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Tideglusib significantly reduced cerebral infarct volume at both 24h and 7days after HI injury. Tideglusib also increased phosphorylated GSK-3beta(Ser9) and Akt (显示 AKT1 ELISA试剂盒)(Ser473)
Therefore our study identifies a compartmentalized PtdIns(3,4,5)P3/AKT (显示 AKT1 ELISA试剂盒)/GSK3beta signaling axis at cilia in SHH (显示 SHH ELISA试剂盒)-dependent medulloblastoma that is regulated by INPP5E (显示 INPP5E ELISA试剂盒) to maintain tumor cell cilia, promote SHH (显示 SHH ELISA试剂盒) signaling and thereby medulloblastoma progression.
B-cell receptor controls fitness of MYC (显示 MYC ELISA试剂盒)-driven lymphoma cells via GSK3beta inhibition
These findings suggest that protein tyrosine phosphatase SHP-1 (显示 PTPN6 ELISA试剂盒) may act as a positive regulator of osteoblast differentiation through direct association with and dephosphorylation of GSK3beta.
CREB (显示 CREB1 ELISA试剂盒) was found to bind to GSK3beta promoter and essential for cAMP-mediated regulation of GSK3beta.
GSK-3beta participates in early pancreatitis-induced acinar-to-ductal metaplasia and the progression towards pre-malignant pancreatic intraepithelial neoplasia.
These observations demonstrate that oxidative stress destabilizes PRMT4 (显示 CARM1 ELISA试剂盒) via GSK-3beta signaling to impede lung epithelial cell migration that may hinder the lung repair and regeneration process.
changes in GSK-3beta activity and/or levels regulate the production and subsequent secretion of fractalkine (显示 CX3CL1 ELISA试剂盒), a chemokine (显示 CCL1 ELISA试剂盒) involved in the immune response that has been linked to AD and to other different neurological disorders.
The activation of brain GSK-3beta expression is increased in an animal model of depressive syndrome.
Findings suggest that atorvastatin attenuates diabetes-associated renal injury by reducing reactive oxygen species (ROS (显示 ROS1 ELISA试剂盒)) generation, RhoA (显示 RHOA ELISA试剂盒) activity and normalizing Akt (显示 AKT1 ELISA试剂盒)/GSK3beta signaling pathways.
Our results reveal a new mechanism of ZNF322A (显示 ZNF322A ELISA试剂盒) oncoprotein destruction regulated by the CK1delta/GSK3beta/FBXW7a axis. Deregulation of this signaling axis results in ZNF322A (显示 ZNF322A ELISA试剂盒) overexpression and promotes cancer progression
The present work identified GSK-3beta as a new interacting protein for D1R (显示 DRD1 ELISA试剂盒) functional regulation and revealed a novel mechanism for GSK-3beta-regulated D1R (显示 DRD1 ELISA试剂盒) function which may underlie D1R (显示 DRD1 ELISA试剂盒) dysfunction in schizophrenia.
The ovarian cancer cell lines BG-1 (显示 ACSBG1 ELISA试剂盒) and UCI-101 were transfected with the let-7 reporter and surveyed with a library of kinase inhibitors in order to identify pathways affecting let-7 activity. Among the inhibitors causing changes in endogenous let-7 abundance, the lowering of GSK-3beta function specifically increased let-7 levels and lowered luciferase activity.
Taken together, this study reveals evidence demonstrating a mechanism by which the LPR6/ GSK3beta/E2F1 (显示 E2F1 ELISA试剂盒) axis-upregulated LSH (显示 HELLS ELISA试剂盒) promoted gliomas.
High GSK3B expression is associated with glioblastoma.
AKT (显示 AKT1 ELISA试剂盒)/GSK-3beta-mediated stabilization of SP1 (显示 PSG1 ELISA试剂盒) is required for TGF-beta (显示 TGFB1 ELISA试剂盒) induced up-regulation of NKG2DLs.
These findings reveal that Endoplasmic reticulum stress engages the GSK3beta-TIP60 (显示 KAT5 ELISA试剂盒)-ULK1 (显示 ULK1 ELISA试剂盒) pathway to increase autophagy.
The data indicate that the AC023115.3-miR (显示 MLXIP ELISA试剂盒)-26a-GSK3beta signaling axis plays an important role in reducing the chemoresistance of glioma.
Results demonstrated that expression of total GSK3beta is significantly high in the cancer tissues of esophageal squamous cell carcinoma (ESCC) patients but the phosphorylated form is decreased in cancer tissues. Also, the study found that inhibition of either GSK3beta or STAT3 (显示 STAT3 ELISA试剂盒) alone resulted in a significant decrease in ESCC cell viability and migration, indicating their contribution to the malignancy phenotype.
our findings identify the miR (显示 MLXIP ELISA试剂盒)-410/Gsk3beta/beta-catenin (显示 CTNNB1 ELISA试剂盒) signaling axis is a novel molecular circuit in inducing stemness of non-small cells lung cancer
Novel roles for Plk (显示 PLK1 ELISA试剂盒) and GSK3 regulation of ADAM13 (显示 ADAM33 ELISA试剂盒) function in cranial neural crest cell migration.
Interaction with Snail1 (显示 SNAI1 ELISA试剂盒)/2, and Twist function more generally, is regulated by GSK-3-beta-mediated phosphorylation of conserved sites in the WR domain.
These data suggest that the interactions of beta-catenin (显示 CTNNB1 ELISA试剂盒) with alpha-catenin (显示 CTNNA1 ELISA试剂盒) and GSK-3beta exert opposing effects on the terminal projections of ventral optic axons.
Both active and inactive forms of Gsk3b mediate the cooperative signaling during angiogenesis in zebrafish embryos.
a novel negative, Gsk3beta-independent control mechanism of beta-catenin and implicates Ccr7 as a long-hypothesized GPCR regulating vertebrate axis formation.
The regulatory target of Wnts and Igfs, GSK3beta, is inefficiently inactivated in male fin regenerates compared with females. Pharmacological inhibition of GSK3 in males increases blastemal proliferation and restores regenerative pattern.
2-OST (显示 HS2ST1 ELISA试剂盒) functions within the Wnt (显示 WNT2 ELISA试剂盒) pathway, downstream of Wnt (显示 WNT2 ELISA试剂盒) ligand signaling and upstream of Gsk3beta and beta-catenin (显示 CTNNB1 ELISA试剂盒) intracellular localization and function
Data show that GSK-3beta inhibition was sufficient to stimulate MG dedifferentiation and the formation of multipotent retinal progenitors that were capable of differentiating into all major retinal cell types.
GSK3alpha, but not GSK3beta, is necessary in cardiomyocyte survival
Gsk3b regulates the maintenance of neural progenitors at the midbrain-hindbrain boundary in concert with E(Spl (显示 SGPL1 ELISA试剂盒)) factor activity.
A newly developed highly active GSK3beta inhibitor AR-534, reduced human TAU phosphorylation in TAU transgenic zebrafish.
Five different isoforms of GSK3beta identified from porcine tissues, splice variants exhibit differential activity towards glycogen synthase.
scratching-induced injury and repair of bronchial epithelial cells may involve inhibition of GSK3beta activity which can lead to activation of the downstream signaling through beta-catenin (显示 CTNNB1 ELISA试剂盒)
There was no correlation of infarct size with expression or phosphorylation of p70S6K (显示 RPS6KB1 ELISA试剂盒) or GSK3beta in ischemic postconditioning.
GSK3B and phosphorylated GSK3B regulate milk synthesis and proliferation dairy cow mammary epithelial cells.
GSK3B serine phosphorylation was positively correlated with embryo development
results suggest that Nav1.7-Ca2+ influx-protein kinase C-alpha pathway activated ERK1/ERK2 and p38, which increased phosphorylation of glycogen synthase kinase-3beta, decreasing tau phosphorylation
IGF-I (显示 IGF1 ELISA试剂盒) down-regulated functional IGF-I receptor (显示 IGF1R ELISA试剂盒) via GSK-3beta inhibition and mTOR (显示 FRAP1 ELISA试剂盒) activation; constitutive activity of GSK-3beta maintained IGF-I receptor (显示 IGF1R ELISA试剂盒) level in nonstimulated cells.
These results suggest that phospholipids and sulfatide and heparin may function as effective stimulators for autophosphorylation of GSK-3beta and for the GSK-3beta-mediated phosphorylation of SH-binding proteins, including MBP (显示 MBP ELISA试剂盒) and tau protein.
cAMP/PKA regulation of GSK3beta/beta-catenin (显示 CTNNB1 ELISA试剂盒) signaling contributes to the increase in progesterone production in corpus luteum.
The protein encoded by this gene is a serine-threonine kinase, belonging to the glycogen synthase kinase subfamily. It is involved in energy metabolism, neuronal cell development, and body pattern formation. Polymorphisms in this gene have been implicated in modifying risk of Parkinson disease, and studies in mice show that overexpression of this gene may be relevant to the pathogenesis of Alzheimer disease. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, glycogen synthase kinase-3 beta
, serine/threonine-protein kinase GSK3B
, factor A
, GSK3beta isoform
, intracellular kinase
, glycogen synthase kinase 3 beta variant 1
, glycogen synthase kinase 3 beta variant 2
, glycogen synthase kinase 3 beta variant 3
, glycogen synthase kinase 3 beta variant 4