PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 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 18322101-10 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 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 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 15691529-4 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 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 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 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 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 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 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. Valproic Acid 257-260 glycogen synthase kinase 3 beta Mus musculus 24-28 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 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 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 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 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 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 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 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