dex-mediated apoptosis of osteoblasts is facilitated by GSK3beta, but prevented by p38-MAPK. Dexamethasone 27-30 glycogen synthase kinase 3 beta Mus musculus 83-91 19542610-2 2009 Results showed that GSK3 beta overexpression significantly increased PKB phosphorylation at the S473 site but not the T308 site. t308 118-122 glycogen synthase kinase 3 beta Mus musculus 20-29 18801732-3 2008 We initially found that injecting fasted mice with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) markedly increased Ser-9 phosphorylation of hepatic GSK3beta within 15 min. Serine 124-127 glycogen synthase kinase 3 beta Mus musculus 157-165 18778410-8 2008 Our results further show that the inhibition of GSK3 may play a role in mediating the improved glucose tolerance phenotype in Tg(PRDX3) mice. Glucose 95-102 glycogen synthase kinase 3 beta Mus musculus 48-52 19014379-6 2008 Inhibition of the Akt/GSK3beta signaling pathway by acute or chronic LiCl treatment revealed changes in HuR, HuD, pGSK3beta, p-Akt, and beta-catenin protein levels. Lithium Chloride 69-73 glycogen synthase kinase 3 beta Mus musculus 22-30 18952597-5 2008 But beta-catenin inhibition was significantly reduced by GSK3beta RNA interference or GSK3beta inhibitor lithium chloride and proteasome inhibitor MG132. Lithium Chloride 105-121 glycogen synthase kinase 3 beta Mus musculus 86-94 19014379-6 2008 Inhibition of the Akt/GSK3beta signaling pathway by acute or chronic LiCl treatment revealed changes in HuR, HuD, pGSK3beta, p-Akt, and beta-catenin protein levels. pgsk3beta 114-123 glycogen synthase kinase 3 beta Mus musculus 22-30 18701453-0 2008 Glycogen synthase kinase 3beta is a novel regulator of high glucose- and high insulin-induced extracellular matrix protein synthesis in renal proximal tubular epithelial cells. Glucose 60-67 glycogen synthase kinase 3 beta Mus musculus 0-30 18701453-2 2008 We tested the hypothesis that inactivation of glycogen synthase kinase 3beta (GSK3beta) by high glucose and high insulin induces increase in synthesis of laminin beta1 via activation of eIF2Bepsilon. Glucose 96-103 glycogen synthase kinase 3 beta Mus musculus 46-76 18701453-2 2008 We tested the hypothesis that inactivation of glycogen synthase kinase 3beta (GSK3beta) by high glucose and high insulin induces increase in synthesis of laminin beta1 via activation of eIF2Bepsilon. Glucose 96-103 glycogen synthase kinase 3 beta Mus musculus 78-86 18701453-3 2008 Both high glucose and high insulin induced Ser-9 phosphorylation and inactivation of GSK3beta at 2 h that lasted for up to 48 h. This was associated with dephosphorylation of eIF2Bepsilon and eEF2, and increase in phosphorylation of 4E-BP1 and eIF4E. Glucose 10-17 glycogen synthase kinase 3 beta Mus musculus 85-93 18701453-5 2008 Incubation with selective kinase inhibitors showed that high glucose- and high insulin-induced laminin beta1 synthesis and phosphorylation of GSK3beta were dependent on PI 3-kinase, Erk, and mTOR. Glucose 61-68 glycogen synthase kinase 3 beta Mus musculus 142-150 18701453-7 2008 Dominant negative Akt, but not dominant negative p70S6 kinase, inhibited GSK3beta phosphorylation induced by high glucose and high insulin, suggesting Akt but not p70S6 kinase was upstream of GSK3beta. Glucose 114-121 glycogen synthase kinase 3 beta Mus musculus 73-81 18701453-10 2008 GSK3beta and eIF2Bepsilon play a role in augmented protein synthesis associated with high glucose- and high insulin-stimulated hypertrophy and matrix accumulation in renal disease in type 2 diabetes. Glucose 90-97 glycogen synthase kinase 3 beta Mus musculus 0-8 18723505-10 2008 Sildenafil also enhanced the Bcl-2/Bax ratio, phosphorylation of Akt, ERK1/2, and glycogen synthase kinase 3beta. Sildenafil Citrate 0-10 glycogen synthase kinase 3 beta Mus musculus 82-112 18936328-11 2008 Wortmannin, a phosphoinositide 3-kinase inhibitor, attenuated basal phosphorylation of Akt and glycogen synthase kinase-3beta and blocked cardiac protection in Cav-3 OE mice. Wortmannin 0-10 glycogen synthase kinase 3 beta Mus musculus 95-125 18723505-13 2008 Moreover, our results demonstrate that sildenafil activates a PKG-dependent novel signaling cascade that involves activation of ERK and inhibition of glycogen synthase kinase 3beta leading to cytoprotection. Sildenafil Citrate 39-49 glycogen synthase kinase 3 beta Mus musculus 150-180 18449906-5 2008 Interestingly, heparin induces glycogen synthase kinase-3beta (GSK-3beta) inhibition, beta-catenin stabilization and morphological differentiation in both N2a cells and in rat primary hippocampal neuronal cultures. Heparin 15-22 glycogen synthase kinase 3 beta Mus musculus 63-72 18768685-7 2008 Systemic application of the GSK-3 inhibitor lithium to spinal cord-lesioned rats suppresses the activity of this kinase around lesion. Lithium 44-51 glycogen synthase kinase 3 beta Mus musculus 28-33 18768685-8 2008 Treatments with GSK-3 inhibitors including a clinical dose of lithium to rats with thoracic spinal cord transection or contusion injuries induce significant descending corticospinal and serotonergic axon sprouting in caudal spinal cord and promote locomotor functional recovery. Lithium 62-69 glycogen synthase kinase 3 beta Mus musculus 16-21 18768685-9 2008 Our studies suggest that GSK-3 signal is an important therapeutic target for promoting functional recovery of adult CNS injuries and that administration of GSK-3 inhibitors may facilitate the development of an effective treatment to white matter injuries including spinal cord trauma given the wide use of lithium in humans. Lithium 306-313 glycogen synthase kinase 3 beta Mus musculus 25-30 18768685-9 2008 Our studies suggest that GSK-3 signal is an important therapeutic target for promoting functional recovery of adult CNS injuries and that administration of GSK-3 inhibitors may facilitate the development of an effective treatment to white matter injuries including spinal cord trauma given the wide use of lithium in humans. Lithium 306-313 glycogen synthase kinase 3 beta Mus musculus 156-161 18616637-6 2008 Inhibition of Gsk3beta by lithium or Cdk5 by roscovitine reduced tau phosphorylation at Ser(396). Lithium 26-33 glycogen synthase kinase 3 beta Mus musculus 14-22 18616637-6 2008 Inhibition of Gsk3beta by lithium or Cdk5 by roscovitine reduced tau phosphorylation at Ser(396). Roscovitine 45-56 glycogen synthase kinase 3 beta Mus musculus 14-22 18616637-6 2008 Inhibition of Gsk3beta by lithium or Cdk5 by roscovitine reduced tau phosphorylation at Ser(396). Serine 88-91 glycogen synthase kinase 3 beta Mus musculus 14-22 18602000-9 2008 These results demonstrated that GSK3beta is implicated in the regulation of melanogenesis and that pharmacological inhibition of its activity could increase melanin synthesis through mechanisms probably not restricted to Wnt/beta-catenin pathway activation. Melanins 157-164 glycogen synthase kinase 3 beta Mus musculus 32-40 18694957-7 2008 Mice lacking expression of GSK-3beta in skeletal muscle are also viable but, in contrast to the liver-deleted animals, display improved glucose tolerance that is coupled with enhanced insulin-stimulated glycogen synthase regulation and glycogen deposition. Glucose 136-143 glycogen synthase kinase 3 beta Mus musculus 27-36 18694957-7 2008 Mice lacking expression of GSK-3beta in skeletal muscle are also viable but, in contrast to the liver-deleted animals, display improved glucose tolerance that is coupled with enhanced insulin-stimulated glycogen synthase regulation and glycogen deposition. Glycogen 203-211 glycogen synthase kinase 3 beta Mus musculus 27-36 18688045-5 2008 Inhibition of GSK3beta by LiCl reversed the loss in protection in PI3Kgamma(-/-) hearts. Lithium Chloride 26-30 glycogen synthase kinase 3 beta Mus musculus 14-22 18543255-0 2008 Staurosporine rapidly commits 3T3-F442A cells to the formation of adipocytes by activation of GSK-3beta and mobilization of calcium. Staurosporine 0-13 glycogen synthase kinase 3 beta Mus musculus 94-103 18619545-5 2008 Lithium, a GSK-3beta inhibitor, promoted Nrf2 transcriptional activity towards an Antioxidant-Response-Element (ARE) luciferase reporter and cooperated with sulforaphane (SFN) to induce this reporter and to increase the protein levels of heme oxygenase-1 (HO-1), coded by a representative ARE-containing gene. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 11-20 18619545-6 2008 Conversely, ARE activation by SFN was attenuated by over-expression of active GSK-3beta. sulforaphane 30-33 glycogen synthase kinase 3 beta Mus musculus 78-87 18369660-3 2008 Replacement of the serines in the PKB/SGK consensus sequences by alanine (gsk3 ( KI )) confers resistance of GSK3 to PKB/SGK. Serine 19-26 glycogen synthase kinase 3 beta Mus musculus 74-78 18369660-3 2008 Replacement of the serines in the PKB/SGK consensus sequences by alanine (gsk3 ( KI )) confers resistance of GSK3 to PKB/SGK. Serine 19-26 glycogen synthase kinase 3 beta Mus musculus 109-113 18369660-12 2008 During high-salt diet, urinary vasopressin excretion increased to significantly higher levels in gsk3 ( KI ) than in gsk3 ( WT ) mice. Salts 12-16 glycogen synthase kinase 3 beta Mus musculus 97-101 18369660-3 2008 Replacement of the serines in the PKB/SGK consensus sequences by alanine (gsk3 ( KI )) confers resistance of GSK3 to PKB/SGK. Alanine 65-72 glycogen synthase kinase 3 beta Mus musculus 74-78 18369660-13 2008 After water deprivation, body weight decreased faster in gsk3 ( KI ) than in gsk3 ( WT ) mice. Water 6-11 glycogen synthase kinase 3 beta Mus musculus 57-61 18369660-15 2008 The observations disclose a role of PKB/SGK-dependent GSK3 activity in the regulation of steroid hormone release, renal water and electrolyte excretion and blood pressure control. Steroids 89-104 glycogen synthase kinase 3 beta Mus musculus 54-58 18369660-3 2008 Replacement of the serines in the PKB/SGK consensus sequences by alanine (gsk3 ( KI )) confers resistance of GSK3 to PKB/SGK. Alanine 65-72 glycogen synthase kinase 3 beta Mus musculus 109-113 18369660-15 2008 The observations disclose a role of PKB/SGK-dependent GSK3 activity in the regulation of steroid hormone release, renal water and electrolyte excretion and blood pressure control. Water 120-125 glycogen synthase kinase 3 beta Mus musculus 54-58 18369660-8 2008 were significantly lower, but 24-h urinary aldosterone was significantly higher, and corticosterone excretion tended to be higher in gsk3 ( KI ) than in gsk3 ( WT ) mice. Corticosterone 85-99 glycogen synthase kinase 3 beta Mus musculus 133-137 18616990-7 2008 VO(OPT) treatment rescued decreased phosphorylation of glycogen synthesis kinase 3beta (GSK-3beta) at Ser-9. Serine 102-105 glycogen synthase kinase 3 beta Mus musculus 88-97 18640245-2 2008 A recent study demonstrated that combined treatment with lithium and VPA elicits synergistic neuroprotective effects against glutamate excitotoxicity in cultured brain neurons, and the synergy involves potentiated inhibition of glycogen synthase kinase-3 (GSK-3) activity through enhanced GSK-3 serine phosphorylation [Leng Y, Liang MH, Ren M, Marinova Z, Leeds P, Chuang DM (2008) Synergistic neuroprotective effects of lithium and valproic acid or other histone deacetylase inhibitors in neurons: roles of glycogen synthase kinase-3 inhibition. Serine 295-301 glycogen synthase kinase 3 beta Mus musculus 228-254 18550525-4 2008 Inhibitors of GSK3 greatly reduced (>75%) the activating STAT3 tyrosine phosphorylation in mouse primary astrocytes, microglia, and macrophage-derived RAW264.7 cells induced by interferon-gamma (IFNgamma), IFNalpha, interleukin-6, or insulin. Tyrosine 66-74 glycogen synthase kinase 3 beta Mus musculus 14-18 18632640-6 2008 GSK-3beta inhibition with SB216763 or SB415286 also decreased apoptosis in the subgranular zone of the hippocampus in irradiated mice, leading to improved cognitive function in irradiated animals. SB 216763 26-34 glycogen synthase kinase 3 beta Mus musculus 0-9 18583716-3 2008 The aim of this study was to verify the role of GSK-3 using a targeted mouse line lacking the critical N-terminal serine within GSK-3beta (Ser9) and the highly homologous GSK-3alpha (Ser21), which when phosphorylated results in kinase inactivation. Serine 114-120 glycogen synthase kinase 3 beta Mus musculus 128-137 18579278-1 2008 Glycogen synthase kinase-3beta (GSK-3beta) is an enzyme that phosphorylates glycogen synthase, thereby inhibiting glycogen synthesis. Glycogen 76-84 glycogen synthase kinase 3 beta Mus musculus 0-30 18579278-1 2008 Glycogen synthase kinase-3beta (GSK-3beta) is an enzyme that phosphorylates glycogen synthase, thereby inhibiting glycogen synthesis. Glycogen 76-84 glycogen synthase kinase 3 beta Mus musculus 32-41 18632640-6 2008 GSK-3beta inhibition with SB216763 or SB415286 also decreased apoptosis in the subgranular zone of the hippocampus in irradiated mice, leading to improved cognitive function in irradiated animals. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 38-46 glycogen synthase kinase 3 beta Mus musculus 0-9 18430969-2 2008 Previously, we showed that glycogen synthase kinase-3 (GSK-3) phosphorylates IRS-1 at Ser(332). Serine 86-89 glycogen synthase kinase 3 beta Mus musculus 27-53 18566399-2 2008 We investigated whether lithium, an inhibitor of glycogen synthase kinase-3 (GSK3), can ameliorate EAE in mice. Lithium 24-31 glycogen synthase kinase 3 beta Mus musculus 49-75 18566399-2 2008 We investigated whether lithium, an inhibitor of glycogen synthase kinase-3 (GSK3), can ameliorate EAE in mice. Lithium 24-31 glycogen synthase kinase 3 beta Mus musculus 77-81 18566399-8 2008 These results demonstrate that lithium suppresses EAE and identify GSK3 as a new target for inhibition that may be useful for therapeutic intervention of multiple sclerosis and other autoimmune and inflammatory diseases afflicting the CNS. Lithium 31-38 glycogen synthase kinase 3 beta Mus musculus 67-71 18460467-4 2008 Here we establish that dephosphorylation of CRMP2 at the residues targeted by GSK3 (Ser-518/Thr-514/Thr-509) is carried out by a protein phosphatase 1 family member in vitro, in neuroblastoma cells, and primary cortical neurons. Serine 84-87 glycogen synthase kinase 3 beta Mus musculus 78-82 18460467-4 2008 Here we establish that dephosphorylation of CRMP2 at the residues targeted by GSK3 (Ser-518/Thr-514/Thr-509) is carried out by a protein phosphatase 1 family member in vitro, in neuroblastoma cells, and primary cortical neurons. Threonine 92-95 glycogen synthase kinase 3 beta Mus musculus 78-82 18460467-4 2008 Here we establish that dephosphorylation of CRMP2 at the residues targeted by GSK3 (Ser-518/Thr-514/Thr-509) is carried out by a protein phosphatase 1 family member in vitro, in neuroblastoma cells, and primary cortical neurons. Threonine 100-103 glycogen synthase kinase 3 beta Mus musculus 78-82 18430969-2 2008 Previously, we showed that glycogen synthase kinase-3 (GSK-3) phosphorylates IRS-1 at Ser(332). Serine 86-89 glycogen synthase kinase 3 beta Mus musculus 55-60 18430969-3 2008 However, the fact that GSK-3 requires prephosphorylation of its substrates suggested that Ser(336) on IRS-1 was the "priming" site phosphorylated by an as yet unknown protein kinase. Serine 90-93 glycogen synthase kinase 3 beta Mus musculus 23-28 18430969-11 2008 Taken together, our results suggest that IRS-1 is sequentially phosphorylated by PKCbetaII and GSK-3 at Ser(336) and Ser(332). Serine 104-107 glycogen synthase kinase 3 beta Mus musculus 95-100 18302991-8 2008 In vitro addition of lithium chloride, a GSK3beta inhibitor, significantly shifted the acrophase of all genes by 4.2-4.7 h oscillation in BMSCs; however, only the male murine BMSCs displayed a significant increase in the length of the period of oscillation. Lithium Chloride 21-37 glycogen synthase kinase 3 beta Mus musculus 41-49 18392047-8 2008 The self-renewal ability of NSCs from NPC1-/- mice was restored by an NOS inhibitor, L-NAME, which resulted in the inhibition of GSK3beta and caspase-3. NG-Nitroarginine Methyl Ester 85-91 glycogen synthase kinase 3 beta Mus musculus 129-137 18377926-9 2008 Alcohol reduced phosphorylation of Akt and GSK-3beta as well as GSK-3beta expression and the effect was exaggerated by ADH. Alcohols 0-7 glycogen synthase kinase 3 beta Mus musculus 43-52 18377926-9 2008 Alcohol reduced phosphorylation of Akt and GSK-3beta as well as GSK-3beta expression and the effect was exaggerated by ADH. Alcohols 0-7 glycogen synthase kinase 3 beta Mus musculus 64-73 18520779-1 2008 Lithium modulates glycogen synthase kinase 3beta (GSK-3beta), a kinase involved in Alzheimer disease-related tau pathology. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 18-48 18520779-1 2008 Lithium modulates glycogen synthase kinase 3beta (GSK-3beta), a kinase involved in Alzheimer disease-related tau pathology. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 50-59 18520779-4 2008 Lithium also reduced both the levels and activity of GSK-3beta and the activity of cyclin-dependent kinase 5 and reduced hyperphosphorylation of 3 different phosphoepitopes of tau: Ser199, Ser212, and Ser396. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 53-62 18520779-6 2008 Both lithium and SB415286, a specific inhibitor of GSK-3beta, reduced apoptosis in vitro. Lithium 5-12 glycogen synthase kinase 3 beta Mus musculus 51-60 18520779-6 2008 Both lithium and SB415286, a specific inhibitor of GSK-3beta, reduced apoptosis in vitro. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 17-25 glycogen synthase kinase 3 beta Mus musculus 51-60 18520779-7 2008 Taken together, these in vivo and in vitro findings of lithium-mediated reductions in GSK-3beta and cyclin-dependent kinase 5 activities, tau phosphorylation, apoptotic activity, and cell death provide a strong rationale for the use of lithium as a potential treatment in neurodegenerative diseases. Lithium 55-62 glycogen synthase kinase 3 beta Mus musculus 86-95 18084742-0 2008 Cordycepin (3"-deoxyadenosine) inhibits the growth of B16-BL6 mouse melanoma cells through the stimulation of adenosine A3 receptor followed by glycogen synthase kinase-3beta activation and cyclin D1 suppression. cordycepin 0-10 glycogen synthase kinase 3 beta Mus musculus 144-174 18084742-0 2008 Cordycepin (3"-deoxyadenosine) inhibits the growth of B16-BL6 mouse melanoma cells through the stimulation of adenosine A3 receptor followed by glycogen synthase kinase-3beta activation and cyclin D1 suppression. cordycepin 12-29 glycogen synthase kinase 3 beta Mus musculus 144-174 18084742-5 2008 Next, indirubin, a glycogen synthase kinase-3beta (GSK-3beta) inhibitor, antagonized the growth suppression induced by cordycepin. indirubin 6-15 glycogen synthase kinase 3 beta Mus musculus 19-49 18084742-5 2008 Next, indirubin, a glycogen synthase kinase-3beta (GSK-3beta) inhibitor, antagonized the growth suppression induced by cordycepin. indirubin 6-15 glycogen synthase kinase 3 beta Mus musculus 51-60 18490522-9 2008 In GSK3beta-S9A mice, only CsA, but not postconditioning or SB21, reduced infarct size. Cyclosporine 27-30 glycogen synthase kinase 3 beta Mus musculus 3-11 18490522-10 2008 Postconditioning, CsA, and SB21 all improved the resistance of the mPTP in wild-type mice, but only CsA did so in GSK3beta-S9A mice. Cyclosporine 100-103 glycogen synthase kinase 3 beta Mus musculus 114-122 18469539-0 2008 Glycogen synthase kinase-3beta heterozygote knockout mice as a model of findings in postmortem schizophrenia brain or as a model of behaviors mimicking lithium action: negative results. Lithium 152-159 glycogen synthase kinase 3 beta Mus musculus 0-30 18217188-0 2008 17beta-estradiol attenuates glycogen synthase kinase-3beta activation and tau hyperphosphorylation in Akt-independent manner. Estradiol 0-16 glycogen synthase kinase 3 beta Mus musculus 28-58 18268048-10 2008 Administration of GSK-3beta inhibitors lithium chloride and L803-mts restored glucose homeostasis and rescued the glucose intolerance and impaired insulin response in L-Stat3(-/-) mice. Lithium Chloride 39-55 glycogen synthase kinase 3 beta Mus musculus 18-27 18268048-10 2008 Administration of GSK-3beta inhibitors lithium chloride and L803-mts restored glucose homeostasis and rescued the glucose intolerance and impaired insulin response in L-Stat3(-/-) mice. Glucose 78-85 glycogen synthase kinase 3 beta Mus musculus 18-27 18268048-8 2008 During feeding, both mRNA and protein levels of GSK-3beta decreased in Stat3(f/+) mice, which reflected the need of hepatocytes for insulin to induce glycogen synthesis. Glycogen 150-158 glycogen synthase kinase 3 beta Mus musculus 48-57 17222948-7 2008 In contrast to the deficiency in PS1, mutant PS1 activated GSK-3beta by decreasing phosphorylation on Ser-9, which correlated with increased phosphorylation of protein tau at Ser-396-Ser-404 (PHF1/AD2 epitope). Serine 102-105 glycogen synthase kinase 3 beta Mus musculus 59-68 18027881-3 2008 Inhibition of GSK-3beta by SB216763 or by over-expression of a dominant negative mutant of GSK-3beta significantly enhanced TNF-alpha expression in LPS-stimulated cardiomyocytes, in association with an increase in p65 phosphorylation. SB 216763 27-35 glycogen synthase kinase 3 beta Mus musculus 14-23 18322101-10 2008 An additive increase in GSK-3 serine phosphorylation was also observed in mice chronically treated with lithium and VPA. Serine 30-36 glycogen synthase kinase 3 beta Mus musculus 24-29 18295757-1 2008 Olanzapine was investigated as an inhibitor of glycogen synthase kinase-3beta (GSK-3beta) in an attempt to evaluate its effect on blood glucose level. Glucose 136-143 glycogen synthase kinase 3 beta Mus musculus 79-88 18295757-2 2008 The investigation included simulated docking experiments to fit olanzapine within the binding pocket of GSK-3beta followed by in vitro enzyme inhibition assay as well as in vivo subchronic animal treatment. Olanzapine 64-74 glycogen synthase kinase 3 beta Mus musculus 104-113 18295757-3 2008 Olanzapine was found to readily fit within the binding pocket of GSK-3beta in a low energy orientation characterized with optimal attractive interactions bridging the tricyclic thienobenzodiazepine nitrogen and sulfur atoms of olanzapine and the residue of VAL-135 of GSK-3beta. Olanzapine 0-10 glycogen synthase kinase 3 beta Mus musculus 65-74 18295757-3 2008 Olanzapine was found to readily fit within the binding pocket of GSK-3beta in a low energy orientation characterized with optimal attractive interactions bridging the tricyclic thienobenzodiazepine nitrogen and sulfur atoms of olanzapine and the residue of VAL-135 of GSK-3beta. Olanzapine 0-10 glycogen synthase kinase 3 beta Mus musculus 268-277 18295757-3 2008 Olanzapine was found to readily fit within the binding pocket of GSK-3beta in a low energy orientation characterized with optimal attractive interactions bridging the tricyclic thienobenzodiazepine nitrogen and sulfur atoms of olanzapine and the residue of VAL-135 of GSK-3beta. thienobenzodiazepine 177-197 glycogen synthase kinase 3 beta Mus musculus 65-74 18295757-3 2008 Olanzapine was found to readily fit within the binding pocket of GSK-3beta in a low energy orientation characterized with optimal attractive interactions bridging the tricyclic thienobenzodiazepine nitrogen and sulfur atoms of olanzapine and the residue of VAL-135 of GSK-3beta. Nitrogen 198-206 glycogen synthase kinase 3 beta Mus musculus 65-74 18295757-3 2008 Olanzapine was found to readily fit within the binding pocket of GSK-3beta in a low energy orientation characterized with optimal attractive interactions bridging the tricyclic thienobenzodiazepine nitrogen and sulfur atoms of olanzapine and the residue of VAL-135 of GSK-3beta. Sulfur 211-217 glycogen synthase kinase 3 beta Mus musculus 65-74 18295757-3 2008 Olanzapine was found to readily fit within the binding pocket of GSK-3beta in a low energy orientation characterized with optimal attractive interactions bridging the tricyclic thienobenzodiazepine nitrogen and sulfur atoms of olanzapine and the residue of VAL-135 of GSK-3beta. Olanzapine 227-237 glycogen synthase kinase 3 beta Mus musculus 65-74 18295757-3 2008 Olanzapine was found to readily fit within the binding pocket of GSK-3beta in a low energy orientation characterized with optimal attractive interactions bridging the tricyclic thienobenzodiazepine nitrogen and sulfur atoms of olanzapine and the residue of VAL-135 of GSK-3beta. Valine 257-260 glycogen synthase kinase 3 beta Mus musculus 65-74 18295757-5 2008 Moreover; olanzapine was found to potently inhibit recombinant GSK-3beta in vitro (IC(50) value=91.0 nM). Olanzapine 10-20 glycogen synthase kinase 3 beta Mus musculus 63-72 18295757-6 2008 Our findings strongly suggest that olanzapine has significant GSK-3beta inhibition activity that could justify some of its pharmacological effects and glucose metabolic disturbances. Olanzapine 35-45 glycogen synthase kinase 3 beta Mus musculus 62-71 18295757-0 2008 Olanzapine inhibits glycogen synthase kinase-3beta: an investigation by docking simulation and experimental validation. Olanzapine 0-10 glycogen synthase kinase 3 beta Mus musculus 20-50 18295757-1 2008 Olanzapine was investigated as an inhibitor of glycogen synthase kinase-3beta (GSK-3beta) in an attempt to evaluate its effect on blood glucose level. Olanzapine 0-10 glycogen synthase kinase 3 beta Mus musculus 47-77 18295757-1 2008 Olanzapine was investigated as an inhibitor of glycogen synthase kinase-3beta (GSK-3beta) in an attempt to evaluate its effect on blood glucose level. Olanzapine 0-10 glycogen synthase kinase 3 beta Mus musculus 79-88 18219478-2 2008 However, despite recent progress in our understanding of the role of GSK3 in the regulation of glucose metabolism in peripheral tissues, the involvement of GSK3 in islet beta cell growth and function in vivo is unknown. Glucose 95-102 glycogen synthase kinase 3 beta Mus musculus 69-73 18219478-7 2008 In MIN6 cells, the activity of GSK3beta was regulated by glucose, in a fashion largely dependent on phosphatidylinositol 3-kinase. Glucose 57-64 glycogen synthase kinase 3 beta Mus musculus 31-39 18336525-4 2008 Consistent with these findings, in a double transgenic mice model (Tet/GSK-3beta/VLW) overexpressing the enzyme glycogen synthase kinase-3beta (GSK-3beta) and tau with a triple FTDP-17 mutation (VLW) with AD-like neurodegeneration, phosphorylation at sites Ser(199/202)-Thr(205) was greater than truncated tau. tetramethylenedisulfotetramine 67-70 glycogen synthase kinase 3 beta Mus musculus 112-142 18336525-4 2008 Consistent with these findings, in a double transgenic mice model (Tet/GSK-3beta/VLW) overexpressing the enzyme glycogen synthase kinase-3beta (GSK-3beta) and tau with a triple FTDP-17 mutation (VLW) with AD-like neurodegeneration, phosphorylation at sites Ser(199/202)-Thr(205) was greater than truncated tau. Serine 257-260 glycogen synthase kinase 3 beta Mus musculus 112-142 18336525-4 2008 Consistent with these findings, in a double transgenic mice model (Tet/GSK-3beta/VLW) overexpressing the enzyme glycogen synthase kinase-3beta (GSK-3beta) and tau with a triple FTDP-17 mutation (VLW) with AD-like neurodegeneration, phosphorylation at sites Ser(199/202)-Thr(205) was greater than truncated tau. Threonine 270-273 glycogen synthase kinase 3 beta Mus musculus 112-142 18190791-2 2008 We previously reported that ethanol-induced apoptotic neurodegeneration in the postnatal day 7 (P7) mice is associated with decreases in phosphorylation levels of Akt, glycogen synthase kinase-3beta (GSK-3beta), and AMP-activated protein kinase (AMPK), and alteration in lipid profiles in the brain. Ethanol 28-35 glycogen synthase kinase 3 beta Mus musculus 168-198 18190791-2 2008 We previously reported that ethanol-induced apoptotic neurodegeneration in the postnatal day 7 (P7) mice is associated with decreases in phosphorylation levels of Akt, glycogen synthase kinase-3beta (GSK-3beta), and AMP-activated protein kinase (AMPK), and alteration in lipid profiles in the brain. Ethanol 28-35 glycogen synthase kinase 3 beta Mus musculus 200-209 18190791-4 2008 Immunoblot and immunohistochemical analyses showed that lithium significantly blocked ethanol-induced caspase-3 activation and reduction in phosphorylation levels of Akt, GSK-3beta, and AMPK. Lithium 56-63 glycogen synthase kinase 3 beta Mus musculus 171-180 18190791-4 2008 Immunoblot and immunohistochemical analyses showed that lithium significantly blocked ethanol-induced caspase-3 activation and reduction in phosphorylation levels of Akt, GSK-3beta, and AMPK. Ethanol 86-93 glycogen synthase kinase 3 beta Mus musculus 171-180 18190791-6 2008 These results suggest that Akt, GSK-3beta, and AMPK are involved in ethanol-induced neurodegeneration and the neuroprotective effects of lithium by modulating both apoptotic and survival pathways. Ethanol 68-75 glycogen synthase kinase 3 beta Mus musculus 32-41 18190791-6 2008 These results suggest that Akt, GSK-3beta, and AMPK are involved in ethanol-induced neurodegeneration and the neuroprotective effects of lithium by modulating both apoptotic and survival pathways. Lithium 137-144 glycogen synthase kinase 3 beta Mus musculus 32-41 18322101-2 2008 Lithium, a glycogen synthase kinase-3 (GSK-3) inhibitor, and VPA, a histone deacetylase (HDAC) inhibitor, have neuroprotective effects. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 39-44 18322101-6 2008 Combined treatment with lithium and VPA potentiated serine phosphorylation of GSK-3 alpha and beta isoforms and inhibition of GSK-3 enzyme activity. Lithium 24-31 glycogen synthase kinase 3 beta Mus musculus 78-83 18322101-6 2008 Combined treatment with lithium and VPA potentiated serine phosphorylation of GSK-3 alpha and beta isoforms and inhibition of GSK-3 enzyme activity. Valproic Acid 36-39 glycogen synthase kinase 3 beta Mus musculus 78-83 18322101-6 2008 Combined treatment with lithium and VPA potentiated serine phosphorylation of GSK-3 alpha and beta isoforms and inhibition of GSK-3 enzyme activity. Serine 52-58 glycogen synthase kinase 3 beta Mus musculus 78-83 18322101-10 2008 An additive increase in GSK-3 serine phosphorylation was also observed in mice chronically treated with lithium and VPA. Lithium 104-111 glycogen synthase kinase 3 beta Mus musculus 24-29 18322101-10 2008 An additive increase in GSK-3 serine phosphorylation was also observed in mice chronically treated with lithium and VPA. Valproic Acid 116-119 glycogen synthase kinase 3 beta Mus musculus 24-29 18322101-11 2008 Together, for the first time, our results demonstrate synergistic neuroprotective effects of lithium and HDAC inhibitors and suggest that GSK-3 inhibition is a likely molecular target for the synergistic neuroprotection. Lithium 93-100 glycogen synthase kinase 3 beta Mus musculus 138-143 18322105-2 2008 Here we show that young p25 overexpressing mice have enhanced cdk5 activity but reduced GSK3beta activity attributable to phosphorylation at the inhibitory GSK3beta-serine 9 (GSK3beta-S9) site. Serine 165-171 glycogen synthase kinase 3 beta Mus musculus 156-164 18322105-2 2008 Here we show that young p25 overexpressing mice have enhanced cdk5 activity but reduced GSK3beta activity attributable to phosphorylation at the inhibitory GSK3beta-serine 9 (GSK3beta-S9) site. Serine 165-171 glycogen synthase kinase 3 beta Mus musculus 156-164 18288891-6 2008 Crossing these mice with those having haploinsufficiency for Gsk-3beta (Gsk-3beta+/-) reduced insulin resistance by augmenting whole-body glucose disposal, and significantly reduced beta-cell mass. Glucose 138-145 glycogen synthase kinase 3 beta Mus musculus 61-70 18195042-6 2008 Nonetheless, inhibition of GSK-3 catalytic activity with lithium or SB216763 protects GSK-3alpha/beta(S21A/S9A) neurons from death. Lithium 57-64 glycogen synthase kinase 3 beta Mus musculus 27-32 18195042-6 2008 Nonetheless, inhibition of GSK-3 catalytic activity with lithium or SB216763 protects GSK-3alpha/beta(S21A/S9A) neurons from death. SB 216763 68-76 glycogen synthase kinase 3 beta Mus musculus 27-32 18029441-4 2008 It was found that the stress activator anisomycin enhanced the ability of GSK-3 to phosphorylate IRS-2. Anisomycin 39-49 glycogen synthase kinase 3 beta Mus musculus 74-79 18029441-7 2008 IRS-2 deletion mutants enabled us to localize the GSK-3 and JNK phosphorylation sites to serines 484 and 488, respectively. Serine 89-96 glycogen synthase kinase 3 beta Mus musculus 50-55 18029441-9 2008 Treatment of H4IIE liver cells with anisomycin inhibited insulin-induced tyrosine phosphorylation of IRS-2; inhibition was reversed by pretreatment with the JNK and GSK-3 inhibitors. Anisomycin 36-46 glycogen synthase kinase 3 beta Mus musculus 165-170 18029441-10 2008 Moreover, overexpression of JNK and GSK-3 in H4IIE cells reduced insulin-induced tyrosine phosphorylation of IRS-2 and its association with the p85 regulatory subunit of phosphatidylinositol 3-kinase. Tyrosine 81-89 glycogen synthase kinase 3 beta Mus musculus 36-41 18029441-12 2008 Together, our data indicate that IRS-2 is sequentially phosphorylated by JNK and GSK-3 at serines 484/488 and provide evidence for their inhibitory role in hepatic insulin signaling. Serine 90-97 glycogen synthase kinase 3 beta Mus musculus 81-86 18260796-11 2008 Our data show that simvastatin treatment increases phosphorylation of v-akt murine thymoma viral oncogene homolog (Akt), glycogen synthase kinase-3beta (GSK-3beta), and cAMP response element-binding proteins (CREB); elevates the expression of BDNF and VEGF in the DG; increases cell proliferation and differentiation in the DG; and enhances the recovery of spatial learning. Simvastatin 19-30 glycogen synthase kinase 3 beta Mus musculus 121-151 18260796-11 2008 Our data show that simvastatin treatment increases phosphorylation of v-akt murine thymoma viral oncogene homolog (Akt), glycogen synthase kinase-3beta (GSK-3beta), and cAMP response element-binding proteins (CREB); elevates the expression of BDNF and VEGF in the DG; increases cell proliferation and differentiation in the DG; and enhances the recovery of spatial learning. Simvastatin 19-30 glycogen synthase kinase 3 beta Mus musculus 153-162 18288891-6 2008 Crossing these mice with those having haploinsufficiency for Gsk-3beta (Gsk-3beta+/-) reduced insulin resistance by augmenting whole-body glucose disposal, and significantly reduced beta-cell mass. Glucose 138-145 glycogen synthase kinase 3 beta Mus musculus 72-81 18003720-9 2008 Injection of glucose containing 2-deoxy-[3H]glucose and [14C]glucose also resulted in similar rates of muscle glucose uptake and glycogen synthesis in vivo between wild-type and GSK3 knockin mice. Glucose 13-20 glycogen synthase kinase 3 beta Mus musculus 178-182 18191226-2 2008 Here we show that lithium, a pharmacological agent used for the management of psychiatric disorders such as bipolar disorder, schizophrenia, and depression, regulates Akt/glycogen synthase kinase 3 (GSK3) signaling and related behaviors in mice by disrupting a signaling complex composed of Akt, beta-arrestin 2, and protein phosphatase 2A. Lithium 18-25 glycogen synthase kinase 3 beta Mus musculus 199-203 18191226-3 2008 When administered to beta-arrestin 2 knockout mice, lithium fails to affect Akt/GSK3 signaling and induce behavioral changes associated with GSK3 inhibition as it does in normal animals. Lithium 52-59 glycogen synthase kinase 3 beta Mus musculus 141-145 17961518-0 2007 Arsenic inhibits neurofilament transport and induces perikaryal accumulation of phosphorylated neurofilaments: roles of JNK and GSK-3beta. Arsenic 0-7 glycogen synthase kinase 3 beta Mus musculus 128-137 17901358-4 2007 Tg-GSK-3beta-DN exhibited concentric hypertrophy at baseline, accompanied by upregulation of the alpha-myosin heavy chain gene and increases in cardiac function, as evidenced by a significantly greater Emax after dobutamine infusion and percentage of contraction in isolated cardiac myocytes, indicating that inhibition of GSK-3beta induces well-compensated hypertrophy. Dobutamine 213-223 glycogen synthase kinase 3 beta Mus musculus 3-12 17901358-6 2007 Induction of the GSK-3beta transgene in tetracycline-regulatable wild-type GSK-3beta mice induced left ventricular dysfunction and premature death, accompanied by increases in apoptosis and fibrosis. Tetracycline 40-52 glycogen synthase kinase 3 beta Mus musculus 17-26 17901358-6 2007 Induction of the GSK-3beta transgene in tetracycline-regulatable wild-type GSK-3beta mice induced left ventricular dysfunction and premature death, accompanied by increases in apoptosis and fibrosis. Tetracycline 40-52 glycogen synthase kinase 3 beta Mus musculus 75-84 18003720-4 2008 The aim of this study was to investigate if dephosphorylation of GS mediated via GSK3 is required for normal glycogen synthesis in skeletal muscle with insulin. Glycogen 109-117 glycogen synthase kinase 3 beta Mus musculus 81-85 18003720-8 2008 Incubation of isolated soleus muscle in Krebs buffer containing 5.5 mM glucose in the presence or absence of insulin revealed that the levels of G-6-P, the rate of [14C]glucose incorporation into glycogen, and an increase in total glycogen content were similar between wild-type and GSK3 knockin mice. Glucose 71-78 glycogen synthase kinase 3 beta Mus musculus 283-287 18074481-8 2007 In the treatment group, the potent and selective GSK-3beta inhibitor 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) was administered 1 hr and 6 hrs after the first injection of cerulein (10 mg/kg, intraperitoneally). 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 69-118 glycogen synthase kinase 3 beta Mus musculus 49-58 18074481-8 2007 In the treatment group, the potent and selective GSK-3beta inhibitor 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8) was administered 1 hr and 6 hrs after the first injection of cerulein (10 mg/kg, intraperitoneally). 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 120-126 glycogen synthase kinase 3 beta Mus musculus 49-58 17726008-8 2007 Furthermore, GSK3beta phosphorylates specific serines and threonines in the N terminus of MEKK4. Threonine 58-68 glycogen synthase kinase 3 beta Mus musculus 13-21 17726008-7 2007 Inhibition of GSK3beta kinase activity with SB216763 results in enhanced MEKK4 kinase activity and increased JNK and p38 activation, indicating that an active state of GSK3beta is required for binding and inhibition of MEKK4 dimerization. SB 216763 44-52 glycogen synthase kinase 3 beta Mus musculus 14-22 17556716-9 2007 MEASUREMENTS AND MAIN RESULTS: Intravenous administration of 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8), a selective glycogen synthase kinase-3beta inhibitor, significantly inhibited ovalbumin-induced increases in total cell counts, eosinophil counts, and IL-5, IL-13, and eotaxin levels recovered in bronchoalveolar lavage fluid in a dose-dependent manner. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 61-110 glycogen synthase kinase 3 beta Mus musculus 133-163 17726008-7 2007 Inhibition of GSK3beta kinase activity with SB216763 results in enhanced MEKK4 kinase activity and increased JNK and p38 activation, indicating that an active state of GSK3beta is required for binding and inhibition of MEKK4 dimerization. SB 216763 44-52 glycogen synthase kinase 3 beta Mus musculus 168-176 17726008-8 2007 Furthermore, GSK3beta phosphorylates specific serines and threonines in the N terminus of MEKK4. Serine 46-53 glycogen synthase kinase 3 beta Mus musculus 13-21 17908561-2 2007 GSK-3 activity is elevated in human and rodent models of diabetes, and various GSK-3 inhibitors improve glucose tolerance and insulin sensitivity in rodent models of obesity and diabetes. Glucose 104-111 glycogen synthase kinase 3 beta Mus musculus 0-5 17908561-2 2007 GSK-3 activity is elevated in human and rodent models of diabetes, and various GSK-3 inhibitors improve glucose tolerance and insulin sensitivity in rodent models of obesity and diabetes. Glucose 104-111 glycogen synthase kinase 3 beta Mus musculus 79-84 17682063-5 2007 Mutational analysis of MafA and pharmacological inhibition of GSK3 in MIN6 beta cells strongly suggest that the rate of MafA protein degradation is regulated by glucose, that MafA is constitutively phosphorylated by GSK3, and that phosphorylation is a prerequisite for rapid degradation of MafA under low-glucose conditions. Glucose 161-168 glycogen synthase kinase 3 beta Mus musculus 62-66 17682063-5 2007 Mutational analysis of MafA and pharmacological inhibition of GSK3 in MIN6 beta cells strongly suggest that the rate of MafA protein degradation is regulated by glucose, that MafA is constitutively phosphorylated by GSK3, and that phosphorylation is a prerequisite for rapid degradation of MafA under low-glucose conditions. Glucose 305-312 glycogen synthase kinase 3 beta Mus musculus 62-66 17682063-5 2007 Mutational analysis of MafA and pharmacological inhibition of GSK3 in MIN6 beta cells strongly suggest that the rate of MafA protein degradation is regulated by glucose, that MafA is constitutively phosphorylated by GSK3, and that phosphorylation is a prerequisite for rapid degradation of MafA under low-glucose conditions. Glucose 305-312 glycogen synthase kinase 3 beta Mus musculus 216-220 17786208-3 2007 The cleidocranial dysplasia in heterozygous Runx2-deficient mice was significantly rescued by the genetic insufficiency of GSK-3beta or the oral administration of lithium chloride, a selective inhibitor of GSK-3beta. Lithium Chloride 163-179 glycogen synthase kinase 3 beta Mus musculus 206-215 17299510-1 2007 Lithium inhibits glycogen synthase kinase-3 (GSK-3) at therapeutic concentrations; however, it is unclear if this inhibition and its downstream effects on specific signaling pathways are relevant to the treatment of bipolar disorder and depression. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 17-43 17299510-1 2007 Lithium inhibits glycogen synthase kinase-3 (GSK-3) at therapeutic concentrations; however, it is unclear if this inhibition and its downstream effects on specific signaling pathways are relevant to the treatment of bipolar disorder and depression. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 45-50 17299510-10 2007 The results of this study, in which beta-catenin transgenic mice exhibited behaviors identical to those observed in lithium-treated mice, are consistent with the hypothesis that the behavioral effects of lithium in these models are mediated through its direct inhibition of GSK-3 and the consequent increase in beta-catenin. Lithium 116-123 glycogen synthase kinase 3 beta Mus musculus 274-279 17299510-10 2007 The results of this study, in which beta-catenin transgenic mice exhibited behaviors identical to those observed in lithium-treated mice, are consistent with the hypothesis that the behavioral effects of lithium in these models are mediated through its direct inhibition of GSK-3 and the consequent increase in beta-catenin. Lithium 204-211 glycogen synthase kinase 3 beta Mus musculus 274-279 17650175-9 2007 Additionally, although DMHF did not inhibit cAMP production by alpha-MSH, both CRE binding protein (CREB) phosphorylation and the reduction of glycogen synthase kinase-3beta phosphorylation by alpha-MSH were blocked by DMHF. furaneol 23-27 glycogen synthase kinase 3 beta Mus musculus 143-173 17662302-7 2007 Despite microtubule disruption evidenced on deconvolution microscopy, vincristine activated a prosurvival pathway resulting in increased phosphorylation of Akt, ERK and GSK-3beta and in reduced cytochrome C release into the cytosol. Vincristine 70-81 glycogen synthase kinase 3 beta Mus musculus 169-178 17417726-3 2007 In this study, we evaluated the expressions of molecules associated with the GSK3beta signaling pathway, following the induction of an excitotoxic lesion in mouse brain by kainic acid (KA) injection, which caused pyramidal cell degeneration in the hippocampal CA3 region. Kainic Acid 172-183 glycogen synthase kinase 3 beta Mus musculus 77-85 17545163-8 2007 Insulin-stimulated phosphorylation of IR, IRS proteins, Akt/protein kinase B, glycogen synthase kinase 3beta, and p70(S6K) was impaired in DHet mouse muscle and liver and was differentially improved by PTP1B deficiency. dhet 139-143 glycogen synthase kinase 3 beta Mus musculus 78-108 17548347-6 2007 Genotoxic stress induced by camptothecin treatment of NPCs stabilized p53, which formed a complex with GSK3beta and activated Bax and caspase-3. Camptothecin 28-40 glycogen synthase kinase 3 beta Mus musculus 103-111 17548347-7 2007 Camptothecin-induced activation of caspase-3 was reduced by GSK3 inhibitors in both bax(+)(/)(+) and bax(-/-) NPCs. Camptothecin 0-12 glycogen synthase kinase 3 beta Mus musculus 60-64 17650175-9 2007 Additionally, although DMHF did not inhibit cAMP production by alpha-MSH, both CRE binding protein (CREB) phosphorylation and the reduction of glycogen synthase kinase-3beta phosphorylation by alpha-MSH were blocked by DMHF. furaneol 219-223 glycogen synthase kinase 3 beta Mus musculus 143-173 17333113-7 2007 FAK was also found to interact downstream with insulin receptor substrate-1, phosphatidylinositol 3-kinase and protein kinase C and glycogen synthase kinase 3beta, leading to translocation of glucose transporter 4 and resulting in the regulation of glucose uptake. Glucose 192-199 glycogen synthase kinase 3 beta Mus musculus 111-162 17552518-8 2007 The present chemistry, modeling, and biology efforts have identified 3-benzofuranyl-4-indolylmaleimides as potent and relatively selective GSK-3beta inhibitors. 3-benzofuranyl-4-indolylmaleimides 69-103 glycogen synthase kinase 3 beta Mus musculus 139-148 17322282-7 2007 In these lungs, tyrosine phosphorylation of beta-catenin and serine/threonine phosphorylation of Akt, glycogen synthase kinase 3beta (GSK3beta), and ERK1/2 increased significantly with peak effects at 60 min. Tyrosine 16-24 glycogen synthase kinase 3 beta Mus musculus 134-142 17322282-7 2007 In these lungs, tyrosine phosphorylation of beta-catenin and serine/threonine phosphorylation of Akt, glycogen synthase kinase 3beta (GSK3beta), and ERK1/2 increased significantly with peak effects at 60 min. Threonine 68-77 glycogen synthase kinase 3 beta Mus musculus 102-132 17322282-7 2007 In these lungs, tyrosine phosphorylation of beta-catenin and serine/threonine phosphorylation of Akt, glycogen synthase kinase 3beta (GSK3beta), and ERK1/2 increased significantly with peak effects at 60 min. Threonine 68-77 glycogen synthase kinase 3 beta Mus musculus 134-142 17568620-7 2007 In this study, diosgenin inhibited the reduction of Akt and GSK 3beta phosphorylation induced by LY294,002, a PI3K inhibitor. ly294 97-102 glycogen synthase kinase 3 beta Mus musculus 60-69 17510631-4 2007 Here, we have generated transgenic mice with conditional (tetracycline system) expression of dominant-negative-GSK-3 as an alternative genetic approach to predict the outcome of chronic GSK-3 inhibition, either per se, or in combination with mouse models of disease. Tetracycline 58-70 glycogen synthase kinase 3 beta Mus musculus 111-116 17510631-6 2007 Tet/DN-GSK-3 mice showed increased neuronal apoptosis and impaired motor coordination. tetramethylenedisulfotetramine 0-3 glycogen synthase kinase 3 beta Mus musculus 7-12 17468512-0 2007 Akt GSK-3 pathway as a target in genistein-induced inhibition of TRAMP prostate cancer progression toward a poorly differentiated phenotype. Genistein 33-42 glycogen synthase kinase 3 beta Mus musculus 4-9 17468512-5 2007 Incorporation of genistein in the diet significantly inhibited the activation of Akt, restored the activation of GSK-3beta, reduced cyclin D1 levels post-transcriptionally and maintained the expression of the cadherin-1 complex via down-regulation of snail-1. Genistein 17-26 glycogen synthase kinase 3 beta Mus musculus 113-122 17468512-6 2007 By identifying the Akt-GSK-3 pathway and subsequently its downstream effectors, as targets for genistein chemopreventive action, we have elucidated one possible mechanism by which genistein decreases the proliferative potential, retards cancer progression and maintains the integrity of the prostatic epithelial cells in vivo. Genistein 95-104 glycogen synthase kinase 3 beta Mus musculus 23-28 17484726-0 2007 Regulation of PI3K/Akt/GSK-3 pathway by cannabinoids in the brain. Cannabinoids 40-52 glycogen synthase kinase 3 beta Mus musculus 23-28 17484726-9 2007 In addition, THC increased the phosphorylation of glycogen synthase kinase 3 beta. Dronabinol 13-16 glycogen synthase kinase 3 beta Mus musculus 50-81 17880775-0 2007 Glycogen synthase kinase-3beta inhibition attenuates the development of bleomycin-induced lung injury. Bleomycin 72-81 glycogen synthase kinase 3 beta Mus musculus 0-30 17880775-2 2007 The aim of this study is to investigate the effects of TDZD-8, a potent and selective GSK-3beta inhibitor, on the development of lung injury caused by administration of bleomycin (BLM). 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 55-61 glycogen synthase kinase 3 beta Mus musculus 86-95 17880775-2 2007 The aim of this study is to investigate the effects of TDZD-8, a potent and selective GSK-3beta inhibitor, on the development of lung injury caused by administration of bleomycin (BLM). Bleomycin 169-178 glycogen synthase kinase 3 beta Mus musculus 86-95 17880775-2 2007 The aim of this study is to investigate the effects of TDZD-8, a potent and selective GSK-3beta inhibitor, on the development of lung injury caused by administration of bleomycin (BLM). Bleomycin 180-183 glycogen synthase kinase 3 beta Mus musculus 86-95 17880775-6 2007 Taken together, these results clearly demonstrate treatment with the GSK-3beta inhibitor TDZD-8 reduces the development of lung injury and inflammation induced by BLM in mice. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 89-95 glycogen synthase kinase 3 beta Mus musculus 69-78 17568620-7 2007 In this study, diosgenin inhibited the reduction of Akt and GSK 3beta phosphorylation induced by LY294,002, a PI3K inhibitor. Diosgenin 15-24 glycogen synthase kinase 3 beta Mus musculus 60-69 17215071-4 2007 The Akt inhibitor, 1L-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate, significantly amplified the FGF-2-induced VEGF release, in a dose-dependent manner between 1 and 70microM, while it suppressed the FGF-2-induced phosphorylation of GSK-3beta. 1L-6-hydroxymethyl-chiro-inositol 2(R)-2-O-methyl-3-O-octadecylcarbonate 19-92 glycogen synthase kinase 3 beta Mus musculus 258-267 17043650-6 2007 LiCl, an inhibitor of GSK3beta, abolished inhibitory effect of PTEN on cyclin D2 expression, and TCF members could directly bind to the promoter of cyclin D2 and regulate its transcription in a CREB-dependent manner. Lithium Chloride 0-4 glycogen synthase kinase 3 beta Mus musculus 22-30 17329570-3 2007 First is shown that transient exposure of isolated kidney mesenchymes to structurally different glycogen synthase kinase-3 (GSK3) inhibitors lithium or 6-bromoindirubin-3"-oxime results in abundant epithelial differentiation and full segregation of nephrons. Lithium 141-148 glycogen synthase kinase 3 beta Mus musculus 96-122 17329570-3 2007 First is shown that transient exposure of isolated kidney mesenchymes to structurally different glycogen synthase kinase-3 (GSK3) inhibitors lithium or 6-bromoindirubin-3"-oxime results in abundant epithelial differentiation and full segregation of nephrons. Lithium 141-148 glycogen synthase kinase 3 beta Mus musculus 124-128 17329570-3 2007 First is shown that transient exposure of isolated kidney mesenchymes to structurally different glycogen synthase kinase-3 (GSK3) inhibitors lithium or 6-bromoindirubin-3"-oxime results in abundant epithelial differentiation and full segregation of nephrons. 6-bromoindirubin-3'-oxime 152-177 glycogen synthase kinase 3 beta Mus musculus 96-122 17329570-3 2007 First is shown that transient exposure of isolated kidney mesenchymes to structurally different glycogen synthase kinase-3 (GSK3) inhibitors lithium or 6-bromoindirubin-3"-oxime results in abundant epithelial differentiation and full segregation of nephrons. 6-bromoindirubin-3'-oxime 152-177 glycogen synthase kinase 3 beta Mus musculus 124-128 17254554-3 2007 Previously, we reported that there was the association between lengthening circadian period by lithium and GSK-3 protein and its enzyme activity in the mouse suprachiasmatic nucleus (SCN). Lithium 95-102 glycogen synthase kinase 3 beta Mus musculus 107-112 17416967-7 2007 However, ceramide blocked tau hyperphosphorylation potentially via inhibition of glycogen synthase kinase-3beta. Ceramides 9-17 glycogen synthase kinase 3 beta Mus musculus 81-111 17295926-2 2007 Lithium, a direct inhibitor of glycogen synthase kinase 3 (GSK3) activity, and a mainstay in BPD therapeutics, has been proposed to target GSK3 as a mechanism of mood stabilization. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 59-63 17295926-2 2007 Lithium, a direct inhibitor of glycogen synthase kinase 3 (GSK3) activity, and a mainstay in BPD therapeutics, has been proposed to target GSK3 as a mechanism of mood stabilization. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 139-143 17295926-5 2007 We sought to investigate the role of GSK3 in the mammalian clock mechanism, as a possible mediator of lithium"s therapeutic effects. Lithium 102-109 glycogen synthase kinase 3 beta Mus musculus 37-41 17295926-8 2007 Furthermore, we demonstrate that pharmacological inhibition of GSK3 activity by kenpaullone, a known antagonist of GSK3 activity, as well as by lithium, a direct inhibitor of GSK3 and the most common treatment for BPD, induces a phase delay in mPer2 transcription that resembles the effect observed with GSK3 knockdown. kenpaullone 80-91 glycogen synthase kinase 3 beta Mus musculus 63-67 17105725-6 2007 Ceramide depletion prevented plasma membrane translocation of PKCzeta/lambda, its interaction with Cdc42, and phosphorylation of GSK-3beta, a substrate of PKCzeta/lambda. Ceramides 0-8 glycogen synthase kinase 3 beta Mus musculus 129-138 17053159-1 2007 Casein kinase I (CKI)-epsilon and GSK-3beta phosphorylate beta-catenin at Ser(45) (beta-cat(45)) and Thr(41)/Ser(37,33) (beta-cat(33,37,41)) residues, thereby facilitating its ubiquitination and proteasomal degradation. Serine 74-77 glycogen synthase kinase 3 beta Mus musculus 34-43 17053159-1 2007 Casein kinase I (CKI)-epsilon and GSK-3beta phosphorylate beta-catenin at Ser(45) (beta-cat(45)) and Thr(41)/Ser(37,33) (beta-cat(33,37,41)) residues, thereby facilitating its ubiquitination and proteasomal degradation. Threonine 101-104 glycogen synthase kinase 3 beta Mus musculus 34-43 17053159-1 2007 Casein kinase I (CKI)-epsilon and GSK-3beta phosphorylate beta-catenin at Ser(45) (beta-cat(45)) and Thr(41)/Ser(37,33) (beta-cat(33,37,41)) residues, thereby facilitating its ubiquitination and proteasomal degradation. Serine 109-112 glycogen synthase kinase 3 beta Mus musculus 34-43 17053159-7 2007 Interestingly, GSK-3beta underwent increased phosphorylation at Ser(9), leading to 40% and 70% decreases in its activity at these time points, respectively. Serine 64-67 glycogen synthase kinase 3 beta Mus musculus 15-24 17053159-12 2007 Impairment in linking beta-cat(45) to subsequent GSK-3beta-mediated phosphorylation and degradation may account for increased steady-state levels of both unphosphorylated as well as Ser(45)-phosphorylated beta-catenin, which may be causally linked to increases in cell census during TMCH. Serine 182-185 glycogen synthase kinase 3 beta Mus musculus 49-58 17053159-12 2007 Impairment in linking beta-cat(45) to subsequent GSK-3beta-mediated phosphorylation and degradation may account for increased steady-state levels of both unphosphorylated as well as Ser(45)-phosphorylated beta-catenin, which may be causally linked to increases in cell census during TMCH. tmch 283-287 glycogen synthase kinase 3 beta Mus musculus 49-58 17151860-0 2007 Glycogen synthase kinase 3 inhibition improves insulin-stimulated glucose metabolism but not hypertension in high-fat-fed C57BL/6J mice. Glucose 66-73 glycogen synthase kinase 3 beta Mus musculus 0-26 17151860-1 2007 AIMS/HYPOTHESIS: In the current study, the effect of a highly specific peptide inhibitor of glycogen synthase kinase 3 (GSK3) (L803-mts) on glucose metabolism and BP was examined in a high-fat (HF) fed mouse model of diabetes. Glucose 140-147 glycogen synthase kinase 3 beta Mus musculus 92-118 17151860-1 2007 AIMS/HYPOTHESIS: In the current study, the effect of a highly specific peptide inhibitor of glycogen synthase kinase 3 (GSK3) (L803-mts) on glucose metabolism and BP was examined in a high-fat (HF) fed mouse model of diabetes. Glucose 140-147 glycogen synthase kinase 3 beta Mus musculus 120-124 17151860-1 2007 AIMS/HYPOTHESIS: In the current study, the effect of a highly specific peptide inhibitor of glycogen synthase kinase 3 (GSK3) (L803-mts) on glucose metabolism and BP was examined in a high-fat (HF) fed mouse model of diabetes. Benzo(a)pyrene 163-165 glycogen synthase kinase 3 beta Mus musculus 120-124 16672106-3 2007 We previously reported that serotonin, a major neurotransmitter involved in mood disorders, regulates GSK3 by acutely increasing its N-terminal serine phosphorylation. Serotonin 28-37 glycogen synthase kinase 3 beta Mus musculus 102-106 16672106-3 2007 We previously reported that serotonin, a major neurotransmitter involved in mood disorders, regulates GSK3 by acutely increasing its N-terminal serine phosphorylation. Serine 144-150 glycogen synthase kinase 3 beta Mus musculus 102-106 16672106-4 2007 The present study was undertaken to further determine if atypical antipsychotics, which have therapeutic effects in both mood disorders and schizophrenia, can regulate phospho-Ser-GSK3 and inhibit its activity. Serine 176-179 glycogen synthase kinase 3 beta Mus musculus 180-184 16672106-5 2007 The results showed that acute treatment of mice with risperidone rapidly increased the level of brain phospho-Ser-GSK3 in the cortex, hippocampus, striatum, and cerebellum in a dose-dependent manner. Risperidone 53-64 glycogen synthase kinase 3 beta Mus musculus 114-118 16672106-5 2007 The results showed that acute treatment of mice with risperidone rapidly increased the level of brain phospho-Ser-GSK3 in the cortex, hippocampus, striatum, and cerebellum in a dose-dependent manner. Serine 110-113 glycogen synthase kinase 3 beta Mus musculus 114-118 16672106-6 2007 Regulation of phospho-Ser-GSK3 was a shared effect among several atypical antipsychotics, including olanzapine, clozapine, quetiapine, and ziprasidone. Olanzapine 100-110 glycogen synthase kinase 3 beta Mus musculus 26-30 16672106-6 2007 Regulation of phospho-Ser-GSK3 was a shared effect among several atypical antipsychotics, including olanzapine, clozapine, quetiapine, and ziprasidone. Clozapine 112-121 glycogen synthase kinase 3 beta Mus musculus 26-30 16672106-6 2007 Regulation of phospho-Ser-GSK3 was a shared effect among several atypical antipsychotics, including olanzapine, clozapine, quetiapine, and ziprasidone. Quetiapine Fumarate 123-133 glycogen synthase kinase 3 beta Mus musculus 26-30 16672106-6 2007 Regulation of phospho-Ser-GSK3 was a shared effect among several atypical antipsychotics, including olanzapine, clozapine, quetiapine, and ziprasidone. ziprasidone 139-150 glycogen synthase kinase 3 beta Mus musculus 26-30 16672106-7 2007 In addition, combination treatment of mice with risperidone and a monoamine reuptake inhibitor antidepressant imipramine or fluoxetine elicited larger increases in brain phospho-Ser-GSK3 than each agent alone. Risperidone 48-59 glycogen synthase kinase 3 beta Mus musculus 182-186 16672106-7 2007 In addition, combination treatment of mice with risperidone and a monoamine reuptake inhibitor antidepressant imipramine or fluoxetine elicited larger increases in brain phospho-Ser-GSK3 than each agent alone. Imipramine 110-120 glycogen synthase kinase 3 beta Mus musculus 182-186 16672106-7 2007 In addition, combination treatment of mice with risperidone and a monoamine reuptake inhibitor antidepressant imipramine or fluoxetine elicited larger increases in brain phospho-Ser-GSK3 than each agent alone. Fluoxetine 124-134 glycogen synthase kinase 3 beta Mus musculus 182-186 17242176-7 2007 In addition, we have shown that the regulation of GSK-3alpha and GSK-3beta in cultured oocytes by soluble KL is accomplished through PI3K, since the PI3K-specific inhibitor LY294002 completely abolished the KL-induced phosphorylation of GSK-3alpha and GSK-3beta. Kraft lignin 106-108 glycogen synthase kinase 3 beta Mus musculus 65-74 17242176-7 2007 In addition, we have shown that the regulation of GSK-3alpha and GSK-3beta in cultured oocytes by soluble KL is accomplished through PI3K, since the PI3K-specific inhibitor LY294002 completely abolished the KL-induced phosphorylation of GSK-3alpha and GSK-3beta. Kraft lignin 106-108 glycogen synthase kinase 3 beta Mus musculus 252-261 17242176-7 2007 In addition, we have shown that the regulation of GSK-3alpha and GSK-3beta in cultured oocytes by soluble KL is accomplished through PI3K, since the PI3K-specific inhibitor LY294002 completely abolished the KL-induced phosphorylation of GSK-3alpha and GSK-3beta. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 173-181 glycogen synthase kinase 3 beta Mus musculus 65-74 17242176-7 2007 In addition, we have shown that the regulation of GSK-3alpha and GSK-3beta in cultured oocytes by soluble KL is accomplished through PI3K, since the PI3K-specific inhibitor LY294002 completely abolished the KL-induced phosphorylation of GSK-3alpha and GSK-3beta. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 173-181 glycogen synthase kinase 3 beta Mus musculus 252-261 17242176-7 2007 In addition, we have shown that the regulation of GSK-3alpha and GSK-3beta in cultured oocytes by soluble KL is accomplished through PI3K, since the PI3K-specific inhibitor LY294002 completely abolished the KL-induced phosphorylation of GSK-3alpha and GSK-3beta. Kraft lignin 207-209 glycogen synthase kinase 3 beta Mus musculus 65-74 17241269-2 2007 Numerous intracellular signalling pathways converge on GSK-3 and regulate its activity via inhibitory serine-phosphorylation. Serine 102-108 glycogen synthase kinase 3 beta Mus musculus 55-60 17241269-8 2007 The LTP deficits can be attenuated/rescued by chronic treatment with lithium, a GSK-3 inhibitor. Lithium 69-76 glycogen synthase kinase 3 beta Mus musculus 80-85 17101033-0 2007 Dual alteration of limbic dopamine D1 receptor-mediated signalling and the Akt/GSK3 pathway in dopamine D3 receptor mutants during the development of methamphetamine sensitization. Methamphetamine 150-165 glycogen synthase kinase 3 beta Mus musculus 79-83 17261353-0 2007 Genistein inhibits glutamate-induced apoptotic processes in primary neuronal cell cultures: an involvement of aryl hydrocarbon receptor and estrogen receptor/glycogen synthase kinase-3beta intracellular signaling pathway. Genistein 0-9 glycogen synthase kinase 3 beta Mus musculus 158-188 17261353-0 2007 Genistein inhibits glutamate-induced apoptotic processes in primary neuronal cell cultures: an involvement of aryl hydrocarbon receptor and estrogen receptor/glycogen synthase kinase-3beta intracellular signaling pathway. Glutamic Acid 19-28 glycogen synthase kinase 3 beta Mus musculus 158-188 17261353-8 2007 SB 216763 (1 microM), which preferentially inhibits glycogen synthase kinase-3beta (GSK-3beta), potentiated genistein effects. SB 216763 0-9 glycogen synthase kinase 3 beta Mus musculus 52-82 17261353-8 2007 SB 216763 (1 microM), which preferentially inhibits glycogen synthase kinase-3beta (GSK-3beta), potentiated genistein effects. SB 216763 0-9 glycogen synthase kinase 3 beta Mus musculus 84-93 17261353-8 2007 SB 216763 (1 microM), which preferentially inhibits glycogen synthase kinase-3beta (GSK-3beta), potentiated genistein effects. Genistein 108-117 glycogen synthase kinase 3 beta Mus musculus 84-93 17261353-10 2007 Moreover, this study provided evidence for involvement of aryl hydrocarbon receptor and estrogen receptor/GSK-3beta intracellular signaling pathway in anti-apoptotic action of genistein. Genistein 176-185 glycogen synthase kinase 3 beta Mus musculus 106-115 17130121-5 2007 We further showed that phosphorylation at threonine 286 by GSK-3beta was required for myostatin-stimulated cyclin D1 nuclear export and degradation. Threonine 42-51 glycogen synthase kinase 3 beta Mus musculus 59-68 17295926-9 2007 CONCLUSION: These results confirm GSK3 as a plausible target of lithium action in BPD therapeutics, and suggest the circadian clock mechanism as a significant modulator of lithium"s clinical benefits. Lithium 64-71 glycogen synthase kinase 3 beta Mus musculus 34-38 16806104-2 2007 The mood stabilizer lithium inhibits GSK3beta in vitro and in mouse brain, and this is currently the strongest known potential therapeutic target of lithium. Lithium 20-27 glycogen synthase kinase 3 beta Mus musculus 37-45 16806104-2 2007 The mood stabilizer lithium inhibits GSK3beta in vitro and in mouse brain, and this is currently the strongest known potential therapeutic target of lithium. Lithium 149-156 glycogen synthase kinase 3 beta Mus musculus 37-45 17116346-0 2007 Kainate induces AKT, ERK and cdk5/GSK3beta pathway deregulation, phosphorylates tau protein in mouse hippocampus. Kainic Acid 0-7 glycogen synthase kinase 3 beta Mus musculus 34-42 16803897-2 2006 Over-activation of proline-directed kinases, such as cyclin-dependent kinase 5 (Cdk5) and glycogen synthase kinase 3 (GSK3), has been implicated in the aberrant phosphorylation of tau at proline-directed sites. Proline 19-26 glycogen synthase kinase 3 beta Mus musculus 90-116 16817229-7 2006 Wortmannin and LY294002 suppressed the PDGF-BB-induced phosphorylation of Akt and GSK-3beta. Wortmannin 0-10 glycogen synthase kinase 3 beta Mus musculus 82-91 16817229-7 2006 Wortmannin and LY294002 suppressed the PDGF-BB-induced phosphorylation of Akt and GSK-3beta. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 15-23 glycogen synthase kinase 3 beta Mus musculus 82-91 17145862-5 2006 Lithium treatment of the cultured mouse hippocampal neurons HT-22 induced activation of Akt (1.5-fold), inhibition of GSK-3beta (2.2-fold), and an increase in Bcl-2 protein expression (2-fold). Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 118-127 17059563-0 2006 Chronic lithium administration to FTDP-17 tau and GSK-3beta overexpressing mice prevents tau hyperphosphorylation and neurofibrillary tangle formation, but pre-formed neurofibrillary tangles do not revert. Lithium 8-15 glycogen synthase kinase 3 beta Mus musculus 50-59 17059563-2 2006 Lithium, a widely used drug for affective disorders, inhibits GSK-3 at therapeutically relevant concentrations. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 62-67 17059563-4 2006 We had previously generated a double transgenic model, overexpressing GSK-3beta in a conditional manner, using the Tet-off system and tau protein carrying a triple FTDP-17 (frontotemporal dementia and parkinsonism linked to chromosome 17) mutation. tetramethylenedisulfotetramine 115-118 glycogen synthase kinase 3 beta Mus musculus 70-79 17059563-6 2006 We used this transgenic model to address two issues: first, whether chronic lithium treatment is able to prevent the formation of aberrant tau aggregates that result from the overexpression of FTDP-17 tau and GSK-3beta; second, whether lithium is able to change back already formed NFTs in aged animals. Lithium 76-83 glycogen synthase kinase 3 beta Mus musculus 209-218 17016509-8 2006 CONCLUSIONS AND IMPLICATIONS: Thus, based on these findings we propose that inhibitors of the activity of GSK-3beta, such as TDZD-8, may be useful in the treatment of various inflammatory diseases. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 125-131 glycogen synthase kinase 3 beta Mus musculus 106-115 16855914-2 2006 In the present study, we investigated the effects of cold water stress (CWS) on tau phosphorylation in the mouse hippocampus and the effects of GSK-3beta inhibitor, LiCl, on CWS-induced changes in tau phosphorylation levels by immunoblot analyses. Lithium Chloride 165-169 glycogen synthase kinase 3 beta Mus musculus 144-153 16855914-7 2006 These results suggest that a CWS-induced increase in phosphorylated tau in the hippocampus is mediated, at least partly, by the activation of GSK-3beta. 6-Methylquinazolin-4-Amine 29-32 glycogen synthase kinase 3 beta Mus musculus 142-151 17172987-0 2007 Glycogen synthase kinase 3beta inhibition reduces the development of nonseptic shock induced by zymosan in mice. Zymosan 96-103 glycogen synthase kinase 3 beta Mus musculus 0-30 17172987-2 2007 In the present study, we have investigated the effects of 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8), a glycogen synthase kinase 3beta inhibitor, on the development of nonseptic shock caused by zymosan (dose, 500 mg/kg i.p. 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 109-115 glycogen synthase kinase 3 beta Mus musculus 120-150 17016509-0 2006 Inhibition of glycogen synthase kinase-3beta attenuates the development of carrageenan-induced lung injury in mice. Carrageenan 75-86 glycogen synthase kinase 3 beta Mus musculus 14-44 16806170-3 2006 We have previously shown that keratinocyte migration induced by EGF or staurosporine is dependent on the activity of glycogen synthase kinase-3 (GSK-3). Staurosporine 71-84 glycogen synthase kinase 3 beta Mus musculus 117-143 16806170-3 2006 We have previously shown that keratinocyte migration induced by EGF or staurosporine is dependent on the activity of glycogen synthase kinase-3 (GSK-3). Staurosporine 71-84 glycogen synthase kinase 3 beta Mus musculus 145-150 16806170-4 2006 In the present study, we show that keratinocyte migration induced by TGF-beta1, KGF, EGF, TGF-alpha and staurosporine depends on EGFR signaling, involves autocrine HB-EGF expression and is potently blocked by GSK-3 inhibitors SB-415286 and LiCl. Staurosporine 104-117 glycogen synthase kinase 3 beta Mus musculus 209-214 16803897-2 2006 Over-activation of proline-directed kinases, such as cyclin-dependent kinase 5 (Cdk5) and glycogen synthase kinase 3 (GSK3), has been implicated in the aberrant phosphorylation of tau at proline-directed sites. Proline 19-26 glycogen synthase kinase 3 beta Mus musculus 118-122 16803897-7 2006 Pharmacological inhibition of GSK3 in old transgenic mice by chronic treatment with lithium leads to a reduction of the age-dependent increase in tau hyperphosphorylation. Lithium 84-91 glycogen synthase kinase 3 beta Mus musculus 30-34 16943560-2 2006 Lithium inhibits glycogen synthase kinase 3beta (GSK-3beta) directly or indirectly via stimulation of the kinase Akt-1. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 17-47 16054268-3 2006 Tet/GSK-3beta/VLW transgenic mice show tau hyperphosphorylation in hippocampal neurons. tetramethylenedisulfotetramine 0-3 glycogen synthase kinase 3 beta Mus musculus 4-13 16054268-5 2006 Finally, the atrophy of the hippocampal dentate gyrus observed in Tet/GSK-3beta mice develops much faster in Tet/GSK-3beta/VLW mice. tetramethylenedisulfotetramine 66-69 glycogen synthase kinase 3 beta Mus musculus 70-79 16054268-5 2006 Finally, the atrophy of the hippocampal dentate gyrus observed in Tet/GSK-3beta mice develops much faster in Tet/GSK-3beta/VLW mice. tetramethylenedisulfotetramine 109-112 glycogen synthase kinase 3 beta Mus musculus 113-122 16943560-2 2006 Lithium inhibits glycogen synthase kinase 3beta (GSK-3beta) directly or indirectly via stimulation of the kinase Akt-1. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 49-58 16644257-1 2006 Two leading hypotheses to explain lithium action in bipolar disorder propose either inositol depletion or inhibition of GSK-3 as mechanisms of action. Lithium 34-41 glycogen synthase kinase 3 beta Mus musculus 120-125 16762022-8 2006 Inhibition of GSK-3 by LiCl, but not inhibition of CDK-5 by roscovitine, arrested Abeta secretion and tau phosphorylation. Lithium Chloride 23-27 glycogen synthase kinase 3 beta Mus musculus 14-19 16762022-9 2006 Inhibition of PKC by GF-109203X activated GSK-3, whereas activation of PKC by phorbol-12,13-dibutyrate inhibited GSK-3. bisindolylmaleimide I 21-31 glycogen synthase kinase 3 beta Mus musculus 42-47 16762022-9 2006 Inhibition of PKC by GF-109203X activated GSK-3, whereas activation of PKC by phorbol-12,13-dibutyrate inhibited GSK-3. phorbol-12 78-88 glycogen synthase kinase 3 beta Mus musculus 113-118 16762022-9 2006 Inhibition of PKC by GF-109203X activated GSK-3, whereas activation of PKC by phorbol-12,13-dibutyrate inhibited GSK-3. 13-dibutyrate 89-102 glycogen synthase kinase 3 beta Mus musculus 113-118 16762022-10 2006 These results suggest that endogenously overproduced Abeta induces increased tau phosphorylation through activation of GSK-3, and that inactivation of PKC is at least one of the mechanisms involved in GSK-3 activation. UNII-042A8N37WH 53-58 glycogen synthase kinase 3 beta Mus musculus 119-124 16762022-10 2006 These results suggest that endogenously overproduced Abeta induces increased tau phosphorylation through activation of GSK-3, and that inactivation of PKC is at least one of the mechanisms involved in GSK-3 activation. UNII-042A8N37WH 53-58 glycogen synthase kinase 3 beta Mus musculus 201-206 16514645-5 2006 The sphingosine 1-phosphate-induced phosphorylation of GSK-3beta was suppressed by Akt inhibitor. sphingosine 1-phosphate 4-27 glycogen synthase kinase 3 beta Mus musculus 55-64 16644257-2 2006 Behavioral effects of lithium are mimicked in Gsk-3beta+/- mice, but the contribution of inositol depletion to these behaviors has not been tested. Lithium 22-29 glycogen synthase kinase 3 beta Mus musculus 46-55 16753022-13 2006 DXA analyses revealed significant increases in BMC and BMD in cancellous and cortical bone of OVX rats treated with GSK-3 inhibitor. S-benzyl-N-malonylcysteine 47-50 glycogen synthase kinase 3 beta Mus musculus 116-121 16816383-6 2006 Glycogen synthase kinase 3 (GSK-3beta) serine phosphorylation (inactivation) was blunted in PECAM-1-null ECs after histamine treatment or shear stress. Serine 39-45 glycogen synthase kinase 3 beta Mus musculus 28-37 16816383-6 2006 Glycogen synthase kinase 3 (GSK-3beta) serine phosphorylation (inactivation) was blunted in PECAM-1-null ECs after histamine treatment or shear stress. Histamine 115-124 glycogen synthase kinase 3 beta Mus musculus 28-37 16816383-9 2006 In addition, PECAM-1 modulated the levels of beta-catenin by regulating the activity of GSK-3beta, which in turn affected the serine phosphorylation of beta-catenin and its proteosomal degradation, affecting the ability of the cell to reform adherens junctions in a timely fashion. Serine 126-132 glycogen synthase kinase 3 beta Mus musculus 88-97 16631408-6 2006 Treatment of mice with the GSK-3beta inhibitor TDZD-8 (1 mg/kg/day i.p.) 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione 47-53 glycogen synthase kinase 3 beta Mus musculus 27-36 16631408-9 2006 The degree of staining for nitrotyrosine, PAR, iNOS, and COX-2 was significantly reduced in CII-challenged mice treated with the GSK-3beta inhibitor. 3-nitrotyrosine 27-40 glycogen synthase kinase 3 beta Mus musculus 129-138 16631408-9 2006 The degree of staining for nitrotyrosine, PAR, iNOS, and COX-2 was significantly reduced in CII-challenged mice treated with the GSK-3beta inhibitor. Poly Adenosine Diphosphate Ribose 42-45 glycogen synthase kinase 3 beta Mus musculus 129-138 16631408-9 2006 The degree of staining for nitrotyrosine, PAR, iNOS, and COX-2 was significantly reduced in CII-challenged mice treated with the GSK-3beta inhibitor. N-[(1S)-2-methyl-1-(pyridin-4-ylcarbamoyl)propyl]cyclohexanecarboxamide 92-95 glycogen synthase kinase 3 beta Mus musculus 129-138 16191209-6 2006 Mice treated chronically with lithium exhibited the most prominent elevation in phospho-Ser9-GSK-3beta. Lithium 30-37 glycogen synthase kinase 3 beta Mus musculus 93-102 16601113-5 2006 Interestingly, inhibition of GSK-3beta by antisense oligonucleotides or pharmacological agent (10 mm lithium) potentiated TNF-induced expression of IL-6 and MCP-1 by 2-6-fold suggesting that inhibition of GSK-3beta under inflammatory conditions (exposure to TNF-alpha and IL-1beta) may contribute to enhanced cytokine expression. Oligonucleotides 52-68 glycogen synthase kinase 3 beta Mus musculus 29-38 16601113-5 2006 Interestingly, inhibition of GSK-3beta by antisense oligonucleotides or pharmacological agent (10 mm lithium) potentiated TNF-induced expression of IL-6 and MCP-1 by 2-6-fold suggesting that inhibition of GSK-3beta under inflammatory conditions (exposure to TNF-alpha and IL-1beta) may contribute to enhanced cytokine expression. Lithium 101-108 glycogen synthase kinase 3 beta Mus musculus 29-38 16601113-5 2006 Interestingly, inhibition of GSK-3beta by antisense oligonucleotides or pharmacological agent (10 mm lithium) potentiated TNF-induced expression of IL-6 and MCP-1 by 2-6-fold suggesting that inhibition of GSK-3beta under inflammatory conditions (exposure to TNF-alpha and IL-1beta) may contribute to enhanced cytokine expression. Lithium 101-108 glycogen synthase kinase 3 beta Mus musculus 205-214 16497810-3 2006 LiCl, sodium valproate, and SB415286, three inhibitors of GSK3, dose-dependently blocked ERalpha-mediated transcription. Lithium Chloride 0-4 glycogen synthase kinase 3 beta Mus musculus 58-62 16497810-3 2006 LiCl, sodium valproate, and SB415286, three inhibitors of GSK3, dose-dependently blocked ERalpha-mediated transcription. Valproic Acid 6-22 glycogen synthase kinase 3 beta Mus musculus 58-62 16497810-3 2006 LiCl, sodium valproate, and SB415286, three inhibitors of GSK3, dose-dependently blocked ERalpha-mediated transcription. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 28-36 glycogen synthase kinase 3 beta Mus musculus 58-62 16687499-1 2006 Glycogen synthase kinase-3 (GSK-3) is a ubiquitously expressed serine/threonine kinase that is particularly abundant in the CNS. Serine 63-69 glycogen synthase kinase 3 beta Mus musculus 0-26 16687499-1 2006 Glycogen synthase kinase-3 (GSK-3) is a ubiquitously expressed serine/threonine kinase that is particularly abundant in the CNS. Serine 63-69 glycogen synthase kinase 3 beta Mus musculus 28-33 16687499-7 2006 Furthermore, GSK-3 phosphorylates tau in most serine and threonine residues hyperphosphorylated in PHF (paired helical filament)-tau and GSK-3 activity contributes both to beta-amyloid production and to beta-amyloid-mediated neuronal death. Serine 46-52 glycogen synthase kinase 3 beta Mus musculus 13-18 16687499-7 2006 Furthermore, GSK-3 phosphorylates tau in most serine and threonine residues hyperphosphorylated in PHF (paired helical filament)-tau and GSK-3 activity contributes both to beta-amyloid production and to beta-amyloid-mediated neuronal death. Serine 46-52 glycogen synthase kinase 3 beta Mus musculus 137-142 16687499-7 2006 Furthermore, GSK-3 phosphorylates tau in most serine and threonine residues hyperphosphorylated in PHF (paired helical filament)-tau and GSK-3 activity contributes both to beta-amyloid production and to beta-amyloid-mediated neuronal death. Threonine 57-66 glycogen synthase kinase 3 beta Mus musculus 137-142 16687499-8 2006 In good agreement, mice with conditional overexpression of GSK-3 in forebrain neurons (Tet/GSK-3beta mice) recapitulate aspects of AD neuropathology such as tau hyperphosphorylation, apoptotic neuronal death, and reactive astrocytosis as well as spatial learning deficit. uridine triacetate 157-160 glycogen synthase kinase 3 beta Mus musculus 59-64 16530186-3 2006 We found that GSK3beta became more active (less phosphorylated at serine 9) via decreased Akt phosphorylation, in parallel to c-Jun NH2 terminal kinase activation, which correlated with increased activated caspase 3 and myocardial apoptosis 3 days after streptozotocin (STZ) injection in mice. Streptozocin 254-268 glycogen synthase kinase 3 beta Mus musculus 14-22 16522636-5 2006 Leptin-mediated GSK3beta phosphorylation was prevented by the MEK/ERK inhibitor PD98059, the phosphatidylinositol 3-kinase inhibitor LY294002, or the protein kinase C inhibitor GF109203X. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 133-141 glycogen synthase kinase 3 beta Mus musculus 16-24 16522636-5 2006 Leptin-mediated GSK3beta phosphorylation was prevented by the MEK/ERK inhibitor PD98059, the phosphatidylinositol 3-kinase inhibitor LY294002, or the protein kinase C inhibitor GF109203X. bisindolylmaleimide I 177-186 glycogen synthase kinase 3 beta Mus musculus 16-24 16522636-9 2006 The leptin-induced growth cone spreading was hampered in cortical neurons from Lepr(db/db) mice lacking functional leptin receptors; it was associated with localized Ser-9-GSK3beta phosphorylation and mimicked by the GSK3beta inhibitor SB216763. SB 216763 236-244 glycogen synthase kinase 3 beta Mus musculus 217-225 16522636-4 2006 Moreover, leptin elicited the phosphorylation of the phosphatidylinositol 3-kinase effector Akt and evoked Ser-9 phosphorylation of glycogen synthase kinase-3beta (GSK3beta), an event inactivating this kinase. Serine 107-110 glycogen synthase kinase 3 beta Mus musculus 132-162 16522636-5 2006 Leptin-mediated GSK3beta phosphorylation was prevented by the MEK/ERK inhibitor PD98059, the phosphatidylinositol 3-kinase inhibitor LY294002, or the protein kinase C inhibitor GF109203X. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 80-87 glycogen synthase kinase 3 beta Mus musculus 16-24 16530186-3 2006 We found that GSK3beta became more active (less phosphorylated at serine 9) via decreased Akt phosphorylation, in parallel to c-Jun NH2 terminal kinase activation, which correlated with increased activated caspase 3 and myocardial apoptosis 3 days after streptozotocin (STZ) injection in mice. Serine 66-72 glycogen synthase kinase 3 beta Mus musculus 14-22 16530186-3 2006 We found that GSK3beta became more active (less phosphorylated at serine 9) via decreased Akt phosphorylation, in parallel to c-Jun NH2 terminal kinase activation, which correlated with increased activated caspase 3 and myocardial apoptosis 3 days after streptozotocin (STZ) injection in mice. Streptozocin 270-273 glycogen synthase kinase 3 beta Mus musculus 14-22 16530186-4 2006 However, 28 days after STZ injection, GSK3beta became inactive, which correlated with the enhanced protein kinase C beta2 and p38 mitogen activated protein kinase expression, nuclear translocation of nuclear factor of activated T cells c3, cardiac hypertrophy and fibrosis. Streptozocin 23-26 glycogen synthase kinase 3 beta Mus musculus 38-46 16530186-6 2006 Our results suggest that GSK3beta together with 14-3-3 protein plays essential roles in the signaling of diabetic cardiomyopathy, and treatment with either losartan or tempol prevents these changes. Losartan 156-164 glycogen synthase kinase 3 beta Mus musculus 25-33 16530186-6 2006 Our results suggest that GSK3beta together with 14-3-3 protein plays essential roles in the signaling of diabetic cardiomyopathy, and treatment with either losartan or tempol prevents these changes. tempol 168-174 glycogen synthase kinase 3 beta Mus musculus 25-33 16469950-8 2006 High glucose also regulated glycogen synthase kinase 3beta and c-Jun N-terminal kinase activity, yielding decreased kinase activity and reduced export of NFAT from the nucleus, providing additional mechanisms underlying the glucose-induced NFAT activation. Glucose 5-12 glycogen synthase kinase 3 beta Mus musculus 28-58 16469950-8 2006 High glucose also regulated glycogen synthase kinase 3beta and c-Jun N-terminal kinase activity, yielding decreased kinase activity and reduced export of NFAT from the nucleus, providing additional mechanisms underlying the glucose-induced NFAT activation. Glucose 224-231 glycogen synthase kinase 3 beta Mus musculus 28-58 16434614-7 2006 Glycogen synthase kinase 3beta (GSK3beta) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17beta-estradiol and Delta5-diol treatments were less effective. Serine 62-68 glycogen synthase kinase 3 beta Mus musculus 0-30 16522681-4 2006 In co-cultures of mouse mononuclear spleen cells and osteoblasts, inhibition of GSK3beta with LiCl or exposure to Wnt3a inhibited the formation of tartrate-resistant acid phosphatase-positive multinucleated cells compared with controls. Lithium Chloride 94-98 glycogen synthase kinase 3 beta Mus musculus 80-88 16537926-7 2006 Interestingly, this GSK-3-dependent phosphorylation is regulated via an ERK-dependent priming mechanism, i.e., phosphorylation of serine 130. Serine 130-136 glycogen synthase kinase 3 beta Mus musculus 20-25 16537926-10 2006 Hence, phosphorylation of paxillin on serines 126 and 130, which is mediated by an ERK/GSK-3 dual-kinase mechanism, plays an important role in cytoskeletal rearrangement. Serine 38-45 glycogen synthase kinase 3 beta Mus musculus 87-92 16434614-7 2006 Glycogen synthase kinase 3beta (GSK3beta) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17beta-estradiol and Delta5-diol treatments were less effective. Serine 62-68 glycogen synthase kinase 3 beta Mus musculus 32-40 16434614-7 2006 Glycogen synthase kinase 3beta (GSK3beta) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17beta-estradiol and Delta5-diol treatments were less effective. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 95-99 glycogen synthase kinase 3 beta Mus musculus 0-30 16434614-7 2006 Glycogen synthase kinase 3beta (GSK3beta) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17beta-estradiol and Delta5-diol treatments were less effective. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 95-99 glycogen synthase kinase 3 beta Mus musculus 32-40 16434614-7 2006 Glycogen synthase kinase 3beta (GSK3beta) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17beta-estradiol and Delta5-diol treatments were less effective. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 139-142 glycogen synthase kinase 3 beta Mus musculus 0-30 16434614-7 2006 Glycogen synthase kinase 3beta (GSK3beta) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17beta-estradiol and Delta5-diol treatments were less effective. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 139-142 glycogen synthase kinase 3 beta Mus musculus 32-40 16434614-7 2006 Glycogen synthase kinase 3beta (GSK3beta) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17beta-estradiol and Delta5-diol treatments were less effective. Estradiol 152-168 glycogen synthase kinase 3 beta Mus musculus 0-30 16434614-7 2006 Glycogen synthase kinase 3beta (GSK3beta) phosphorylation (at serine 9) was greatly reduced in MPTP mice; this was completely prevented by PPT, whereas 17beta-estradiol and Delta5-diol treatments were less effective. Estradiol 152-168 glycogen synthase kinase 3 beta Mus musculus 32-40 16434614-10 2006 In nonlesioned mice, 17beta-estradiol and PPT increased phosphorylation of striatal Akt and GSK3beta, whereas the other markers measured remained unchanged. Estradiol 21-37 glycogen synthase kinase 3 beta Mus musculus 92-100 16434614-10 2006 In nonlesioned mice, 17beta-estradiol and PPT increased phosphorylation of striatal Akt and GSK3beta, whereas the other markers measured remained unchanged. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 42-45 glycogen synthase kinase 3 beta Mus musculus 92-100 16434614-11 2006 Delta5-Diol increased GSK3beta phosphorylation less than the PPT treatment. delta5-diol 0-11 glycogen synthase kinase 3 beta Mus musculus 22-30 16434614-12 2006 These results suggest that a pretreatment with estradiol promoted dopamine neuron survival by activating ERalpha and increasing Akt and GSK3beta phosphorylation. Estradiol 47-56 glycogen synthase kinase 3 beta Mus musculus 136-144 16434614-12 2006 These results suggest that a pretreatment with estradiol promoted dopamine neuron survival by activating ERalpha and increasing Akt and GSK3beta phosphorylation. Dopamine 66-74 glycogen synthase kinase 3 beta Mus musculus 136-144 16464655-1 2006 Glycogen synthase kinase-3 (GSK3), which is inhibited by serine-phosphorylation, is involved in the neuropathology of Alzheimer"s disease (AD). Serine 57-63 glycogen synthase kinase 3 beta Mus musculus 0-26 16510873-3 2006 In the absence of Cdc42, degradation of beta-catenin was increased corresponding to a decreased phosphorylation of GSK3beta at Ser 9 and an increased phosphorylation of axin, which is known to be required for binding of beta-catenin to the degradation machinery. Serine 127-130 glycogen synthase kinase 3 beta Mus musculus 115-123 16464655-1 2006 Glycogen synthase kinase-3 (GSK3), which is inhibited by serine-phosphorylation, is involved in the neuropathology of Alzheimer"s disease (AD). Serine 57-63 glycogen synthase kinase 3 beta Mus musculus 28-32 16464655-4 2006 Treatment with memantine, an NMDA receptor antagonist, also increased the serine-phosphorylation of both GSK3 isoforms in mouse brain. Memantine 15-24 glycogen synthase kinase 3 beta Mus musculus 105-109 16464655-4 2006 Treatment with memantine, an NMDA receptor antagonist, also increased the serine-phosphorylation of both GSK3 isoforms in mouse brain. Serine 74-80 glycogen synthase kinase 3 beta Mus musculus 105-109 16464655-5 2006 Co-administration of physostigmine and memantine increased serine-phosphorylated GSK3 levels equally to that achieved by either agent alone, indicating that the actions of these two drugs converge on overlapping pools of GSK3. Physostigmine 21-34 glycogen synthase kinase 3 beta Mus musculus 81-85 16464655-5 2006 Co-administration of physostigmine and memantine increased serine-phosphorylated GSK3 levels equally to that achieved by either agent alone, indicating that the actions of these two drugs converge on overlapping pools of GSK3. Physostigmine 21-34 glycogen synthase kinase 3 beta Mus musculus 221-225 16464655-5 2006 Co-administration of physostigmine and memantine increased serine-phosphorylated GSK3 levels equally to that achieved by either agent alone, indicating that the actions of these two drugs converge on overlapping pools of GSK3. Memantine 39-48 glycogen synthase kinase 3 beta Mus musculus 81-85 16464655-5 2006 Co-administration of physostigmine and memantine increased serine-phosphorylated GSK3 levels equally to that achieved by either agent alone, indicating that the actions of these two drugs converge on overlapping pools of GSK3. Memantine 39-48 glycogen synthase kinase 3 beta Mus musculus 221-225 16464655-5 2006 Co-administration of physostigmine and memantine increased serine-phosphorylated GSK3 levels equally to that achieved by either agent alone, indicating that the actions of these two drugs converge on overlapping pools of GSK3. Serine 59-65 glycogen synthase kinase 3 beta Mus musculus 81-85 16464655-6 2006 Thus, drugs in each class of therapeutic agents used for AD have the common property of increasing the regulatory serine-phosphorylation of GSK3 within common pools of the enzyme. Serine 114-120 glycogen synthase kinase 3 beta Mus musculus 140-144 16543730-0 2006 DOCA-induced phosphorylation of glycogen synthase kinase 3beta. Desoxycorticosterone Acetate 0-4 glycogen synthase kinase 3 beta Mus musculus 32-62 16179343-2 2005 We found that Akt and GSK3 are sensitive to glucose, because fasting decreased and glucose administration increased by severalfold the phosphorylation of Akt and GSK3 in the cerebral cortex and hippocampus of non-diabetic mice. Glucose 83-90 glycogen synthase kinase 3 beta Mus musculus 22-26 16176184-2 2005 Inhibition of GSK3 in animal models of diabetes leads to normalization of blood glucose levels, while high GSK3 activity has been reported in Type II diabetes. Glucose 80-87 glycogen synthase kinase 3 beta Mus musculus 14-18 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Serine 56-62 glycogen synthase kinase 3 beta Mus musculus 17-21 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Serine 56-62 glycogen synthase kinase 3 beta Mus musculus 102-110 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Serine 56-62 glycogen synthase kinase 3 beta Mus musculus 82-86 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Serine 72-75 glycogen synthase kinase 3 beta Mus musculus 17-21 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Serine 72-75 glycogen synthase kinase 3 beta Mus musculus 82-86 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Serine 93-96 glycogen synthase kinase 3 beta Mus musculus 17-21 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Serine 93-96 glycogen synthase kinase 3 beta Mus musculus 102-110 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Serine 93-96 glycogen synthase kinase 3 beta Mus musculus 82-86 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Glycogen 150-158 glycogen synthase kinase 3 beta Mus musculus 17-21 16176184-3 2005 Insulin inhibits GSK3 by promoting phosphorylation of a serine residue (Ser-21 in GSK3alpha, Ser-9 in GSK3beta), thereby relieving GSK3 inhibition of glycogen synthesis in muscle. Glycogen 150-158 glycogen synthase kinase 3 beta Mus musculus 82-86 16176184-9 2005 We suggest for the first time that although pharmacological inhibition of GSK3 reduces hepatic glucose production even in insulin-resistant states, feeding can repress the gluconeogenic genes without inhibiting GSK3. Glucose 95-102 glycogen synthase kinase 3 beta Mus musculus 74-78 16179343-0 2005 Physiological and pathological changes in glucose regulate brain Akt and glycogen synthase kinase-3. Glucose 42-49 glycogen synthase kinase 3 beta Mus musculus 73-99 16179343-2 2005 We found that Akt and GSK3 are sensitive to glucose, because fasting decreased and glucose administration increased by severalfold the phosphorylation of Akt and GSK3 in the cerebral cortex and hippocampus of non-diabetic mice. Glucose 44-51 glycogen synthase kinase 3 beta Mus musculus 22-26 16179343-2 2005 We found that Akt and GSK3 are sensitive to glucose, because fasting decreased and glucose administration increased by severalfold the phosphorylation of Akt and GSK3 in the cerebral cortex and hippocampus of non-diabetic mice. Glucose 44-51 glycogen synthase kinase 3 beta Mus musculus 162-166 16169938-0 2006 Long-term treatment with novel glycogen synthase kinase-3 inhibitor improves glucose homeostasis in ob/ob mice: molecular characterization in liver and muscle. Glucose 77-84 glycogen synthase kinase 3 beta Mus musculus 31-57 16169938-12 2006 Our studies show that long-term treatment with GSK-3 inhibitor improves glucose homeostasis in ob/ob mice and demonstrates a novel role of GSK-3 in regulating hepatic CREB activity and expression of muscle GLUT4. Glucose 72-79 glycogen synthase kinase 3 beta Mus musculus 47-52 16223856-10 2006 The Wnt3a-treated cells showed nuclear accumulation of beta-catenin, and a GSK3 inhibitor, SB216763, mimicked the mitogenic activity of Wnt3a. SB 216763 91-99 glycogen synthase kinase 3 beta Mus musculus 75-79 16179343-2 2005 We found that Akt and GSK3 are sensitive to glucose, because fasting decreased and glucose administration increased by severalfold the phosphorylation of Akt and GSK3 in the cerebral cortex and hippocampus of non-diabetic mice. Glucose 83-90 glycogen synthase kinase 3 beta Mus musculus 162-166 16179343-3 2005 Brain Akt and GSK3 phosphorylation also increased after streptozotocin administration (3 days), which increased blood glucose and depleted blood insulin, indicating regulation by glucose availability even with deficient insulin. Streptozocin 56-70 glycogen synthase kinase 3 beta Mus musculus 14-18 16179343-3 2005 Brain Akt and GSK3 phosphorylation also increased after streptozotocin administration (3 days), which increased blood glucose and depleted blood insulin, indicating regulation by glucose availability even with deficient insulin. Glucose 118-125 glycogen synthase kinase 3 beta Mus musculus 14-18 16179343-4 2005 Changes in Akt and GSK3 phosphorylation and activities in epididymal fat were opposite to those of brain after streptozotocin treatment. Streptozocin 111-125 glycogen synthase kinase 3 beta Mus musculus 19-23 16179343-5 2005 Streptozotocin-induced hyperglycemia and increased brain Akt and GSK3 phosphorylation were reversed by lowering blood glucose with insulin administration. Streptozocin 0-14 glycogen synthase kinase 3 beta Mus musculus 65-69 16179343-5 2005 Streptozotocin-induced hyperglycemia and increased brain Akt and GSK3 phosphorylation were reversed by lowering blood glucose with insulin administration. Glucose 118-125 glycogen synthase kinase 3 beta Mus musculus 65-69 16179343-7 2005 Thus, the Akt-GSK3 signaling pathway is regulated in mouse brain in vivo in response to physiological and pathological changes in insulin and glucose. Glucose 142-149 glycogen synthase kinase 3 beta Mus musculus 14-18 16293698-1 2005 One of the well characterized cell biologic actions of lithium is the inhibition of glycogen synthase kinase-3beta and the consequent activation of canonical Wnt signaling. Lithium 55-62 glycogen synthase kinase 3 beta Mus musculus 84-114 16277616-6 2005 We found that brief incubations of mouse hippocampal slices with (R,S)-3,5-dihydroxyphenylglycine (DHPG) resulted in increased phosphorylation of Akt and Gsk3beta. (r,s)-3,5-dihydroxyphenylglycine 65-97 glycogen synthase kinase 3 beta Mus musculus 154-162 16277616-6 2005 We found that brief incubations of mouse hippocampal slices with (R,S)-3,5-dihydroxyphenylglycine (DHPG) resulted in increased phosphorylation of Akt and Gsk3beta. 3,5-dihydroxyphenylglycine 99-103 glycogen synthase kinase 3 beta Mus musculus 154-162 16155008-2 2005 Here, we report that stimulation of NMDARs in cultured rat hippocampal or cortical neurons and in the adult mouse brain in vivo disinhibited glycogen synthase kinase 3beta (GSK3beta) by protein phosphatase 1(PP1)-mediated dephosphorylation of GSK3beta at the serine 9 residue. Serine 259-265 glycogen synthase kinase 3 beta Mus musculus 141-171 16288045-3 2005 We found that the resistance to the antiproliferative effects of gefitinib, in vitro as well as in vivo in nude mice models, was associated with uncoupling between EGFR and MAPK inhibition, and that GSK-3beta activation and degradation of its target cyclin D1 were indicators of a high cell sensitivity to gefitinib. Gefitinib 65-74 glycogen synthase kinase 3 beta Mus musculus 199-208 16288045-3 2005 We found that the resistance to the antiproliferative effects of gefitinib, in vitro as well as in vivo in nude mice models, was associated with uncoupling between EGFR and MAPK inhibition, and that GSK-3beta activation and degradation of its target cyclin D1 were indicators of a high cell sensitivity to gefitinib. Gefitinib 306-315 glycogen synthase kinase 3 beta Mus musculus 199-208 16155008-2 2005 Here, we report that stimulation of NMDARs in cultured rat hippocampal or cortical neurons and in the adult mouse brain in vivo disinhibited glycogen synthase kinase 3beta (GSK3beta) by protein phosphatase 1(PP1)-mediated dephosphorylation of GSK3beta at the serine 9 residue. Serine 259-265 glycogen synthase kinase 3 beta Mus musculus 173-181 16086373-5 2005 Increased phosphorylation of GSK-3 (Ser(9/21)), TSC2(Thr(1462)), and mTOR(Ser(2448)) was observed. Serine 36-39 glycogen synthase kinase 3 beta Mus musculus 29-34 16139797-7 2005 Further, GSK3 inhibitor lithium blocked Pin1 binding to C99 by decreasing Thr668 phosphorylation and attenuated Abeta generation, explaining the inhibitory effect of lithium on Abeta generation. Lithium 24-31 glycogen synthase kinase 3 beta Mus musculus 9-13 16139797-7 2005 Further, GSK3 inhibitor lithium blocked Pin1 binding to C99 by decreasing Thr668 phosphorylation and attenuated Abeta generation, explaining the inhibitory effect of lithium on Abeta generation. UNII-042A8N37WH 112-117 glycogen synthase kinase 3 beta Mus musculus 9-13 16139797-7 2005 Further, GSK3 inhibitor lithium blocked Pin1 binding to C99 by decreasing Thr668 phosphorylation and attenuated Abeta generation, explaining the inhibitory effect of lithium on Abeta generation. Lithium 166-173 glycogen synthase kinase 3 beta Mus musculus 9-13 16192643-6 2005 Increases in inactive GSK-3beta occurred early in postnatal development, well before neuronal loss, and were most prominent in structures with intracellular cholesterol accumulation, suggesting a contribution to subsequent degeneration. Cholesterol 157-168 glycogen synthase kinase 3 beta Mus musculus 22-31 15980066-0 2005 Ser-557-phosphorylated mCRY2 is degraded upon synergistic phosphorylation by glycogen synthase kinase-3 beta. Serine 0-3 glycogen synthase kinase 3 beta Mus musculus 77-108 15980066-5 2005 Importantly, phosphorylation of mCRY2 at Ser-557 allows subsequent phosphorylation at Ser-553 by glycogen synthase kinase-3beta (GSK-3beta), resulting in efficient degradation of mCRY2 by a proteasome pathway. Serine 41-44 glycogen synthase kinase 3 beta Mus musculus 97-127 15980066-6 2005 As assessed by phosphorylation of GSK-3beta at Ser-9, which negatively regulates the kinase activity, GSK-3beta exhibits a circadian rhythm in its activity with a peak from late night to early morning when Ser-557 of mCRY2 is highly phosphorylated. Serine 206-209 glycogen synthase kinase 3 beta Mus musculus 34-43 15980066-5 2005 Importantly, phosphorylation of mCRY2 at Ser-557 allows subsequent phosphorylation at Ser-553 by glycogen synthase kinase-3beta (GSK-3beta), resulting in efficient degradation of mCRY2 by a proteasome pathway. Serine 41-44 glycogen synthase kinase 3 beta Mus musculus 129-138 15980066-6 2005 As assessed by phosphorylation of GSK-3beta at Ser-9, which negatively regulates the kinase activity, GSK-3beta exhibits a circadian rhythm in its activity with a peak from late night to early morning when Ser-557 of mCRY2 is highly phosphorylated. Serine 206-209 glycogen synthase kinase 3 beta Mus musculus 102-111 15980066-5 2005 Importantly, phosphorylation of mCRY2 at Ser-557 allows subsequent phosphorylation at Ser-553 by glycogen synthase kinase-3beta (GSK-3beta), resulting in efficient degradation of mCRY2 by a proteasome pathway. Serine 86-89 glycogen synthase kinase 3 beta Mus musculus 97-127 15980066-5 2005 Importantly, phosphorylation of mCRY2 at Ser-557 allows subsequent phosphorylation at Ser-553 by glycogen synthase kinase-3beta (GSK-3beta), resulting in efficient degradation of mCRY2 by a proteasome pathway. Serine 86-89 glycogen synthase kinase 3 beta Mus musculus 129-138 15980066-6 2005 As assessed by phosphorylation of GSK-3beta at Ser-9, which negatively regulates the kinase activity, GSK-3beta exhibits a circadian rhythm in its activity with a peak from late night to early morning when Ser-557 of mCRY2 is highly phosphorylated. Serine 47-50 glycogen synthase kinase 3 beta Mus musculus 34-43 15980066-6 2005 As assessed by phosphorylation of GSK-3beta at Ser-9, which negatively regulates the kinase activity, GSK-3beta exhibits a circadian rhythm in its activity with a peak from late night to early morning when Ser-557 of mCRY2 is highly phosphorylated. Serine 47-50 glycogen synthase kinase 3 beta Mus musculus 102-111 16103100-8 2005 Enzastaurin treatment also suppresses GSK3beta phosphorylation to a similar extent in peripheral blood mononuclear cells (PBMCs) from these treated mice. enzastaurin 0-11 glycogen synthase kinase 3 beta Mus musculus 38-46 16039605-5 2005 In addition, we showed hyperphosphorylation of c-Jun N-terminal kinase (JNK) and glycogen synthase kinase 3 beta (GSK-3 beta) at serine 9. Serine 129-135 glycogen synthase kinase 3 beta Mus musculus 81-112 16039605-5 2005 In addition, we showed hyperphosphorylation of c-Jun N-terminal kinase (JNK) and glycogen synthase kinase 3 beta (GSK-3 beta) at serine 9. Serine 129-135 glycogen synthase kinase 3 beta Mus musculus 114-124 15972822-4 2005 Exposing serum-shocked NIH3T3 cells to lithium chloride, a specific inhibitor of GSK-3beta, increases GSK-3beta phosphorylation and delays the phase of rhythmic clock gene expression. Lithium Chloride 39-55 glycogen synthase kinase 3 beta Mus musculus 81-90 15972822-4 2005 Exposing serum-shocked NIH3T3 cells to lithium chloride, a specific inhibitor of GSK-3beta, increases GSK-3beta phosphorylation and delays the phase of rhythmic clock gene expression. Lithium Chloride 39-55 glycogen synthase kinase 3 beta Mus musculus 102-111 15961082-0 2005 Role of the PDK1-PKB-GSK3 pathway in regulating glycogen synthase and glucose uptake in the heart. Glucose 70-77 glycogen synthase kinase 3 beta Mus musculus 21-25 16082208-2 2005 By binding to GSK3, Frat prevents the phosphorylation and concomitant degradation of beta-catenin and allows the activation of downstream target genes by beta-catenin/TCF complexes. tcf 167-170 glycogen synthase kinase 3 beta Mus musculus 14-18 15878878-5 2005 By analyzing cellular proteins that regulate beta-catenin stabilities, it was found that RONDelta160 activates the protein disheveled (DVL) and inactivates glycogen synthase kinase-3beta by Ser-9 residue phosphorylation. rondelta160 89-100 glycogen synthase kinase 3 beta Mus musculus 156-186 15878878-5 2005 By analyzing cellular proteins that regulate beta-catenin stabilities, it was found that RONDelta160 activates the protein disheveled (DVL) and inactivates glycogen synthase kinase-3beta by Ser-9 residue phosphorylation. Serine 190-193 glycogen synthase kinase 3 beta Mus musculus 156-186 15792956-3 2005 Kinase activity of ERK1/2 for Elk-1 and Akt for glycogen synthase kinase-3beta was also potently enhanced by silibinin pretreatment. Silybin 109-118 glycogen synthase kinase 3 beta Mus musculus 48-78 15741651-4 2005 Although the uptake of TG precursors is not stimulated in 3T3-L1 cells with impaired mitochondrial activity, we found a strong stimulation of glucose uptake in AA-treated cells mediated by calcium and phosphatidylinositol 3-kinase/Akt1/glycogen synthase kinase 3beta, a pathway known to trigger the translocation of glucose transporter 4 to the plasma membrane in response to insulin. Glucose 142-149 glycogen synthase kinase 3 beta Mus musculus 236-266 15880264-3 2005 It was found that the application of wortmannin alone only transitorily increased the activity of GSK-3 (about 1 h) and the level of tau hyperphosphorylation at Ser396/Ser404 and Ser199/Ser202 sites (no longer than 3 h); however, a prolonged and intense activation of GSK-3 (over 12 h) and enhanced tau hyperphosphorylation (about 24 h) were observed when these two selective kinase inhibitors were applied together. Wortmannin 37-47 glycogen synthase kinase 3 beta Mus musculus 98-103 15880264-3 2005 It was found that the application of wortmannin alone only transitorily increased the activity of GSK-3 (about 1 h) and the level of tau hyperphosphorylation at Ser396/Ser404 and Ser199/Ser202 sites (no longer than 3 h); however, a prolonged and intense activation of GSK-3 (over 12 h) and enhanced tau hyperphosphorylation (about 24 h) were observed when these two selective kinase inhibitors were applied together. Wortmannin 37-47 glycogen synthase kinase 3 beta Mus musculus 268-273 15585669-0 2005 Lithium treatment inhibits renal GSK-3 activity and promotes cyclooxygenase 2-dependent polyuria. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 33-38 15585669-2 2005 In vitro studies indicate that lithium can induce renal medullary interstitial cell cyclooxygenase 2 (COX2) protein expression via inhibition of glycogen synthase kinase-3beta (GSK-3beta). Lithium 31-38 glycogen synthase kinase 3 beta Mus musculus 145-175 15585669-2 2005 In vitro studies indicate that lithium can induce renal medullary interstitial cell cyclooxygenase 2 (COX2) protein expression via inhibition of glycogen synthase kinase-3beta (GSK-3beta). Lithium 31-38 glycogen synthase kinase 3 beta Mus musculus 177-186 15572521-6 2005 Inhibition of phosphatidylinositol 3-kinase (responsible for Akt activation) either by wortmanin or LY-294002 prevented Li(+)- or BIO-induced Akt phosphorylation and reduces cell survival without altering the phosphorylation state of GSK3beta. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 100-109 glycogen synthase kinase 3 beta Mus musculus 234-242 15585669-12 2005 Lithium also decreased renal medullary GSK-3beta activity, and this was temporally related to increased COX2 expression in the kidney from lithium-treated mice, consistent with a tonic in vivo suppression of COX2 expression by GSK-3 activity. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 39-48 15585669-12 2005 Lithium also decreased renal medullary GSK-3beta activity, and this was temporally related to increased COX2 expression in the kidney from lithium-treated mice, consistent with a tonic in vivo suppression of COX2 expression by GSK-3 activity. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 39-44 15585669-13 2005 In conclusion, these findings temporally link decreased GSK-3 activity to enhanced renal COX2 expression and COX2-derived urine PGE(2) excretion. Prostaglandins E 128-131 glycogen synthase kinase 3 beta Mus musculus 56-61 15740721-4 2005 When the cells were incubated simultaneously with calyculin A and melatonin (25 microM or 50 microM), the calyculin A-induced decrease in cell viability, tau hyperphosphorylation, PP-2A/GSK-3 imbalance and oxidative stress were attenuated accordingly. calyculin A 50-61 glycogen synthase kinase 3 beta Mus musculus 186-191 15777744-12 2005 Finally, we found that LiCl and SB216773 displayed different profiles in the TaqMan panel evidencing their distinct inhibitory action toward GSK-3beta. Lithium Chloride 23-27 glycogen synthase kinase 3 beta Mus musculus 141-150 15777744-12 2005 Finally, we found that LiCl and SB216773 displayed different profiles in the TaqMan panel evidencing their distinct inhibitory action toward GSK-3beta. sb216773 32-40 glycogen synthase kinase 3 beta Mus musculus 141-150 15740721-4 2005 When the cells were incubated simultaneously with calyculin A and melatonin (25 microM or 50 microM), the calyculin A-induced decrease in cell viability, tau hyperphosphorylation, PP-2A/GSK-3 imbalance and oxidative stress were attenuated accordingly. Melatonin 66-75 glycogen synthase kinase 3 beta Mus musculus 186-191 15740721-4 2005 When the cells were incubated simultaneously with calyculin A and melatonin (25 microM or 50 microM), the calyculin A-induced decrease in cell viability, tau hyperphosphorylation, PP-2A/GSK-3 imbalance and oxidative stress were attenuated accordingly. calyculin A 50-59 glycogen synthase kinase 3 beta Mus musculus 186-191 15740721-5 2005 These results suggest (i) that calyculin A induces tau hyperphosphorylation not only by inhibition of PP-2A, but also by activation of GSK-3 in N2a cells; (ii) that melatonin efficiently attenuates the calyculin A-induced damages through not only its antioxidant effect but also its modulation to the phosphorylation system. calyculin A 31-42 glycogen synthase kinase 3 beta Mus musculus 135-140 15659239-0 2005 Anesthesia and post-mortem interval profoundly influence the regulatory serine phosphorylation of glycogen synthase kinase-3 in mouse brain. Serine 72-78 glycogen synthase kinase 3 beta Mus musculus 98-124 15691529-0 2005 Hypoxia activates glycogen synthase kinase-3 in mouse brain in vivo: protection by mood stabilizers and imipramine. Imipramine 104-114 glycogen synthase kinase 3 beta Mus musculus 18-44 15691529-1 2005 BACKGROUND: Glycogen synthase kinase-3 (GSK3), which is primarily regulated by an inhibitory phosphorylation of an N-terminal serine, has been implicated as contributing to mood disorders by the finding that it is inhibited by the mood stabilizer lithium. Serine 126-132 glycogen synthase kinase 3 beta Mus musculus 12-38 15691529-1 2005 BACKGROUND: Glycogen synthase kinase-3 (GSK3), which is primarily regulated by an inhibitory phosphorylation of an N-terminal serine, has been implicated as contributing to mood disorders by the finding that it is inhibited by the mood stabilizer lithium. Serine 126-132 glycogen synthase kinase 3 beta Mus musculus 40-44 15691529-1 2005 BACKGROUND: Glycogen synthase kinase-3 (GSK3), which is primarily regulated by an inhibitory phosphorylation of an N-terminal serine, has been implicated as contributing to mood disorders by the finding that it is inhibited by the mood stabilizer lithium. Lithium 247-254 glycogen synthase kinase 3 beta Mus musculus 12-38 15691529-1 2005 BACKGROUND: Glycogen synthase kinase-3 (GSK3), which is primarily regulated by an inhibitory phosphorylation of an N-terminal serine, has been implicated as contributing to mood disorders by the finding that it is inhibited by the mood stabilizer lithium. Lithium 247-254 glycogen synthase kinase 3 beta Mus musculus 40-44 15691529-2 2005 METHODS: This study tested if the antidepressant imipramine or the mood stabilizers lithium and sodium valproate regulated pathophysiological serine-dephosphorylation of GSK3 caused by hypoxia in mouse brain in vivo. Imipramine 49-59 glycogen synthase kinase 3 beta Mus musculus 170-174 15691529-2 2005 METHODS: This study tested if the antidepressant imipramine or the mood stabilizers lithium and sodium valproate regulated pathophysiological serine-dephosphorylation of GSK3 caused by hypoxia in mouse brain in vivo. Lithium 84-91 glycogen synthase kinase 3 beta Mus musculus 170-174 15691529-2 2005 METHODS: This study tested if the antidepressant imipramine or the mood stabilizers lithium and sodium valproate regulated pathophysiological serine-dephosphorylation of GSK3 caused by hypoxia in mouse brain in vivo. Valproic Acid 96-112 glycogen synthase kinase 3 beta Mus musculus 170-174 15691529-2 2005 METHODS: This study tested if the antidepressant imipramine or the mood stabilizers lithium and sodium valproate regulated pathophysiological serine-dephosphorylation of GSK3 caused by hypoxia in mouse brain in vivo. Serine 142-148 glycogen synthase kinase 3 beta Mus musculus 170-174 15691529-3 2005 RESULTS: Hypoxia caused rapid serine-dephosphorylation of both isoforms of GSK3, GSK3beta and GSK3alpha, in mouse cerebral cortex, hippocampus, and striatum. Serine 30-36 glycogen synthase kinase 3 beta Mus musculus 75-79 15691529-3 2005 RESULTS: Hypoxia caused rapid serine-dephosphorylation of both isoforms of GSK3, GSK3beta and GSK3alpha, in mouse cerebral cortex, hippocampus, and striatum. Serine 30-36 glycogen synthase kinase 3 beta Mus musculus 81-89 15691529-4 2005 Pretreatment of mice with imipramine, sodium valproate, or lithium attenuated hypoxia-induced serine-dephosphorylation of GSK3beta and GSK3alpha in all three brain regions. Imipramine 26-36 glycogen synthase kinase 3 beta Mus musculus 122-130 15691529-4 2005 Pretreatment of mice with imipramine, sodium valproate, or lithium attenuated hypoxia-induced serine-dephosphorylation of GSK3beta and GSK3alpha in all three brain regions. Valproic Acid 38-54 glycogen synthase kinase 3 beta Mus musculus 122-130 15691529-4 2005 Pretreatment of mice with imipramine, sodium valproate, or lithium attenuated hypoxia-induced serine-dephosphorylation of GSK3beta and GSK3alpha in all three brain regions. Lithium 59-66 glycogen synthase kinase 3 beta Mus musculus 122-130 15691529-4 2005 Pretreatment of mice with imipramine, sodium valproate, or lithium attenuated hypoxia-induced serine-dephosphorylation of GSK3beta and GSK3alpha in all three brain regions. Serine 94-100 glycogen synthase kinase 3 beta Mus musculus 122-130 15691529-5 2005 CONCLUSIONS: These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects. Imipramine 44-54 glycogen synthase kinase 3 beta Mus musculus 157-161 15691529-5 2005 CONCLUSIONS: These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects. Imipramine 44-54 glycogen synthase kinase 3 beta Mus musculus 237-241 15691529-5 2005 CONCLUSIONS: These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects. Serine 129-135 glycogen synthase kinase 3 beta Mus musculus 157-161 15691529-5 2005 CONCLUSIONS: These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects. Serine 129-135 glycogen synthase kinase 3 beta Mus musculus 237-241 15691529-5 2005 CONCLUSIONS: These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects. Serine 211-217 glycogen synthase kinase 3 beta Mus musculus 157-161 15691529-5 2005 CONCLUSIONS: These results demonstrate that imipramine and mood stabilizers are capable of blocking pathophysiologically induced serine-dephosphorylation of GSK3, supporting the hypothesis that stabilization of serine-phosphorylation of GSK3 contributes to their therapeutic effects. Serine 211-217 glycogen synthase kinase 3 beta Mus musculus 237-241 15673569-4 2005 Murine ES cells express elevated levels of Myc and following LIF withdrawal, Myc mRNA levels collapse and Myc protein becomes phosphorylated on threonine 58 (T58), triggering its GSK3beta dependent degradation. Threonine 144-153 glycogen synthase kinase 3 beta Mus musculus 179-187 15723650-10 2005 Half of the mutations were detected at codon 37 or 41, encoding serine and threonine that are direct targets for phosphorylation by glycogen synthase kinase-3beta. Serine 64-70 glycogen synthase kinase 3 beta Mus musculus 132-162 15723650-10 2005 Half of the mutations were detected at codon 37 or 41, encoding serine and threonine that are direct targets for phosphorylation by glycogen synthase kinase-3beta. Threonine 75-84 glycogen synthase kinase 3 beta Mus musculus 132-162 15659239-3 2005 GSK3 is inhibited by phosphorylation of serine-9 or serine-21 in GSK3beta and GSK3alpha, respectively. Serine 40-46 glycogen synthase kinase 3 beta Mus musculus 0-4 15659239-3 2005 GSK3 is inhibited by phosphorylation of serine-9 or serine-21 in GSK3beta and GSK3alpha, respectively. Serine 40-46 glycogen synthase kinase 3 beta Mus musculus 65-73 15659239-3 2005 GSK3 is inhibited by phosphorylation of serine-9 or serine-21 in GSK3beta and GSK3alpha, respectively. Serine 52-58 glycogen synthase kinase 3 beta Mus musculus 0-4 15659239-3 2005 GSK3 is inhibited by phosphorylation of serine-9 or serine-21 in GSK3beta and GSK3alpha, respectively. Serine 52-58 glycogen synthase kinase 3 beta Mus musculus 65-73 15659239-4 2005 This study found that accurate measurements of phospho-Ser-GSK3 in brain are confounded by a rapid post-mortem dephosphorylation, with approximately 90% dephosphorylation of both GSK3 isoforms occurring within 2 min post-mortem. Serine 55-58 glycogen synthase kinase 3 beta Mus musculus 59-63 15659239-5 2005 Furthermore, three anesthetics, pentobarbital, halothane and chloral hydrate, each caused large in vivo increases in the serine phosphorylation of both GSK3beta and GSK3alpha in several regions of mouse brain. Pentobarbital 32-45 glycogen synthase kinase 3 beta Mus musculus 152-160 15659239-5 2005 Furthermore, three anesthetics, pentobarbital, halothane and chloral hydrate, each caused large in vivo increases in the serine phosphorylation of both GSK3beta and GSK3alpha in several regions of mouse brain. Halothane 47-56 glycogen synthase kinase 3 beta Mus musculus 152-160 15659239-5 2005 Furthermore, three anesthetics, pentobarbital, halothane and chloral hydrate, each caused large in vivo increases in the serine phosphorylation of both GSK3beta and GSK3alpha in several regions of mouse brain. Chloral Hydrate 61-76 glycogen synthase kinase 3 beta Mus musculus 152-160 15659239-5 2005 Furthermore, three anesthetics, pentobarbital, halothane and chloral hydrate, each caused large in vivo increases in the serine phosphorylation of both GSK3beta and GSK3alpha in several regions of mouse brain. Serine 121-127 glycogen synthase kinase 3 beta Mus musculus 152-160 15659239-6 2005 Thus, studies of the phosphorylation state of GSK3 in brain, and perhaps in other tissues, need to take into account post-mortem changes and the effects of anesthetics and there is a direct correlation between anesthesia and high levels of serine-phosphorylated GSK3. Serine 240-246 glycogen synthase kinase 3 beta Mus musculus 46-50 15466861-4 2004 Inhibition of glycogen synthase kinase-3beta by LiCl treatment further increased PC1-mediated NFAT activity. Lithium Chloride 48-52 glycogen synthase kinase 3 beta Mus musculus 14-44 15956784-5 2005 We show that an acute change in phospholipid composition, by addition of dipalmitoyl-phophatidylcholine, leads to GLUT1 translocation to the plasma membrane in conjunction to an increase of Akt and GSK3beta phosphorylation, which are sensitive to PI3K and PLD inhibitors. Phospholipids 32-44 glycogen synthase kinase 3 beta Mus musculus 198-206 15956784-5 2005 We show that an acute change in phospholipid composition, by addition of dipalmitoyl-phophatidylcholine, leads to GLUT1 translocation to the plasma membrane in conjunction to an increase of Akt and GSK3beta phosphorylation, which are sensitive to PI3K and PLD inhibitors. dipalmitoyl-phophatidylcholine 73-103 glycogen synthase kinase 3 beta Mus musculus 198-206 16196280-2 2005 After N2a cells were treated with the specific inhibitor (wortmannin) of phosphoinositol-3 kinase (PI-3K) or treated with wortmannin and the specific inhibitor (LiCl) of glycogen synthase kinase-3 (GSK-3), GSK-3 activity and neurofilament phosphorylation were detected by using GSK-3 activity assay, Western blots and immunofluoresence. Lithium Chloride 161-165 glycogen synthase kinase 3 beta Mus musculus 170-196 16196280-3 2005 Our results showed that after treatment of N2a cells with wortmannin for 1 h, overactivation of GSK-3 caused a reduced staining with antibody SMI32 and an enhanced staining with antibody SMI31. Wortmannin 58-68 glycogen synthase kinase 3 beta Mus musculus 96-101 16196280-4 2005 When N2a cells were treated with wortmannin and LiCl, the activity of GSK-3 was reduced substantially. Wortmannin 33-43 glycogen synthase kinase 3 beta Mus musculus 70-75 16196280-4 2005 When N2a cells were treated with wortmannin and LiCl, the activity of GSK-3 was reduced substantially. Lithium Chloride 48-52 glycogen synthase kinase 3 beta Mus musculus 70-75 15617833-2 2005 We report that nabumetone decreased uninvolved intestinal mucosal beta-catenin levels in the MIN mouse with a concomitant increase in glycogen synthase kinase (GSK)-3beta levels, an enzyme that targets beta-catenin for destruction. Nabumetone 15-25 glycogen synthase kinase 3 beta Mus musculus 134-170 15525634-7 2005 We now show that beta-catenin and the glycogen synthase kinase-3beta inhibitor lithium do not activate glu mRNA or glu promoter expression in pancreatic cell lines. Lithium 79-86 glycogen synthase kinase 3 beta Mus musculus 38-68 15476703-0 2004 Inactivation of glycogen synthase kinase-3beta protects against kainic acid-induced neurotoxicity in vivo. Kainic Acid 64-75 glycogen synthase kinase 3 beta Mus musculus 16-46 15466414-7 2004 Instead, the increased JNK activation observed in GSK-3beta-/- MEFs was associated with an increased proliferative response to LPA, which was reduced by the inhibition of JNK. lysophosphatidic acid 127-130 glycogen synthase kinase 3 beta Mus musculus 50-59 15466414-8 2004 Ectopic expression of GSK-3beta in GSK-3beta-negative MEFs restrained LPA-triggered JNK phosphorylation and induced a concomitant decrease in the mitogenic response to LPA compatible with GSK-3beta through the inhibition of JNK activation, thus limiting LPA-induced cell proliferation. lysophosphatidic acid 70-73 glycogen synthase kinase 3 beta Mus musculus 22-31 15466414-8 2004 Ectopic expression of GSK-3beta in GSK-3beta-negative MEFs restrained LPA-triggered JNK phosphorylation and induced a concomitant decrease in the mitogenic response to LPA compatible with GSK-3beta through the inhibition of JNK activation, thus limiting LPA-induced cell proliferation. lysophosphatidic acid 70-73 glycogen synthase kinase 3 beta Mus musculus 35-44 15466414-8 2004 Ectopic expression of GSK-3beta in GSK-3beta-negative MEFs restrained LPA-triggered JNK phosphorylation and induced a concomitant decrease in the mitogenic response to LPA compatible with GSK-3beta through the inhibition of JNK activation, thus limiting LPA-induced cell proliferation. lysophosphatidic acid 70-73 glycogen synthase kinase 3 beta Mus musculus 35-44 15466414-8 2004 Ectopic expression of GSK-3beta in GSK-3beta-negative MEFs restrained LPA-triggered JNK phosphorylation and induced a concomitant decrease in the mitogenic response to LPA compatible with GSK-3beta through the inhibition of JNK activation, thus limiting LPA-induced cell proliferation. lysophosphatidic acid 168-171 glycogen synthase kinase 3 beta Mus musculus 22-31 15466414-8 2004 Ectopic expression of GSK-3beta in GSK-3beta-negative MEFs restrained LPA-triggered JNK phosphorylation and induced a concomitant decrease in the mitogenic response to LPA compatible with GSK-3beta through the inhibition of JNK activation, thus limiting LPA-induced cell proliferation. lysophosphatidic acid 168-171 glycogen synthase kinase 3 beta Mus musculus 22-31 15466414-9 2004 Mutation analysis indicated that GSK-3beta kinase activity was required for GSK-3beta to optimally inhibit LPA-stimulated JNK activation. lysophosphatidic acid 107-110 glycogen synthase kinase 3 beta Mus musculus 33-42 15466414-9 2004 Mutation analysis indicated that GSK-3beta kinase activity was required for GSK-3beta to optimally inhibit LPA-stimulated JNK activation. lysophosphatidic acid 107-110 glycogen synthase kinase 3 beta Mus musculus 76-85 15466414-10 2004 Thus GSK-3beta serves as a physiological switch to specifically repress JNK activation in response to LPA, sphingosine-1-phosphate, or the epidermal growth factor. lysophosphatidic acid 102-105 glycogen synthase kinase 3 beta Mus musculus 5-14 15466414-10 2004 Thus GSK-3beta serves as a physiological switch to specifically repress JNK activation in response to LPA, sphingosine-1-phosphate, or the epidermal growth factor. sphingosine 1-phosphate 107-130 glycogen synthase kinase 3 beta Mus musculus 5-14 15579172-1 2004 Valproic acid (VPA) has long been used as an antiepileptic drug and recently as a mood stabilizer, and evidence is increasing that VPA exerts neuroprotective effects through changes in a variety of intracellular signalling pathways including upregulation of Bcl-2 protein with an antiapoptotic property and inhibiting glycogen synthase kinase 3-beta, which is considered to promote cell survival. Valproic Acid 0-13 glycogen synthase kinase 3 beta Mus musculus 318-349 15579172-1 2004 Valproic acid (VPA) has long been used as an antiepileptic drug and recently as a mood stabilizer, and evidence is increasing that VPA exerts neuroprotective effects through changes in a variety of intracellular signalling pathways including upregulation of Bcl-2 protein with an antiapoptotic property and inhibiting glycogen synthase kinase 3-beta, which is considered to promote cell survival. Valproic Acid 15-18 glycogen synthase kinase 3 beta Mus musculus 318-349 15579172-1 2004 Valproic acid (VPA) has long been used as an antiepileptic drug and recently as a mood stabilizer, and evidence is increasing that VPA exerts neuroprotective effects through changes in a variety of intracellular signalling pathways including upregulation of Bcl-2 protein with an antiapoptotic property and inhibiting glycogen synthase kinase 3-beta, which is considered to promote cell survival. Valproic Acid 131-134 glycogen synthase kinase 3 beta Mus musculus 318-349 15466414-3 2004 In the present study, we demonstrated that homozygous disruption of glycogen synthase kinase 3beta (GSK-3beta) dramatically sensitized mouse embryonic fibroblasts (MEFs) to JNK activation induced by lysophosphatidic acid (LPA) and sphingosine-1-phosphate, two prototype ligands for G protein-coupled receptors. lysophosphatidic acid 199-220 glycogen synthase kinase 3 beta Mus musculus 68-98 15466414-3 2004 In the present study, we demonstrated that homozygous disruption of glycogen synthase kinase 3beta (GSK-3beta) dramatically sensitized mouse embryonic fibroblasts (MEFs) to JNK activation induced by lysophosphatidic acid (LPA) and sphingosine-1-phosphate, two prototype ligands for G protein-coupled receptors. lysophosphatidic acid 199-220 glycogen synthase kinase 3 beta Mus musculus 100-109 15466414-3 2004 In the present study, we demonstrated that homozygous disruption of glycogen synthase kinase 3beta (GSK-3beta) dramatically sensitized mouse embryonic fibroblasts (MEFs) to JNK activation induced by lysophosphatidic acid (LPA) and sphingosine-1-phosphate, two prototype ligands for G protein-coupled receptors. lysophosphatidic acid 222-225 glycogen synthase kinase 3 beta Mus musculus 68-98 15466414-3 2004 In the present study, we demonstrated that homozygous disruption of glycogen synthase kinase 3beta (GSK-3beta) dramatically sensitized mouse embryonic fibroblasts (MEFs) to JNK activation induced by lysophosphatidic acid (LPA) and sphingosine-1-phosphate, two prototype ligands for G protein-coupled receptors. lysophosphatidic acid 222-225 glycogen synthase kinase 3 beta Mus musculus 100-109 15466414-3 2004 In the present study, we demonstrated that homozygous disruption of glycogen synthase kinase 3beta (GSK-3beta) dramatically sensitized mouse embryonic fibroblasts (MEFs) to JNK activation induced by lysophosphatidic acid (LPA) and sphingosine-1-phosphate, two prototype ligands for G protein-coupled receptors. sphingosine 1-phosphate 231-254 glycogen synthase kinase 3 beta Mus musculus 68-98 15466414-3 2004 In the present study, we demonstrated that homozygous disruption of glycogen synthase kinase 3beta (GSK-3beta) dramatically sensitized mouse embryonic fibroblasts (MEFs) to JNK activation induced by lysophosphatidic acid (LPA) and sphingosine-1-phosphate, two prototype ligands for G protein-coupled receptors. sphingosine 1-phosphate 231-254 glycogen synthase kinase 3 beta Mus musculus 100-109 15466414-6 2004 The increased JNK activation induced by LPA in GSK-3beta null MEFs was insufficient to trigger apoptotic cell death or growth inhibition. lysophosphatidic acid 40-43 glycogen synthase kinase 3 beta Mus musculus 47-56 15591023-8 2004 The whole pathway activated by ACTH to destabilize c-Myc protein in Y1 cells might comprise the following steps: ACTH receptor -->cAMP/PKA --> Akt deactivation -->GSK3 activity liberation --> c-Myc Thr58 phosphorylation. Cyclic AMP 133-137 glycogen synthase kinase 3 beta Mus musculus 172-176 15476703-5 2004 Indeed, GSK-3beta phosphorylation occurred in response to kainic acid exclusively in the affected hippocampus, but not as a consequence of ERK activation. Kainic Acid 58-69 glycogen synthase kinase 3 beta Mus musculus 8-17 15476703-7 2004 A role for GSK-3beta inhibition in cell survival was further supported by the fact that pharmacological inhibition of GSK-3beta using lithium chloride was protective against kainic acid-induced excitotoxicity in hippocampal slice cultures. Lithium Chloride 134-150 glycogen synthase kinase 3 beta Mus musculus 11-20 15476703-7 2004 A role for GSK-3beta inhibition in cell survival was further supported by the fact that pharmacological inhibition of GSK-3beta using lithium chloride was protective against kainic acid-induced excitotoxicity in hippocampal slice cultures. Lithium Chloride 134-150 glycogen synthase kinase 3 beta Mus musculus 118-127 15476703-7 2004 A role for GSK-3beta inhibition in cell survival was further supported by the fact that pharmacological inhibition of GSK-3beta using lithium chloride was protective against kainic acid-induced excitotoxicity in hippocampal slice cultures. Kainic Acid 174-185 glycogen synthase kinase 3 beta Mus musculus 11-20 15476703-7 2004 A role for GSK-3beta inhibition in cell survival was further supported by the fact that pharmacological inhibition of GSK-3beta using lithium chloride was protective against kainic acid-induced excitotoxicity in hippocampal slice cultures. Kainic Acid 174-185 glycogen synthase kinase 3 beta Mus musculus 118-127 15170327-5 2004 Both lithium and VPA are known to be glycogen synthase kinase-3 (GSK3) inhibitors. Lithium 5-12 glycogen synthase kinase 3 beta Mus musculus 37-63 15375789-1 2004 Glycogen synthase kinase-3 (GSK-3) protein levels and activity are elevated in skeletal muscle in type 2 diabetes, and inversely correlated with both glycogen synthase activity and insulin-stimulated glucose disposal. Glucose 200-207 glycogen synthase kinase 3 beta Mus musculus 0-26 15375789-1 2004 Glycogen synthase kinase-3 (GSK-3) protein levels and activity are elevated in skeletal muscle in type 2 diabetes, and inversely correlated with both glycogen synthase activity and insulin-stimulated glucose disposal. Glucose 200-207 glycogen synthase kinase 3 beta Mus musculus 28-33 15252041-1 2004 Glycogen synthase kinase (GSK)-3beta is a constitutively active, proline-directed serine/threonine kinase that controls growth modulation and tumorigenesis through multiple intracellular signaling pathways. Proline 65-72 glycogen synthase kinase 3 beta Mus musculus 0-36 15288510-0 2004 Phosphatidylinositol-3 kinase/Akt and GSK-3 mediated cytoprotective effect of epigallocatechin gallate on oxidative stress-injured neuronal-differentiated N18D3 cells. epigallocatechin gallate 78-102 glycogen synthase kinase 3 beta Mus musculus 38-43 15288510-3 2004 This study was designed to investigate whether EGCG plays a cytoprotective role by activating phosphatidylinositol-3 kinase (PI3K)/Akt-dependent anti-apoptotic pathway and inhibiting glycogen synthase kinase-3 (GSK-3) activity in oxidative stressed N18D3 neural cells. epigallocatechin gallate 47-51 glycogen synthase kinase 3 beta Mus musculus 183-209 15288510-3 2004 This study was designed to investigate whether EGCG plays a cytoprotective role by activating phosphatidylinositol-3 kinase (PI3K)/Akt-dependent anti-apoptotic pathway and inhibiting glycogen synthase kinase-3 (GSK-3) activity in oxidative stressed N18D3 neural cells. epigallocatechin gallate 47-51 glycogen synthase kinase 3 beta Mus musculus 211-216 15288510-6 2004 MTT assay and trypan blue staining showed that EGCG and z-VAD-fmk significantly increased cell viability, and IR of PI3K, phospho-Akt and phospho-GSK-3 beta was significantly increased in the cells treated with EGCG, but not in z-VAD-fmk treated. epigallocatechin gallate 47-51 glycogen synthase kinase 3 beta Mus musculus 146-156 15039769-2 2004 GSK3beta is inhibited by phosphorylation on serine-9 and is a target of the mood stabilizer lithium. Serine 44-50 glycogen synthase kinase 3 beta Mus musculus 0-8 15039769-2 2004 GSK3beta is inhibited by phosphorylation on serine-9 and is a target of the mood stabilizer lithium. Lithium 92-99 glycogen synthase kinase 3 beta Mus musculus 0-8 15039769-3 2004 Following administration to mice of d-fenfluramine to stimulate serotonin (5HT) release and reduce its reuptake, and clorgyline to inhibit 5HT catabolism, levels of phospho-Ser9-GSK3beta were 300-400% of control levels in the prefrontal cortex, hippocampus, and striatum. Dexfenfluramine 36-50 glycogen synthase kinase 3 beta Mus musculus 178-186 15039769-3 2004 Following administration to mice of d-fenfluramine to stimulate serotonin (5HT) release and reduce its reuptake, and clorgyline to inhibit 5HT catabolism, levels of phospho-Ser9-GSK3beta were 300-400% of control levels in the prefrontal cortex, hippocampus, and striatum. Clorgyline 117-127 glycogen synthase kinase 3 beta Mus musculus 178-186 15039769-4 2004 Treatment with monoamine reuptake inhibitors fluoxetine and imipramine also increased the level of phospho-Ser9-GSK3beta. monoamine 15-24 glycogen synthase kinase 3 beta Mus musculus 112-120 15039769-4 2004 Treatment with monoamine reuptake inhibitors fluoxetine and imipramine also increased the level of phospho-Ser9-GSK3beta. Fluoxetine 45-55 glycogen synthase kinase 3 beta Mus musculus 112-120 15039769-4 2004 Treatment with monoamine reuptake inhibitors fluoxetine and imipramine also increased the level of phospho-Ser9-GSK3beta. Imipramine 60-70 glycogen synthase kinase 3 beta Mus musculus 112-120 15308623-6 2004 Mutation of serine 37 (a target of GSK3beta) to an alanine renders beta-catenin resistant to the degradatory action of PPARgamma. Serine 12-18 glycogen synthase kinase 3 beta Mus musculus 35-43 15308623-6 2004 Mutation of serine 37 (a target of GSK3beta) to an alanine renders beta-catenin resistant to the degradatory action of PPARgamma. Alanine 51-58 glycogen synthase kinase 3 beta Mus musculus 35-43 15367685-5 2004 Similarly, these effectors activate the phosphorylation of T188 within an ectopic C/EBPbeta overexpressed in Swiss mouse fibroblasts, and this event involves both MEK1 and GSK3 activity. Solvent Yellow 21 59-63 glycogen synthase kinase 3 beta Mus musculus 172-176 15286700-16 2004 Consistently, treatment of W53 with selective inhibitors of GSK3 such as SB415286 and lithium salts resulted in increased levels of c-Myc. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 73-81 glycogen synthase kinase 3 beta Mus musculus 60-64 15286700-16 2004 Consistently, treatment of W53 with selective inhibitors of GSK3 such as SB415286 and lithium salts resulted in increased levels of c-Myc. Lithium 86-93 glycogen synthase kinase 3 beta Mus musculus 60-64 15350841-12 2004 Furthermore, myocardial protein extracts of mice revealed GSK3beta inactivation after administration of pravastatin intraperitoneally. Pravastatin 104-115 glycogen synthase kinase 3 beta Mus musculus 58-66 15282284-0 2004 Glycogen synthase kinase-3beta haploinsufficiency mimics the behavioral and molecular effects of lithium. Lithium 97-104 glycogen synthase kinase 3 beta Mus musculus 0-30 15282284-5 2004 Remarkably, these lithium-sensitive behaviors are also observed in mice lacking one copy of the gene encoding glycogen synthase kinase-3beta (Gsk-3beta), a well established direct target of lithium. Lithium 18-25 glycogen synthase kinase 3 beta Mus musculus 110-140 15282284-5 2004 Remarkably, these lithium-sensitive behaviors are also observed in mice lacking one copy of the gene encoding glycogen synthase kinase-3beta (Gsk-3beta), a well established direct target of lithium. Lithium 18-25 glycogen synthase kinase 3 beta Mus musculus 142-151 15282284-5 2004 Remarkably, these lithium-sensitive behaviors are also observed in mice lacking one copy of the gene encoding glycogen synthase kinase-3beta (Gsk-3beta), a well established direct target of lithium. Lithium 190-197 glycogen synthase kinase 3 beta Mus musculus 110-140 15282284-5 2004 Remarkably, these lithium-sensitive behaviors are also observed in mice lacking one copy of the gene encoding glycogen synthase kinase-3beta (Gsk-3beta), a well established direct target of lithium. Lithium 190-197 glycogen synthase kinase 3 beta Mus musculus 142-151 15282284-6 2004 In addition, chronic lithium induces molecular changes consistent with inhibition of GSK-3 within regions of the brain that are paralleled in Gsk-3beta+/- heterozygous mice. Lithium 21-28 glycogen synthase kinase 3 beta Mus musculus 85-90 15282284-6 2004 In addition, chronic lithium induces molecular changes consistent with inhibition of GSK-3 within regions of the brain that are paralleled in Gsk-3beta+/- heterozygous mice. Lithium 21-28 glycogen synthase kinase 3 beta Mus musculus 142-151 15282284-8 2004 These observations support a central role for GSK-3beta in mediating behavioral responses to lithium. Lithium 93-100 glycogen synthase kinase 3 beta Mus musculus 46-55 15170327-5 2004 Both lithium and VPA are known to be glycogen synthase kinase-3 (GSK3) inhibitors. Lithium 5-12 glycogen synthase kinase 3 beta Mus musculus 65-69 15170327-5 2004 Both lithium and VPA are known to be glycogen synthase kinase-3 (GSK3) inhibitors. Valproic Acid 17-20 glycogen synthase kinase 3 beta Mus musculus 37-63 15170327-5 2004 Both lithium and VPA are known to be glycogen synthase kinase-3 (GSK3) inhibitors. Valproic Acid 17-20 glycogen synthase kinase 3 beta Mus musculus 65-69 15170327-6 2004 Our studies reveal that GSK3beta is a potential downstream kinase, which modulates APP processing because inhibition of GSK3 activity by either a dominant negative GSK3beta kinase-deficient construct or GSK3beta antisense oligonucleotide mimics lithium and VPA effects. Oligonucleotides 222-237 glycogen synthase kinase 3 beta Mus musculus 24-28 15170327-6 2004 Our studies reveal that GSK3beta is a potential downstream kinase, which modulates APP processing because inhibition of GSK3 activity by either a dominant negative GSK3beta kinase-deficient construct or GSK3beta antisense oligonucleotide mimics lithium and VPA effects. Lithium 245-252 glycogen synthase kinase 3 beta Mus musculus 24-28 15170327-6 2004 Our studies reveal that GSK3beta is a potential downstream kinase, which modulates APP processing because inhibition of GSK3 activity by either a dominant negative GSK3beta kinase-deficient construct or GSK3beta antisense oligonucleotide mimics lithium and VPA effects. Valproic Acid 257-260 glycogen synthase kinase 3 beta Mus musculus 24-28 15044068-5 2004 Pharmacological inhibition of GSK-3beta with lithium chloride in the sensitive parental neuronal cells results in an increased tolerance to glutamate and hydrogen peroxide, suggesting that GSK-3beta is involved in the control of oxidative stress resistance in these cells. Lithium Chloride 45-61 glycogen synthase kinase 3 beta Mus musculus 30-39 15099877-3 2004 Lithium can mimic increased activity of the Wnt/beta-catenin pathway by blocking the activity of glycogen synthase kinase-3beta. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 97-127 15099877-10 2004 This action of lithium is associated with decreased expression of estrogen receptors-alpha, beta-catenin and glycogen synthase kinase-3beta in the uterus. Lithium 15-22 glycogen synthase kinase 3 beta Mus musculus 109-139 15044068-5 2004 Pharmacological inhibition of GSK-3beta with lithium chloride in the sensitive parental neuronal cells results in an increased tolerance to glutamate and hydrogen peroxide, suggesting that GSK-3beta is involved in the control of oxidative stress resistance in these cells. Lithium Chloride 45-61 glycogen synthase kinase 3 beta Mus musculus 189-198 15044068-5 2004 Pharmacological inhibition of GSK-3beta with lithium chloride in the sensitive parental neuronal cells results in an increased tolerance to glutamate and hydrogen peroxide, suggesting that GSK-3beta is involved in the control of oxidative stress resistance in these cells. Glutamic Acid 140-149 glycogen synthase kinase 3 beta Mus musculus 30-39 15044068-5 2004 Pharmacological inhibition of GSK-3beta with lithium chloride in the sensitive parental neuronal cells results in an increased tolerance to glutamate and hydrogen peroxide, suggesting that GSK-3beta is involved in the control of oxidative stress resistance in these cells. Glutamic Acid 140-149 glycogen synthase kinase 3 beta Mus musculus 189-198 15044068-5 2004 Pharmacological inhibition of GSK-3beta with lithium chloride in the sensitive parental neuronal cells results in an increased tolerance to glutamate and hydrogen peroxide, suggesting that GSK-3beta is involved in the control of oxidative stress resistance in these cells. Hydrogen Peroxide 154-171 glycogen synthase kinase 3 beta Mus musculus 30-39 15044068-5 2004 Pharmacological inhibition of GSK-3beta with lithium chloride in the sensitive parental neuronal cells results in an increased tolerance to glutamate and hydrogen peroxide, suggesting that GSK-3beta is involved in the control of oxidative stress resistance in these cells. Hydrogen Peroxide 154-171 glycogen synthase kinase 3 beta Mus musculus 189-198 15090054-0 2004 Effect of lithium on the circadian rhythms of locomotor activity and glycogen synthase kinase-3 protein expression in the mouse suprachiasmatic nuclei. Lithium 10-17 glycogen synthase kinase 3 beta Mus musculus 69-95 15044694-0 2004 Lithium antagonizes dopamine-dependent behaviors mediated by an AKT/glycogen synthase kinase 3 signaling cascade. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 68-94 15044694-0 2004 Lithium antagonizes dopamine-dependent behaviors mediated by an AKT/glycogen synthase kinase 3 signaling cascade. Dopamine 20-28 glycogen synthase kinase 3 beta Mus musculus 68-94 15044694-3 2004 Here, we used a pharmacogenetic approach to show that DA can exert its behavioral effects by acting on a lithium-sensitive signaling cascade involving Akt/PKB and glycogen synthase kinase 3 (GSK-3). Lithium 105-112 glycogen synthase kinase 3 beta Mus musculus 163-189 15044694-3 2004 Here, we used a pharmacogenetic approach to show that DA can exert its behavioral effects by acting on a lithium-sensitive signaling cascade involving Akt/PKB and glycogen synthase kinase 3 (GSK-3). Lithium 105-112 glycogen synthase kinase 3 beta Mus musculus 191-196 15044694-4 2004 In the mouse striatum, increased DA neurotransmission arising either from administration of amphetamine or from the lack of the DA transporter results in inactivation of Akt and concomitant activation of GSK-3alpha and GSK-3beta. Amphetamine 92-103 glycogen synthase kinase 3 beta Mus musculus 219-228 15044694-7 2004 These data support the involvement of GSK-3 as an important mediator of DA and lithium action in vivo and suggest that modulation of the Akt/GSK-3 pathway might be relevant to DA-related disorders, such as attention deficit hyperactivity disorder and schizophrenia. Lithium 79-86 glycogen synthase kinase 3 beta Mus musculus 38-43 15044694-7 2004 These data support the involvement of GSK-3 as an important mediator of DA and lithium action in vivo and suggest that modulation of the Akt/GSK-3 pathway might be relevant to DA-related disorders, such as attention deficit hyperactivity disorder and schizophrenia. Lithium 79-86 glycogen synthase kinase 3 beta Mus musculus 141-146 15090054-2 2004 In the present study, we examined Drosophila shaggy ortholog glycogen synthase kinase-3 (GSK-3) protein expression in the SCN after lithium treatment. Lithium 132-139 glycogen synthase kinase 3 beta Mus musculus 61-87 15090054-4 2004 The decreased expression of GSK-3 and increased expression of phosphorylated GSK-3 (pGSK-3) resulted in an antiphasic circadian rhythm between the two in the SCN of lithium-treated mice housed under both light-dark and constant dark conditions. pgsk-3 84-90 glycogen synthase kinase 3 beta Mus musculus 77-82 15090054-4 2004 The decreased expression of GSK-3 and increased expression of phosphorylated GSK-3 (pGSK-3) resulted in an antiphasic circadian rhythm between the two in the SCN of lithium-treated mice housed under both light-dark and constant dark conditions. Lithium 165-172 glycogen synthase kinase 3 beta Mus musculus 28-33 15090054-4 2004 The decreased expression of GSK-3 and increased expression of phosphorylated GSK-3 (pGSK-3) resulted in an antiphasic circadian rhythm between the two in the SCN of lithium-treated mice housed under both light-dark and constant dark conditions. Lithium 165-172 glycogen synthase kinase 3 beta Mus musculus 77-82 14691449-5 2004 Further mechanistic studies in vitro revealed that these responses were counteracted by the selective A(3)AR antagonist MRS 1523 and by the GSK-3 beta inhibitors lithium and SB216763, confirming that the observed effects were A(3)AR and GSK-3 beta mediated. Lithium 162-169 glycogen synthase kinase 3 beta Mus musculus 140-150 14691449-5 2004 Further mechanistic studies in vitro revealed that these responses were counteracted by the selective A(3)AR antagonist MRS 1523 and by the GSK-3 beta inhibitors lithium and SB216763, confirming that the observed effects were A(3)AR and GSK-3 beta mediated. SB 216763 174-182 glycogen synthase kinase 3 beta Mus musculus 140-150 14691449-5 2004 Further mechanistic studies in vitro revealed that these responses were counteracted by the selective A(3)AR antagonist MRS 1523 and by the GSK-3 beta inhibitors lithium and SB216763, confirming that the observed effects were A(3)AR and GSK-3 beta mediated. SB 216763 174-182 glycogen synthase kinase 3 beta Mus musculus 237-247 15559765-4 2004 PX-316 administered intraperitoneally to mice at 150 mg/kg inhibits Akt activation in HT-29 human tumor xenografts up to 78% at 10 h with recovery to 34% at 48 h. Phosphorylation of GSK-3beta, a downstream target of Akt, is also inhibited. 1-((1-O-octadecyl-2-O-methylglycero)phospho)-3-deoxy-myo-inositol 0-6 glycogen synthase kinase 3 beta Mus musculus 182-191 15062551-6 2004 Addition of DHEA prevented phosphorylation of both Akt and glycogen synthase kinase-3 beta (GSK-3beta), downstream effector molecules of the phosphatidylinositol 3-kinase (PI3K) pathway. Dehydroepiandrosterone 12-16 glycogen synthase kinase 3 beta Mus musculus 59-90 15062551-6 2004 Addition of DHEA prevented phosphorylation of both Akt and glycogen synthase kinase-3 beta (GSK-3beta), downstream effector molecules of the phosphatidylinositol 3-kinase (PI3K) pathway. Dehydroepiandrosterone 12-16 glycogen synthase kinase 3 beta Mus musculus 92-101 15062551-7 2004 Further IGF-I was able to sustain Akt activity and thus preventing GSK-3beta activation in the presence of DHEA. Dehydroepiandrosterone 107-111 glycogen synthase kinase 3 beta Mus musculus 67-76 14745448-1 2004 AKT-GSK3beta signaling is a target of lithium and as such has been implicated in the pathogenesis of mood disorders. Lithium 38-45 glycogen synthase kinase 3 beta Mus musculus 4-12 14745448-3 2004 Specifically, we present convergent evidence for a decrease in AKT1 protein levels and levels of phosphorylation of GSK3beta at Ser9 in the peripheral lymphocytes and brains of individuals with schizophrenia; a significant association between schizophrenia and an AKT1 haplotype associated with lower AKT1 protein levels; and a greater sensitivity to the sensorimotor gating-disruptive effect of amphetamine, conferred by AKT1 deficiency. Amphetamine 396-407 glycogen synthase kinase 3 beta Mus musculus 116-124 14651959-1 2003 Glycogen synthase kinase-3 (GSK3) and cyclin-dependent kinase 5 (CDK5) are related serine/threonine kinases that have been well studied for their role in tau hyperphosphorylation, however, little is known about their significance in APP processing. Serine 83-89 glycogen synthase kinase 3 beta Mus musculus 0-26 14651959-1 2003 Glycogen synthase kinase-3 (GSK3) and cyclin-dependent kinase 5 (CDK5) are related serine/threonine kinases that have been well studied for their role in tau hyperphosphorylation, however, little is known about their significance in APP processing. Serine 83-89 glycogen synthase kinase 3 beta Mus musculus 28-32 14651959-3 2003 Specific inhibition of cellular GSK3 by lithium or GSK3beta antisense elicits a reduction in Abeta. Lithium 40-47 glycogen synthase kinase 3 beta Mus musculus 32-36 14534419-5 2003 Treatment of NPCs with lithium, a specific inhibitor of glycogen synthase kinase 3beta (GSK3beta), significantly suppressed apoptosis. Lithium 23-30 glycogen synthase kinase 3 beta Mus musculus 56-86 14664817-4 2003 These events can be mimicked by lithium (Li(+)), which inhibits GSK-3 activity. Lithium 32-39 glycogen synthase kinase 3 beta Mus musculus 64-69 14664817-5 2003 Both Li(+) and the GSK-3 inhibitor SB415286 induced neurite outgrowth of Neuro-2a cells. 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione 35-43 glycogen synthase kinase 3 beta Mus musculus 19-24 14663202-2 2003 In SH-SY5Y cells, primary cortical neurons, and mouse brain, the portion of active GSK3 beta (not phosphorylated on serine-9) was 5- to 8-fold greater in nuclei and mitochondria than in cytosol. Serine 116-122 glycogen synthase kinase 3 beta Mus musculus 83-92 14534419-5 2003 Treatment of NPCs with lithium, a specific inhibitor of glycogen synthase kinase 3beta (GSK3beta), significantly suppressed apoptosis. Lithium 23-30 glycogen synthase kinase 3 beta Mus musculus 88-96 12796505-0 2003 Inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3) in response to lithium. Lithium 80-87 glycogen synthase kinase 3 beta Mus musculus 58-63 14632202-6 2003 Interestingly, we have recently reported that cAMP-elevating agents, through a phosphatidylinositol-3-kinase/AKT inhibition and a glycogen synthase kinase 3beta activation, may stimulate microphthalmia associated transcription factor binding to its target sequence, suggesting that inhibition of the phosphatidylinositol-3-kinase is implicated in the stimulation of melanogenesis at different levels. Cyclic AMP 46-50 glycogen synthase kinase 3 beta Mus musculus 130-160 12796505-3 2003 Lithium is a direct inhibitor of GSK-3 and has been widely used to test the putative role of GSK-3 in multiple settings. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 33-38 12796505-3 2003 Lithium is a direct inhibitor of GSK-3 and has been widely used to test the putative role of GSK-3 in multiple settings. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 93-98 12796505-5 2003 For example, lithium is known to increase the inhibitory N-terminal phosphorylation of GSK-3, but the target of lithium responsible for this indirect regulation has not been identified. Lithium 13-20 glycogen synthase kinase 3 beta Mus musculus 87-92 12796505-5 2003 For example, lithium is known to increase the inhibitory N-terminal phosphorylation of GSK-3, but the target of lithium responsible for this indirect regulation has not been identified. Lithium 112-119 glycogen synthase kinase 3 beta Mus musculus 87-92 12796505-7 2003 We show here, using the GSK-3 interaction domain peptide, as well as small molecule inhibitors of GSK-3, that lithium induces GSK-3 N-terminal phosphorylation through direct inhibition of GSK-3 itself. Lithium 110-117 glycogen synthase kinase 3 beta Mus musculus 24-29 12796505-7 2003 We show here, using the GSK-3 interaction domain peptide, as well as small molecule inhibitors of GSK-3, that lithium induces GSK-3 N-terminal phosphorylation through direct inhibition of GSK-3 itself. Lithium 110-117 glycogen synthase kinase 3 beta Mus musculus 98-103 12796505-7 2003 We show here, using the GSK-3 interaction domain peptide, as well as small molecule inhibitors of GSK-3, that lithium induces GSK-3 N-terminal phosphorylation through direct inhibition of GSK-3 itself. Lithium 110-117 glycogen synthase kinase 3 beta Mus musculus 98-103 12796505-7 2003 We show here, using the GSK-3 interaction domain peptide, as well as small molecule inhibitors of GSK-3, that lithium induces GSK-3 N-terminal phosphorylation through direct inhibition of GSK-3 itself. Lithium 110-117 glycogen synthase kinase 3 beta Mus musculus 98-103 12714590-10 2003 Moreover, inhibition of GSK-3beta with lithium prevented aberrant tau phosphorylation in the DN-ILK-expressing cells. Lithium 39-46 glycogen synthase kinase 3 beta Mus musculus 24-33 12770514-0 2003 Effects of a glycogen synthase kinase-3 inhibitor, lithium, in adenomatous polyposis coli mutant mice. Lithium 51-58 glycogen synthase kinase 3 beta Mus musculus 13-39 12770514-5 2003 We therefore investigated the effects of a GSK-3 inhibitor, lithium, in a murine model predisposed to the formation of tumors due to activation of the Wnt pathway-the adenomatous polyposis coli (APC) multiple intestinal neoplasia (min) mouse. Lithium 60-67 glycogen synthase kinase 3 beta Mus musculus 43-48 12770514-8 2003 The APC (min) mouse has previously been shown to be a robust indicator of tumorigenesis, with large increases in tumor number observed in response to a variety of agents; thus, our results suggest that lithium-and perhaps other inhibitors of GSK-3-pose a low risk for the development of cancers of the Wnt pathway. Lithium 202-209 glycogen synthase kinase 3 beta Mus musculus 242-247 12668682-0 2003 Lithium stabilizes the CCAAT/enhancer-binding protein alpha (C/EBPalpha) through a glycogen synthase kinase 3 (GSK3)-independent pathway involving direct inhibition of proteasomal activity. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 83-109 12626660-3 2003 Here, we present a novel class of specific phosphorylated peptides inhibitors of GSK-3, which in sharp contrast to other protein kinase inhibitors that are ATP analogs, are substrate-competitive. Adenosine Triphosphate 156-159 glycogen synthase kinase 3 beta Mus musculus 81-86 12626660-4 2003 We show that the GSK-3 peptide inhibitor activated glycogen synthase activity 2.5-fold in human embryonic kidney 293 cells, and increased glucose uptake in primary mouse adipocytes in the absence or presence of insulin compared with cells treated with two respective peptide controls. Glucose 138-145 glycogen synthase kinase 3 beta Mus musculus 17-22 12626660-6 2003 administration of GSK-3 peptide inhibitor to normal or insulin-resistant obese C57BL/6J mice, improved their performance on glucose tolerance tests compared with control-treated animals. Glucose 124-131 glycogen synthase kinase 3 beta Mus musculus 18-23 12668682-0 2003 Lithium stabilizes the CCAAT/enhancer-binding protein alpha (C/EBPalpha) through a glycogen synthase kinase 3 (GSK3)-independent pathway involving direct inhibition of proteasomal activity. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 111-115 12668682-5 2003 GSK3 is a known C/EBPalpha kinase and treatment of keratinocytes with LiCl, an inhibitor of GSK3 resulted in: (i) a 5-fold increase in C/EBPalpha protein levels, (ii) increased electrophoretic mobility of C/EBPalpha, and (iii) no increase in C/EBPalpha mRNA levels suggesting that GSK3-mediated phosphorylation of C/EBPalpha may target it for proteasomal degradation. Lithium Chloride 70-74 glycogen synthase kinase 3 beta Mus musculus 0-4 12668682-5 2003 GSK3 is a known C/EBPalpha kinase and treatment of keratinocytes with LiCl, an inhibitor of GSK3 resulted in: (i) a 5-fold increase in C/EBPalpha protein levels, (ii) increased electrophoretic mobility of C/EBPalpha, and (iii) no increase in C/EBPalpha mRNA levels suggesting that GSK3-mediated phosphorylation of C/EBPalpha may target it for proteasomal degradation. Lithium Chloride 70-74 glycogen synthase kinase 3 beta Mus musculus 92-96 12668682-5 2003 GSK3 is a known C/EBPalpha kinase and treatment of keratinocytes with LiCl, an inhibitor of GSK3 resulted in: (i) a 5-fold increase in C/EBPalpha protein levels, (ii) increased electrophoretic mobility of C/EBPalpha, and (iii) no increase in C/EBPalpha mRNA levels suggesting that GSK3-mediated phosphorylation of C/EBPalpha may target it for proteasomal degradation. Lithium Chloride 70-74 glycogen synthase kinase 3 beta Mus musculus 92-96 12668682-6 2003 However, a mutant C/EBPalpha containing T to A mutations in the GSK3 phosphorylation sites (T222A and T226A) retained its response to LiCl, and additional pharmacological inhibitors of GSK3 did not alter C/EBPalpha levels indicating the effects of LiCl on C/EBPalpha are GSK3-independent. Lithium Chloride 134-138 glycogen synthase kinase 3 beta Mus musculus 64-68 12668682-6 2003 However, a mutant C/EBPalpha containing T to A mutations in the GSK3 phosphorylation sites (T222A and T226A) retained its response to LiCl, and additional pharmacological inhibitors of GSK3 did not alter C/EBPalpha levels indicating the effects of LiCl on C/EBPalpha are GSK3-independent. Lithium Chloride 248-252 glycogen synthase kinase 3 beta Mus musculus 64-68 12420304-9 2003 Treatment of mouse GVI oocytes with lithium chloride (LiCl), which inhibits both inositol monophosphatase (IMPase) and GSK-3, had no significant influence on oocyte viability, morphology, or development to metaphase II (MII). Lithium Chloride 36-52 glycogen synthase kinase 3 beta Mus musculus 119-124 12721208-3 2003 Immunostaining of testis sections showed that while GSK-3 alpha was ubiquitous in the seminiferous tubules, GSK-3 beta was expressed in premeiotic type B spermatogonia, in both meiotic preleptotene and leptotene spermatocytes, as well as in Sertoli cells in both the mouse and rat. preleptotene 185-197 glycogen synthase kinase 3 beta Mus musculus 108-118 12721208-3 2003 Immunostaining of testis sections showed that while GSK-3 alpha was ubiquitous in the seminiferous tubules, GSK-3 beta was expressed in premeiotic type B spermatogonia, in both meiotic preleptotene and leptotene spermatocytes, as well as in Sertoli cells in both the mouse and rat. leptotene 188-197 glycogen synthase kinase 3 beta Mus musculus 108-118 12420304-9 2003 Treatment of mouse GVI oocytes with lithium chloride (LiCl), which inhibits both inositol monophosphatase (IMPase) and GSK-3, had no significant influence on oocyte viability, morphology, or development to metaphase II (MII). Lithium Chloride 54-58 glycogen synthase kinase 3 beta Mus musculus 119-124 11835406-6 2002 To assess the functional involvement of Wnt signaling in BMP-2 induced chondrogenesis, cultures were treated with lithium chloride, a Wnt-7A mimetic that acts by inhibiting the serine/threonine phosphorylation activity of glycogen synthase kinase-3beta (GSK-3beta). Lithium Chloride 114-130 glycogen synthase kinase 3 beta Mus musculus 222-252 12472906-3 2002 These mice, designated Tet/GSK-3beta, showed many of the biochemical and cellular aspects of AD neuropathology such as tau hyperphosphorylation and somatodendritic localization, decreased nuclear beta-catenin, neuronal death and reactive gliosis. tetramethylenedisulfotetramine 23-26 glycogen synthase kinase 3 beta Mus musculus 27-36 12472906-7 2002 We found a significant increase in GSK-3 activity in the hippocampus of Tet/GSK-3beta mice whereas no tau fibrils could be found even in very old mice. tetramethylenedisulfotetramine 72-75 glycogen synthase kinase 3 beta Mus musculus 35-40 12472906-7 2002 We found a significant increase in GSK-3 activity in the hippocampus of Tet/GSK-3beta mice whereas no tau fibrils could be found even in very old mice. tetramethylenedisulfotetramine 72-75 glycogen synthase kinase 3 beta Mus musculus 76-85 12489109-4 2002 We found that GSK-3 activity was downregulated at the later stages of promotion by tyrosine 216 dephosphorylation and serine 9 phosphorylation. Tyrosine 83-91 glycogen synthase kinase 3 beta Mus musculus 14-19 12489109-4 2002 We found that GSK-3 activity was downregulated at the later stages of promotion by tyrosine 216 dephosphorylation and serine 9 phosphorylation. Serine 118-124 glycogen synthase kinase 3 beta Mus musculus 14-19 12489109-5 2002 The data obtained with Akt-transformed keratinocytes clearly suggested the involvement of Akt in serine 9 phosphorylation of GSK-3beta. Serine 97-103 glycogen synthase kinase 3 beta Mus musculus 125-134 12504922-4 2002 Lithium treatment increased the Ser-9 phosphorylation of GSK3beta both in cells and in mouse brain after chronic administration, but did not alter the phosphorylation of Akt. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 57-65 12504922-4 2002 Lithium treatment increased the Ser-9 phosphorylation of GSK3beta both in cells and in mouse brain after chronic administration, but did not alter the phosphorylation of Akt. Serine 32-35 glycogen synthase kinase 3 beta Mus musculus 57-65 12095987-3 2002 In primary rat neuronal and HT22 cells, FGF1 promoted a time-dependent inactivation of GSK3beta by phosphorylation at serine 9. Serine 118-124 glycogen synthase kinase 3 beta Mus musculus 87-95 11834740-2 2002 It is generally believed that four conserved Ser/Thr residues in the N terminus of beta-catenin are the pivotal targets for the constitutively active serine kinase GSK3. Serine 45-48 glycogen synthase kinase 3 beta Mus musculus 164-168 11834740-2 2002 It is generally believed that four conserved Ser/Thr residues in the N terminus of beta-catenin are the pivotal targets for the constitutively active serine kinase GSK3. Threonine 49-52 glycogen synthase kinase 3 beta Mus musculus 164-168 11834740-8 2002 The epitope is generated upon Wnt signaling as well as upon pharmacological inhibition of GSK3 by lithium, providing formal proof for the regulated phosphorylation of the Ser/Thr residues of beta-catenin by Wnt signaling. Lithium 98-105 glycogen synthase kinase 3 beta Mus musculus 90-94 11834740-8 2002 The epitope is generated upon Wnt signaling as well as upon pharmacological inhibition of GSK3 by lithium, providing formal proof for the regulated phosphorylation of the Ser/Thr residues of beta-catenin by Wnt signaling. Serine 171-174 glycogen synthase kinase 3 beta Mus musculus 90-94 11834740-8 2002 The epitope is generated upon Wnt signaling as well as upon pharmacological inhibition of GSK3 by lithium, providing formal proof for the regulated phosphorylation of the Ser/Thr residues of beta-catenin by Wnt signaling. Threonine 175-178 glycogen synthase kinase 3 beta Mus musculus 90-94 12177184-2 2002 Here we describe that GSK-3 is activated by lysophosphatidic acid (LPA) during neurite retraction in rat cerebellar granule neurons. lysophosphatidic acid 44-65 glycogen synthase kinase 3 beta Mus musculus 22-27 12177184-2 2002 Here we describe that GSK-3 is activated by lysophosphatidic acid (LPA) during neurite retraction in rat cerebellar granule neurons. lysophosphatidic acid 67-70 glycogen synthase kinase 3 beta Mus musculus 22-27 12177184-3 2002 GSK-3 activation correlates with an increase in GSK-3 tyrosine phosphorylation. Tyrosine 54-62 glycogen synthase kinase 3 beta Mus musculus 0-5 12177184-3 2002 GSK-3 activation correlates with an increase in GSK-3 tyrosine phosphorylation. Tyrosine 54-62 glycogen synthase kinase 3 beta Mus musculus 48-53 12177184-4 2002 In addition, LPA induces a GSK-3-mediated hyperphosphorylation of the microtubule-associated protein tau. lysophosphatidic acid 13-16 glycogen synthase kinase 3 beta Mus musculus 27-32 12177184-5 2002 Inhibition of GSK-3 by lithium partially blocks neurite retraction, indicating that GSK-3 activation is important but not essential for the neurite retraction progress. Lithium 23-30 glycogen synthase kinase 3 beta Mus musculus 14-19 12177184-6 2002 GSK-3 activation by LPA in cerebellar granule neurons is neither downstream of Galpha(i) nor downstream of Galpha(q)/phospholipase C, suggesting that it is downstream of Galpha12/13. lysophosphatidic acid 20-23 glycogen synthase kinase 3 beta Mus musculus 0-5 11835406-6 2002 To assess the functional involvement of Wnt signaling in BMP-2 induced chondrogenesis, cultures were treated with lithium chloride, a Wnt-7A mimetic that acts by inhibiting the serine/threonine phosphorylation activity of glycogen synthase kinase-3beta (GSK-3beta). Lithium Chloride 114-130 glycogen synthase kinase 3 beta Mus musculus 254-263 11835406-7 2002 Lithium treatment significantly inhibited BMP-2 stimulation of chondrogenesis as well as GSK-3beta enzymatic activity, and decreased the levels of N-cadherin protein and mRNA. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 89-98 11835406-9 2002 Interestingly, lithium treatment did not affect the ability of BMP-2 to decrease ubiquitination of beta-catenin, although it did reduce the interaction of beta-catenin with GSK-3beta during late chondrogenesis (days 9-13). Lithium 15-22 glycogen synthase kinase 3 beta Mus musculus 173-182 11226152-2 2001 By using the tet-regulated system we have produced conditional transgenic mice overexpressing GSK-3beta in the brain during adulthood while avoiding perinatal lethality due to embryonic transgene expression. tetramethylenedisulfotetramine 13-16 glycogen synthase kinase 3 beta Mus musculus 94-103 11278638-5 2001 Lithium, a GSK-3 inhibitor, increases GH-dependent dephosphorylation of LAP and LIP. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 11-16 11563964-1 2001 Identified originally as a regulator of glycogen metabolism, glycogen synthase kinase-3 (GSK3) is now a well-established component of the Wnt signalling pathway, which is essential for setting up the entire body pattern during embryonic development. Glycogen 40-48 glycogen synthase kinase 3 beta Mus musculus 61-87 11563964-1 2001 Identified originally as a regulator of glycogen metabolism, glycogen synthase kinase-3 (GSK3) is now a well-established component of the Wnt signalling pathway, which is essential for setting up the entire body pattern during embryonic development. Glycogen 40-48 glycogen synthase kinase 3 beta Mus musculus 89-93 11563964-6 2001 Insulin and growth factors inhibit GSK3 by triggering its phosphorylation, turning the N-terminus into a pseudosubstrate inhibitor that competes for binding with the "priming phosphate" of substrates. Phosphates 175-184 glycogen synthase kinase 3 beta Mus musculus 35-39 11154277-6 2001 We also demonstrate that Gas6 activates Akt and concomitantly inhibits GSK3 activity in a wortmannin-dependent manner. Wortmannin 90-100 glycogen synthase kinase 3 beta Mus musculus 71-75 11124803-1 2000 GSK-3beta-dependent phosphorylation of cyclin D1 at Thr-286 promotes the nuclear-to-cytoplasmic redistribution of cyclin D1 during S phase of the cell cycle, but how phosphorylation regulates redistribution has not been resolved. Threonine 52-55 glycogen synthase kinase 3 beta Mus musculus 0-9 10880530-3 2000 Using resting T cells from P14 T cell receptor (TCR)-transgenic mice (specific for the lymphocytic choriomeningitis virus and H-2D(b)), we demonstrated that GSK-3beta was inactivated by serine phosphorylation after viral peptide-specific stimulation in vitro. Serine 186-192 glycogen synthase kinase 3 beta Mus musculus 157-166 10880530-4 2000 To further investigate the role of GSK-3, we have generated a retroviral vector that expresses a constitutively active form of GSK-3beta that has an alanine substitution at the regulatory amino acid, serine 9 (GSK-3betaA9). Alanine 149-156 glycogen synthase kinase 3 beta Mus musculus 127-136 11018055-7 2000 The microtubule stabilizing function of DVL-1 is mimicked by lithium-mediated inhibition of glycogen synthase kinase-3beta (GSK-3beta) and blocked by expression of GSK-3beta. Lithium 61-68 glycogen synthase kinase 3 beta Mus musculus 92-122 11018055-7 2000 The microtubule stabilizing function of DVL-1 is mimicked by lithium-mediated inhibition of glycogen synthase kinase-3beta (GSK-3beta) and blocked by expression of GSK-3beta. Lithium 61-68 glycogen synthase kinase 3 beta Mus musculus 124-133 10894547-6 2000 Lithium treatment (which inhibits GSK-3; refs 8, 9) sensitized wild-type fibroblasts to TNF and inhibited transactivation of NF-kappaB. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 34-39 10221643-7 1999 In contrast, in C57MG fibroblast cells, lithium inactivates GSK-3beta and induces Tcf-controlled transcription. Lithium 40-47 glycogen synthase kinase 3 beta Mus musculus 60-69 10880530-4 2000 To further investigate the role of GSK-3, we have generated a retroviral vector that expresses a constitutively active form of GSK-3beta that has an alanine substitution at the regulatory amino acid, serine 9 (GSK-3betaA9). Serine 200-206 glycogen synthase kinase 3 beta Mus musculus 127-136 10880530-7 2000 In contrast, in vitro assays done in the presence of the GSK-3 inhibitor lithium led to dramatically prolonged T cell proliferation and increased IL-2 production. Lithium 73-80 glycogen synthase kinase 3 beta Mus musculus 57-62 10561508-1 1999 Epidermal growth factor (EGF), insulin-like growth factor 1 (IGF1) and phorbol myristate acetate (PMA) induce the inhibition of glycogen synthase kinase 3 (GSK3) by stimulating the phosphorylation of an N-terminal serine. Tetradecanoylphorbol Acetate 71-96 glycogen synthase kinase 3 beta Mus musculus 128-154 10561508-1 1999 Epidermal growth factor (EGF), insulin-like growth factor 1 (IGF1) and phorbol myristate acetate (PMA) induce the inhibition of glycogen synthase kinase 3 (GSK3) by stimulating the phosphorylation of an N-terminal serine. Tetradecanoylphorbol Acetate 71-96 glycogen synthase kinase 3 beta Mus musculus 156-160 10561508-1 1999 Epidermal growth factor (EGF), insulin-like growth factor 1 (IGF1) and phorbol myristate acetate (PMA) induce the inhibition of glycogen synthase kinase 3 (GSK3) by stimulating the phosphorylation of an N-terminal serine. Serine 214-220 glycogen synthase kinase 3 beta Mus musculus 128-154 10561508-1 1999 Epidermal growth factor (EGF), insulin-like growth factor 1 (IGF1) and phorbol myristate acetate (PMA) induce the inhibition of glycogen synthase kinase 3 (GSK3) by stimulating the phosphorylation of an N-terminal serine. Serine 214-220 glycogen synthase kinase 3 beta Mus musculus 156-160 10545105-3 1999 When the germline heterozygotes were crossed with mice expressing Cre recombinase in the intestines, the serines and threonine encoded by exon 3 and to be phosphorylated by glycogen synthase kinase 3beta (GSK3beta) were deleted in the offspring intestines, which caused adenomatous intestinal polyps resembling those in Apc(Delta716) knockout mice. Serine 105-112 glycogen synthase kinase 3 beta Mus musculus 173-203 10545105-3 1999 When the germline heterozygotes were crossed with mice expressing Cre recombinase in the intestines, the serines and threonine encoded by exon 3 and to be phosphorylated by glycogen synthase kinase 3beta (GSK3beta) were deleted in the offspring intestines, which caused adenomatous intestinal polyps resembling those in Apc(Delta716) knockout mice. Serine 105-112 glycogen synthase kinase 3 beta Mus musculus 205-213 10545105-3 1999 When the germline heterozygotes were crossed with mice expressing Cre recombinase in the intestines, the serines and threonine encoded by exon 3 and to be phosphorylated by glycogen synthase kinase 3beta (GSK3beta) were deleted in the offspring intestines, which caused adenomatous intestinal polyps resembling those in Apc(Delta716) knockout mice. Threonine 117-126 glycogen synthase kinase 3 beta Mus musculus 173-203 10545105-3 1999 When the germline heterozygotes were crossed with mice expressing Cre recombinase in the intestines, the serines and threonine encoded by exon 3 and to be phosphorylated by glycogen synthase kinase 3beta (GSK3beta) were deleted in the offspring intestines, which caused adenomatous intestinal polyps resembling those in Apc(Delta716) knockout mice. Threonine 117-126 glycogen synthase kinase 3 beta Mus musculus 205-213 25152027-9 2014 Moreover, ALA markedly increased PKB/Akt and GSK3beta phosphorylation, and nuclear carbohydrate response element binding protein (ChREBP) expression in livers. Thioctic Acid 10-13 glycogen synthase kinase 3 beta Mus musculus 45-53 9832503-5 1998 Now, we demonstrate that glycogen synthase kinase-3beta (GSK-3beta) phosphorylates cyclin D1 specifically on Thr-286, thereby triggering rapid cyclin D1 turnover. Threonine 109-112 glycogen synthase kinase 3 beta Mus musculus 25-55 9832503-5 1998 Now, we demonstrate that glycogen synthase kinase-3beta (GSK-3beta) phosphorylates cyclin D1 specifically on Thr-286, thereby triggering rapid cyclin D1 turnover. Threonine 109-112 glycogen synthase kinase 3 beta Mus musculus 57-66 8887544-5 1996 Additionally, Wg-induced inactivation of GSK-3 is sensitive to both the protein kinase C (PKC) inhibitor Ro31-8220 and prolonged pre-treatment of 10T1/2 fibroblasts with phorbol ester. Ro 31-8220 105-114 glycogen synthase kinase 3 beta Mus musculus 41-46 8887544-5 1996 Additionally, Wg-induced inactivation of GSK-3 is sensitive to both the protein kinase C (PKC) inhibitor Ro31-8220 and prolonged pre-treatment of 10T1/2 fibroblasts with phorbol ester. Phorbol Esters 170-183 glycogen synthase kinase 3 beta Mus musculus 41-46 33822608-7 2021 Moreover, BCAA peptides significantly increased the muscle glycogen content (22.6 +- 0.9 nmol/mg) via the downregulation of protein kinase B (AKT) and glycogen synthase kinase-3beta (GSK-3beta) while increasing the activity of glycogen synthase (GS). Amino Acids, Branched-Chain 10-14 glycogen synthase kinase 3 beta Mus musculus 151-181 33822608-7 2021 Moreover, BCAA peptides significantly increased the muscle glycogen content (22.6 +- 0.9 nmol/mg) via the downregulation of protein kinase B (AKT) and glycogen synthase kinase-3beta (GSK-3beta) while increasing the activity of glycogen synthase (GS). Peptides 15-23 glycogen synthase kinase 3 beta Mus musculus 151-181 9806907-1 1998 Protein kinase B (PKB) isoforms became activated [and glycogen synthase kinase-3 (GSK3) became inhibited] when mouse Swiss 3T3 fibroblasts were exposed to oxidative stress (H2O2) or heat shock, but not when they were exposed to osmotic shock (0.5 M sorbitol or 0. Hydrogen Peroxide 173-177 glycogen synthase kinase 3 beta Mus musculus 82-86 33803419-3 2021 Quercetin (3,3",4",5,7-pentahydroxyflavone) is known to inhibit glycogen synthase kinase-3beta (GSK3beta), a potent regulator of both pro- and anti-inflammatory effects. Quercetin 0-9 glycogen synthase kinase 3 beta Mus musculus 64-94 33803419-3 2021 Quercetin (3,3",4",5,7-pentahydroxyflavone) is known to inhibit glycogen synthase kinase-3beta (GSK3beta), a potent regulator of both pro- and anti-inflammatory effects. Quercetin 11-42 glycogen synthase kinase 3 beta Mus musculus 64-94 34624485-3 2022 In line with this, 1-(7-chloroquinolin-4-yl)-N-(4-methoxybenzyl)-5-methyl-1H-1,2,3-triazole-4 carboxamide (QTC-4-MeOBnE) is characterized as an inhibitor of beta-secretase, glycogen synthase kinase 3beta, and acetylcholinesterase and has also shown secondary effects underlying the modulation of neurogenesis and synaptic plasticity pathways. 1-(7-chloroquinolin-4-yl)-n-(4-methoxybenzyl)-5-methyl-1h-1,2,3-triazole-4 carboxamide 19-105 glycogen synthase kinase 3 beta Mus musculus 173-203 34624485-3 2022 In line with this, 1-(7-chloroquinolin-4-yl)-N-(4-methoxybenzyl)-5-methyl-1H-1,2,3-triazole-4 carboxamide (QTC-4-MeOBnE) is characterized as an inhibitor of beta-secretase, glycogen synthase kinase 3beta, and acetylcholinesterase and has also shown secondary effects underlying the modulation of neurogenesis and synaptic plasticity pathways. qtc-4-meobne 107-119 glycogen synthase kinase 3 beta Mus musculus 173-203 34735714-8 2021 Meanwhile, melatonin also decreased the expression of p-GSK3beta (glycogen synthase kinase 3 beta), p-Akt, beta-catenin, and its translocation to the nucleus in granulosa cells. Melatonin 11-20 glycogen synthase kinase 3 beta Mus musculus 66-97 34987593-0 2021 Ginsenoside Rd Attenuates Tau Phosphorylation in Olfactory Bulb, Spinal Cord, and Telencephalon by Regulating Glycogen Synthase Kinase 3beta and Cyclin-Dependent Kinase 5. Ginsenosides 0-11 glycogen synthase kinase 3 beta Mus musculus 110-140 34371126-7 2021 Citrate supplemented animals had increased liver PKCalpha activity and altered phosphorylation at serine or threonine residues of components of insulin signaling including IRS-1, Akt, GSK-3 and FoxO1. Citric Acid 0-7 glycogen synthase kinase 3 beta Mus musculus 184-189 34605273-11 2021 Inhibition of glycogen synthase kinase-3 (GSK3), Lyn and Abl signaling pathways prevented the effect of aldosterone on claudin-8 mRNA and protein abundance, suggesting that signaling protein kinases plays a permissive role on the transcriptional activity of the mineralocorticoid receptor.This study shows that signaling via multiple protein kinases working in concert mediates the aldosterone-induced claudin-8 expression in collecting duct. Aldosterone 382-393 glycogen synthase kinase 3 beta Mus musculus 14-40 34246657-6 2021 Mechanistically, beta-hydroxybutyrate inhibition of glycogen synthase kinase 3beta (GSK3beta), a convergent point for myriad signaling pathways regulating Nrf2 activity, seems to contribute. 3-Hydroxybutyric Acid 17-37 glycogen synthase kinase 3 beta Mus musculus 52-82 34400288-0 2021 GSK-3 mediates nuclear translocation of p62/SQSTM1 in MPTP-induced mouse model of Parkinson"s disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 54-58 glycogen synthase kinase 3 beta Mus musculus 0-5 34596681-1 2022 Glycogen synthase kinase 3 (GSK3) is a kinase mediating phosphorylation on serine and threonine amino acid residues of several target molecules. Threonine 86-95 glycogen synthase kinase 3 beta Mus musculus 0-26 34400288-7 2021 Together, our data demonstrate that GSK-3 mediates nuclear translocation of p62 during MPTP-induced parkinsonian neurodegeneration. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 87-91 glycogen synthase kinase 3 beta Mus musculus 36-41 34627204-0 2021 Lactobacillus plantarum PS128 prevents cognitive dysfunction in Alzheimer"s disease mice by modulating propionic acid levels, glycogen synthase kinase 3 beta activity, and gliosis. ps128 24-29 glycogen synthase kinase 3 beta Mus musculus 126-157 34627204-10 2021 CONCLUSIONS: Based on the experimental results, intracerebroventricular injection of streptozotocin accelerates the progression of AD in the 3 x Tg-AD mice, primarily by increasing the levels of gliosis, which were mediated by the propionic acid and glycogen synthase kinase 3 beta pathways. Streptozocin 85-99 glycogen synthase kinase 3 beta Mus musculus 250-281 34627204-11 2021 PS128 supplementation prevents damage induced by intracerebroventricular injection of streptozotocin by regulating the propionic acid levels, glycogen synthase kinase 3 beta activity, and gliosis in 3 x Tg-AD mice. ps128 0-5 glycogen synthase kinase 3 beta Mus musculus 142-173 34627204-11 2021 PS128 supplementation prevents damage induced by intracerebroventricular injection of streptozotocin by regulating the propionic acid levels, glycogen synthase kinase 3 beta activity, and gliosis in 3 x Tg-AD mice. Streptozocin 86-100 glycogen synthase kinase 3 beta Mus musculus 142-173 34690696-1 2021 Glycogen synthase kinase 3 (GSK3) is a proline-directed serine-threonine kinase that is associated with several neurological disorders, including Alzheimer"s disease and fragile X syndrome (FXS). Proline 39-46 glycogen synthase kinase 3 beta Mus musculus 0-26 34690696-1 2021 Glycogen synthase kinase 3 (GSK3) is a proline-directed serine-threonine kinase that is associated with several neurological disorders, including Alzheimer"s disease and fragile X syndrome (FXS). Proline 39-46 glycogen synthase kinase 3 beta Mus musculus 28-32 34690696-1 2021 Glycogen synthase kinase 3 (GSK3) is a proline-directed serine-threonine kinase that is associated with several neurological disorders, including Alzheimer"s disease and fragile X syndrome (FXS). Serine 56-62 glycogen synthase kinase 3 beta Mus musculus 0-26 34690696-1 2021 Glycogen synthase kinase 3 (GSK3) is a proline-directed serine-threonine kinase that is associated with several neurological disorders, including Alzheimer"s disease and fragile X syndrome (FXS). Serine 56-62 glycogen synthase kinase 3 beta Mus musculus 28-32 34690696-2 2021 We tested the efficacy of a novel GSK3 inhibitor AFC03127, which was developed by Angelini Pharma, in comparison to the metabotropic glutamate receptor 5 inhibitor 2-Methyl-6-(phenylethynyl)pyridine hydrochloride (MPEP) and the GSK3 inhibitor SB216763 in in vivo and in vitro assays in Fmr1 KO mice, a mouse model useful for the study of FXS. afc03127 49-57 glycogen synthase kinase 3 beta Mus musculus 34-38 34596681-0 2022 The novel potent GSK3 inhibitor AF3581 reverts fragile X syndrome phenotype. af3581 32-38 glycogen synthase kinase 3 beta Mus musculus 17-21 34596681-1 2022 Glycogen synthase kinase 3 (GSK3) is a kinase mediating phosphorylation on serine and threonine amino acid residues of several target molecules. Serine 75-81 glycogen synthase kinase 3 beta Mus musculus 0-26 34596681-1 2022 Glycogen synthase kinase 3 (GSK3) is a kinase mediating phosphorylation on serine and threonine amino acid residues of several target molecules. Serine 75-81 glycogen synthase kinase 3 beta Mus musculus 28-32 34596681-1 2022 Glycogen synthase kinase 3 (GSK3) is a kinase mediating phosphorylation on serine and threonine amino acid residues of several target molecules. Threonine 86-95 glycogen synthase kinase 3 beta Mus musculus 28-32 34596681-6 2022 In this study we used AF3581, a potent GSK3 inhibitor that we recently discovered, in an in vivo FXS mouse model to elucidate the crucial role of GSK3 in specific behavioral patterns (locomotor activity, sensorimotor gating and social behavior) associated with this disease. af3581 22-28 glycogen synthase kinase 3 beta Mus musculus 39-43 34596681-6 2022 In this study we used AF3581, a potent GSK3 inhibitor that we recently discovered, in an in vivo FXS mouse model to elucidate the crucial role of GSK3 in specific behavioral patterns (locomotor activity, sensorimotor gating and social behavior) associated with this disease. af3581 22-28 glycogen synthase kinase 3 beta Mus musculus 146-150 34729397-9 2021 In addition, CIH induced CBs expression, which subsequently activated insulin-like growth factor-1 receptor (IGF-1R)/AKT/glycogen synthase kinase-3beta (GSK-3beta) axis. cih 13-16 glycogen synthase kinase 3 beta Mus musculus 121-151 34468932-5 2022 Moreover, PRE-084 alleviated LPS-increased Ser 9 de-phosphorylation of glycogen synthase kinase-3 beta (GSK-3beta), LPS-elevated catalytic activity of calcineurin, and LPS-raised percent and frequency of Ca2+ oscillatory BV-2 cells. Serine 43-46 glycogen synthase kinase 3 beta Mus musculus 71-102 34161892-10 2021 DOXY and DOXY+ESC showed a tendency to modulate the functional status of mitogen-activated kinase p42-44 (Phospho-p44/42 MAPK) and of the phosphorylated form of glycogen synthase kinase 3 beta (GSK3beta), revealing a protective profile against inflammation. Doxycycline 9-13 glycogen synthase kinase 3 beta Mus musculus 161-192 34418752-9 2021 However, we observed that multiple genes involved in glycogen generation (Gsk3b, Phka1, Phkb, Phkg1, and Phkg2) and glycogenolysis (Agl and Pygm) had lower mRNA levels in IVF placentas. Glycogen 53-61 glycogen synthase kinase 3 beta Mus musculus 74-79 34161892-10 2021 DOXY and DOXY+ESC showed a tendency to modulate the functional status of mitogen-activated kinase p42-44 (Phospho-p44/42 MAPK) and of the phosphorylated form of glycogen synthase kinase 3 beta (GSK3beta), revealing a protective profile against inflammation. Doxycycline 0-4 glycogen synthase kinase 3 beta Mus musculus 161-192 34266379-3 2021 This study was designed to explore the therapeutic effects of Propofol, both in vivo and in vitro, on lung I/R injury and the underlying mechanisms related to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA-144 (miR-144)/glycogen synthase kinase-3beta (GSK3beta). Propofol 62-70 glycogen synthase kinase 3 beta Mus musculus 246-276 34423266-2 2021 This preliminary study evaluates human AD and transgenic P301L mouse brain tissues using the GSK-3-targeting radiotracers (3H)PF-367 and (3H)OCM-44 in radioligand binding assays. Tritium 123-125 glycogen synthase kinase 3 beta Mus musculus 93-98 34423266-2 2021 This preliminary study evaluates human AD and transgenic P301L mouse brain tissues using the GSK-3-targeting radiotracers (3H)PF-367 and (3H)OCM-44 in radioligand binding assays. Tritium 138-140 glycogen synthase kinase 3 beta Mus musculus 93-98 34423266-5 2021 An evaluation of P301L mouse brain by (3H)/(11C)OCM-44 delineated differences in the B max of GSK-3 between the control and transgenic mice within male subjects. Tritium 39-41 glycogen synthase kinase 3 beta Mus musculus 94-99 33318417-8 2021 Our results show that H2S could prevent nerve injury induced by 1-methyl-4-phenylpyridine, promote the growth of neurospheres, and promote neurogenesis by regulating Akt/glycogen synthase kinase-3beta/beta-catenin pathways in adult neural stem cells. Deuterium 22-25 glycogen synthase kinase 3 beta Mus musculus 170-200 33318417-8 2021 Our results show that H2S could prevent nerve injury induced by 1-methyl-4-phenylpyridine, promote the growth of neurospheres, and promote neurogenesis by regulating Akt/glycogen synthase kinase-3beta/beta-catenin pathways in adult neural stem cells. 1-Methyl-4-phenylpyridinium 64-89 glycogen synthase kinase 3 beta Mus musculus 170-200 33318417-9 2021 These findings confirm that H2S can increase neurogenesis in an adult mouse model of PD by regulating the Akt/glycogen synthase kinase-3beta/beta-catenin signaling pathway. Deuterium 28-31 glycogen synthase kinase 3 beta Mus musculus 110-140 35592888-1 2022 Lithium is an inhibitor of glycogen synthase kinase 3 beta, which is traditionally used in the treatment of bipolar disorders and has antitumor effects. Lithium 0-7 glycogen synthase kinase 3 beta Mus musculus 27-58 34778891-1 2021 Introduction: Glycogen synthase kinase-3beta (GSK-3beta) is a serine/threonine kinase and a negative regulator of cardiac hypertrophy. Serine 62-68 glycogen synthase kinase 3 beta Mus musculus 14-44 35377551-9 2022 Glycogen synthase kinase 3 beta (Gsk3b) mRNA levels were reduced in the hippocampal formations of mice in the chronic stage, which may underlie the elevated brain glycogen content in this model. Glycogen 163-171 glycogen synthase kinase 3 beta Mus musculus 0-31 35377551-9 2022 Glycogen synthase kinase 3 beta (Gsk3b) mRNA levels were reduced in the hippocampal formations of mice in the chronic stage, which may underlie the elevated brain glycogen content in this model. Glycogen 163-171 glycogen synthase kinase 3 beta Mus musculus 33-38 34235177-2 2021 Glycogen synthase kinase 3 (GSK-3) is a serine-threonine kinase involved in several pathways, and its inhibition has been already suggested as a therapeutic strategy for IPF patients. Serine 40-46 glycogen synthase kinase 3 beta Mus musculus 28-33 34235177-5 2021 We found that GSK-3 inhibition down-modulates gene expression and protein levels of MMP-9, MMP-2, and their inhibitors TIMP-1 and TIMP-2 in inflammatory cells harvested from bronchoalveolar lavage fluid (BALF) of mice treated with bleomycin as well as in interstitial alveolar macrophages and cuboidalized epithelial alveolar cells. Bleomycin 231-240 glycogen synthase kinase 3 beta Mus musculus 14-19 34077681-5 2021 Mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (MEK) signaling inhibitor (PD0325901) and glycogen synthase kinase 3 (GSK3) signaling inhibitor (CHIR99021) (also known as 2i) enable cells to maintain naive pluripotency with LIF, and fruquintinib can also promote cells to maintain naive pluripotent state even under serum/LIF condition, whereas VEGF addition limits the pluripotency characteristics in serum/LIF mESCs. Chir 99021 175-184 glycogen synthase kinase 3 beta Mus musculus 120-146 34077681-5 2021 Mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (MEK) signaling inhibitor (PD0325901) and glycogen synthase kinase 3 (GSK3) signaling inhibitor (CHIR99021) (also known as 2i) enable cells to maintain naive pluripotency with LIF, and fruquintinib can also promote cells to maintain naive pluripotent state even under serum/LIF condition, whereas VEGF addition limits the pluripotency characteristics in serum/LIF mESCs. Chir 99021 175-184 glycogen synthase kinase 3 beta Mus musculus 148-152 35594055-4 2022 Priming phosphorylation of murine TRARG1 at serine 84 allows for GSK3-directed phosphorylation at serines 72, 76 and 80. Serine 44-50 glycogen synthase kinase 3 beta Mus musculus 65-69 35594055-4 2022 Priming phosphorylation of murine TRARG1 at serine 84 allows for GSK3-directed phosphorylation at serines 72, 76 and 80. Serine 98-105 glycogen synthase kinase 3 beta Mus musculus 65-69 35489422-7 2022 Our data indicated that BPA exposure impaired cognitive function, disrupted the hippocampal regular cell arrangement, increased blood glucose levels, disturbed the insulin signaling pathway including phosphorylated insulin receptor substrate1 (p-IRS1), protein kinase B (p-AKT), and glycogen synthase kinase 3beta (p-GSK3beta). bisphenol A 24-27 glycogen synthase kinase 3 beta Mus musculus 283-313 35578193-0 2022 Correction: Lactobacillus plantarum PS128 prevents cognitive dysfunction in alzheimer"s disease mice by modulating propionic acid levels, glycogen synthase kinase 3 beta activity, and gliosis. ps128 36-41 glycogen synthase kinase 3 beta Mus musculus 138-169 35143754-1 2022 We previously reported that 2,5-dimethylcelecoxib (DM-C), a derivative of celecoxib, lacks cyclooxygenase-2 inhibitory effects and suppresses cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3). 2,5-dimethylcelecoxib 28-49 glycogen synthase kinase 3 beta Mus musculus 175-201 35456004-4 2022 Studies have indicated the involvement of FMRP in a multitude of cellular pathways, and an absence of FMRP was shown to affect several neurotransmitter receptors, for example, the GABA receptor and intracellular signaling molecules such as Akt, ERK, mTOR, and GSK3. gamma-Aminobutyric Acid 180-184 glycogen synthase kinase 3 beta Mus musculus 260-264 35090935-0 2022 Tanshinone IIA regulates glycogen synthase kinase-3beta-related signaling pathway and ameliorates memory impairment in APP/PS1 transgenic mice. tanshinone 0-10 glycogen synthase kinase 3 beta Mus musculus 25-55 35565964-4 2022 The results also showed that bergapten promotes the phosphorylation of Akt at Ser 473 and glycogen synthase kinase-3beta at Ser 9. 5-Methoxypsoralen 29-38 glycogen synthase kinase 3 beta Mus musculus 90-120 35565964-4 2022 The results also showed that bergapten promotes the phosphorylation of Akt at Ser 473 and glycogen synthase kinase-3beta at Ser 9. Serine 124-127 glycogen synthase kinase 3 beta Mus musculus 90-120 35143754-1 2022 We previously reported that 2,5-dimethylcelecoxib (DM-C), a derivative of celecoxib, lacks cyclooxygenase-2 inhibitory effects and suppresses cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3). 2,5-dimethylcelecoxib 28-49 glycogen synthase kinase 3 beta Mus musculus 203-208 35143754-1 2022 We previously reported that 2,5-dimethylcelecoxib (DM-C), a derivative of celecoxib, lacks cyclooxygenase-2 inhibitory effects and suppresses cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3). Celecoxib 74-83 glycogen synthase kinase 3 beta Mus musculus 175-201 35122996-3 2022 This study explored whether sevoflurane induces neurotoxicity by activating a GSK3beta (glycogen synthase kinase 3beta)/Drp1 (dynamin-related protein-1)-dependent mitochondrial fission and apoptosis. Sevoflurane 28-39 glycogen synthase kinase 3 beta Mus musculus 88-118 35195922-6 2022 In soleus muscles from tumor-bearing mice, insulin-stimulated glucose transport was abrogated concomitantly with abolished insulin-induced TBC1D4 and GSK3 phosphorylation. Glucose 62-69 glycogen synthase kinase 3 beta Mus musculus 150-154 35115156-3 2022 The authors demonstrate that exogenous testosterone administered to immature mice pups around the time of sevoflurane exposure increased brain levels of testosterone, attenuated tau phosphorylation, inhibited glycogen synthase kinase-3beta activation and its interaction/binding with tau, reversed sevoflurane-induced decreases in neuronal activation, and attenuated cognitive impairments. Testosterone 39-51 glycogen synthase kinase 3 beta Mus musculus 209-239 35055183-3 2022 Glycogen synthase kinase 3 (GSK-3) is a multifunctional serine/threonine protein kinase with two isoforms, GSK-3alpha and GSK-3beta, and GSK-3beta plays crucial roles in inflammatory response, which include microglial migration and peripheral immune cell activation. Serine 56-62 glycogen synthase kinase 3 beta Mus musculus 0-26 35166234-3 2022 As the major molecular target of lithium action and a multitasking protein kinase recently implicated in a variety of renal diseases, glycogen synthase kinase 3beta (GSK3beta) is overexpressed and hyperactive with age in glomerular podocytes, correlating with functional and histological signs of kidney aging. Lithium 33-40 glycogen synthase kinase 3 beta Mus musculus 134-164 35159367-4 2022 However, the isoform-specific role of GSK-3 in obesity and glucose intolerance is unclear. Glucose 59-66 glycogen synthase kinase 3 beta Mus musculus 38-43 35159367-6 2022 To overcome these limitations, we created novel mouse models of ROSA26CreERT2-driven, tamoxifen-inducible conditional deletion of GSK-3 that allowed us to delete the gene globally in an isoform-specific and temporal manner. Tamoxifen 86-95 glycogen synthase kinase 3 beta Mus musculus 130-135 35159367-12 2022 In summary, our novel mouse models allowed us to delineate the isoform-specific role of GSK-3 in obesity and glucose tolerance. Glucose 109-116 glycogen synthase kinase 3 beta Mus musculus 88-93 35159367-13 2022 From a translational perspective, our findings underscore the importance of maintaining a healthy weight in patients receiving lithium therapy, which is thought to work by GSK-3 inhibition mechanisms. Lithium 127-134 glycogen synthase kinase 3 beta Mus musculus 172-177 35153671-0 2021 The GSK-3 Inhibitor CT99021 Enhances the Acquisition of Spatial Learning and the Accuracy of Spatial Memory. Chir 99021 20-27 glycogen synthase kinase 3 beta Mus musculus 4-9 35153671-4 2021 Systemic administration of a highly selective GSK-3 inhibitor, CT99021, reversibly blocked NMDAR-dependent LTD in the CA1 region of the hippocampus in anesthetized adult mice. Chir 99021 63-70 glycogen synthase kinase 3 beta Mus musculus 46-51 35096120-7 2022 Moreover, CIG inhibited the activity of calpain and glycogen synthase kinase 3beta (GSK-3beta) and enhanced the activity of protein phosphatase 2A (PP2A) both in vivo and in vitro. 2-AMINO-6-CHLOROPYRAZINE 10-13 glycogen synthase kinase 3 beta Mus musculus 52-82 35055183-3 2022 Glycogen synthase kinase 3 (GSK-3) is a multifunctional serine/threonine protein kinase with two isoforms, GSK-3alpha and GSK-3beta, and GSK-3beta plays crucial roles in inflammatory response, which include microglial migration and peripheral immune cell activation. Serine 56-62 glycogen synthase kinase 3 beta Mus musculus 28-33 35202887-10 2022 We also noticed that liver TGFbetar1 deficiency alleviated LPS/GalN-induced apoptosis and ferroptosis by affecting the phosphorylation of glycogen synthase kinase 3beta and Nrf2, a key antioxidant factor, by up-regulating the levels of glutathione peroxidase 4, XCT, DHODH, and FSP1, and down-regulating transferrin receptor, cyclooxygenase 2, CHAC1, and POR expression. Galactosamine 63-67 glycogen synthase kinase 3 beta Mus musculus 138-168 34516970-7 2022 Furthermore, it reduced the intraneuronal phosphorylated Tau levels in a GSK3-dependent way and increased extracellular phosphorylated Tau levels by reducing the expression of ectoenzyme TNAP. uridine triacetate 57-60 glycogen synthase kinase 3 beta Mus musculus 73-77