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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 (zeige AKT1 ELISA Kits)(Ser473)
Therefore our study identifies a compartmentalized PtdIns(3,4,5)P3/AKT (zeige AKT1 ELISA Kits)/GSK3beta signaling axis at cilia in SHH (zeige SHH ELISA Kits)-dependent medulloblastoma that is regulated by INPP5E (zeige INPP5E ELISA Kits) to maintain tumor cell cilia, promote SHH (zeige SHH ELISA Kits) signaling and thereby medulloblastoma progression.
B-cell receptor controls fitness of MYC (zeige MYC ELISA Kits)-driven lymphoma cells via GSK3beta inhibition
These findings suggest that protein tyrosine phosphatase SHP-1 (zeige PTPN6 ELISA Kits) may act as a positive regulator of osteoblast differentiation through direct association with and dephosphorylation of GSK3beta.
CREB (zeige CREB1 ELISA Kits) 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 (zeige CARM1 ELISA Kits) 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 (zeige CX3CL1 ELISA Kits), a chemokine (zeige CCL1 ELISA Kits) 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 (zeige ROS1 ELISA Kits)) generation, RhoA (zeige RHOA ELISA Kits) activity and normalizing Akt (zeige AKT1 ELISA Kits)/GSK3beta signaling pathways.
Our results reveal a new mechanism of ZNF322A (zeige ZNF322A ELISA Kits) oncoprotein destruction regulated by the CK1delta/GSK3beta/FBXW7a axis. Deregulation of this signaling axis results in ZNF322A (zeige ZNF322A ELISA Kits) overexpression and promotes cancer progression
The present work identified GSK-3beta as a new interacting protein for D1R (zeige DRD1 ELISA Kits) functional regulation and revealed a novel mechanism for GSK-3beta-regulated D1R (zeige DRD1 ELISA Kits) function which may underlie D1R (zeige DRD1 ELISA Kits) dysfunction in schizophrenia.
The ovarian cancer cell lines BG-1 (zeige ACSBG1 ELISA Kits) 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 (zeige E2F1 ELISA Kits) axis-upregulated LSH (zeige HELLS ELISA Kits) promoted gliomas.
High GSK3B expression is associated with glioblastoma.
AKT (zeige AKT1 ELISA Kits)/GSK-3beta-mediated stabilization of SP1 (zeige PSG1 ELISA Kits) is required for TGF-beta (zeige TGFB1 ELISA Kits) induced up-regulation of NKG2DLs.
These findings reveal that Endoplasmic reticulum stress engages the GSK3beta-TIP60 (zeige KAT5 ELISA Kits)-ULK1 (zeige ULK1 ELISA Kits) pathway to increase autophagy.
The data indicate that the AC023115.3-miR (zeige MLXIP ELISA Kits)-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 (zeige STAT3 ELISA Kits) alone resulted in a significant decrease in ESCC cell viability and migration, indicating their contribution to the malignancy phenotype.
our findings identify the miR (zeige MLXIP ELISA Kits)-410/Gsk3beta/beta-catenin (zeige CTNNB1 ELISA Kits) signaling axis is a novel molecular circuit in inducing stemness of non-small cells lung cancer
Novel roles for Plk (zeige PLK1 ELISA Kits) and GSK3 regulation of ADAM13 (zeige ADAM33 ELISA Kits) function in cranial neural crest cell migration.
Interaction with Snail1 (zeige SNAI1 ELISA Kits)/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 (zeige CTNNB1 ELISA Kits) with alpha-catenin (zeige CTNNA1 ELISA Kits) 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 (zeige HS2ST1 ELISA Kits) functions within the Wnt (zeige WNT2 ELISA Kits) pathway, downstream of Wnt (zeige WNT2 ELISA Kits) ligand signaling and upstream of Gsk3beta and beta-catenin (zeige CTNNB1 ELISA Kits) 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 (zeige SGPL1 ELISA Kits)) 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 (zeige CTNNB1 ELISA Kits)
There was no correlation of infarct size with expression or phosphorylation of p70S6K (zeige RPS6KB1 ELISA Kits) 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 (zeige IGF1 ELISA Kits) down-regulated functional IGF-I receptor (zeige IGF1R ELISA Kits) via GSK-3beta inhibition and mTOR (zeige FRAP1 ELISA Kits) activation; constitutive activity of GSK-3beta maintained IGF-I receptor (zeige IGF1R ELISA Kits) 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 (zeige MBP ELISA Kits) and tau protein.
cAMP/PKA regulation of GSK3beta/beta-catenin (zeige CTNNB1 ELISA Kits) 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