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anti-Mouse (Murine) GSK3 beta Antibodies:
anti-Rat (Rattus) GSK3 beta Antibodies:
anti-Human GSK3 beta Antibodies:
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These findings indicated that VPA's neuroprotective effect in the MPP(+)-model of Parkinson's disease is associated with GSK3beta phosphorylation via Akt (show AKT1 Antibodies) and ERK (show EPHB2 Antibodies) activation in the mitochondrial intrinsic apoptotic pathway.
Results support for the hypothesis that GSK3 activity promotes light-induced suprachiasmatic nucleus excitability
the present study determined that GSK3b is required for Epithelial-mesenchymal transition and barrier dysfunction in podocytes under high glucose conditions; therefore, GSK3beta may be a novel target for the treatment of diabetic nephropathy
this study shows that miR (show MLXIP Antibodies)-709 attenuates LPS (show TLR4 Antibodies)-induced inflammatory response via inhibiting GSK-3beta and activating beta-catenin (show CTNNB1 Antibodies)
Data show that glycogen synthase kinase 3 beta (GSK3beta) inhibitor thiadiazolidinone-8 blocks angiotensin II (ang II) induced muscle atrophy, which paves the way for targeted therapy to treat muscle wasting.
results suggest that GSK3 may in part modulate the hypertonic-induced intracellular UT-A1 (show SLC14A2 Antibodies) redistribution and its accumulation on the plasma membrane, which may constitute another mechanism by which GSK3 modulates urine concentration
observations revealed that the alteration of PKB-GSK-3beta axis, Plk-1, and Aurora kinase-A expressions in HSPC compartment due to DNA damage response was associated with the proliferative impairment and apoptosis during aplastic anemia.
Voluntary exercise produces a lasting protective state in the hippocampus, maintained in hippocampal slices by a PI3K-dependent mechanism that precludes its functional disruption in the presence of Abeta (show APP Antibodies) by avoiding GSK3beta activation
The GSK-3beta activity increased, and expression of beta-catenin (show CTNNB1 Antibodies) decreased significantly in the hippocampus of the chronic intermittent hypoxia exposed mice.
GSK3b may up-regulate BK channels, an effect disrupted by lithium or additional expression of AKT (show AKT1 Antibodies) and possibly participating in the regulation of cell volume and excitability.
Neurexin (show NRXN1 Antibodies)-3alpha autoantibodies associate with a severe but potentially treatable novel autoimmune encephalitis in which the antibodies cause a decrease of neurexin (show NRXN1 Antibodies)-3alpha and alter synapse development
Silencing GSK-3beta may have a positive effect on inhibiting the pathologic progression of Alzheimer disease through down-regulating the level of p-Tau
Our results thus suggest that GSK-3beta is a key factor involved in ASK1 (show MAP3K5 Antibodies) activation and reactive oxygen species-induced cell death.
This study revealed that the GSK3-beta inhibitor SB216763 was able to stimulate the proliferation of CD117-positive hAFS cells without influencing their undifferentiated state. Moreover, SB216763 can efficiently promote the neural differentiation of CD117-positive hAFS cells towards neural progenitor cells in the presence of DMEM/F12 and N2 supplement
Association between GSK-3beta rs334558 polymorphism and breast cancer risk in Brazilian population.
Data suggest that melatonin down-regulates adipogenesis via reduction of (a) cAMP synthesis, (b) reactive oxygen species synthesis, (c) phosphorylation of CEBPB (CCAAT-enhancer-binding protein-beta (show CEBPB Antibodies)), and (d) activation of GSK3B (glycogen synthase kinase 3 beta); primary mesenchymal stem cells cultured in adipogenic differentiation media were used in these studies.
flavonoids from Diplotaxis harra display cytotoxic activity against inflammatory and cancer intestinal cells which could depend on GSK3beta inhibition.
Low expression of GSK3B is associated with oral cancer.
These data suggest that BIO, as an inhibitor of GSK-3beta, can suppress Ovarian cancer (OC) development. Therefore, BIO could be a candidate drug for the treatment of OC.
This study suggested mechanistic relationship between miR (show MLXIP Antibodies)-940 and Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) in the development and progression of pancreatic carcinoma through regulation of GSK3beta and sFRP1 (show SFRP1 Antibodies).
Novel roles for Plk (show PLK1 Antibodies) and GSK3 regulation of ADAM13 (show ADAM33 Antibodies) function in cranial neural crest cell migration.
Interaction with Snail1 (show SNAI1 Antibodies)/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 (show CTNNB1 Antibodies) with alpha-catenin (show CTNNA1 Antibodies) 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 (show HS2ST1 Antibodies) functions within the Wnt (show WNT2 Antibodies) pathway, downstream of Wnt (show WNT2 Antibodies) ligand signaling and upstream of Gsk3beta and beta-catenin (show CTNNB1 Antibodies) 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 (show SGPL1 Antibodies)) 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 (show CTNNB1 Antibodies)
There was no correlation of infarct size with expression or phosphorylation of p70S6K (show RPS6KB1 Antibodies) 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 (show IGF1 Antibodies) down-regulated functional IGF-I receptor (show IGF1R Antibodies) via GSK-3beta inhibition and mTOR (show FRAP1 Antibodies) activation; constitutive activity of GSK-3beta maintained IGF-I receptor (show IGF1R Antibodies) 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 (show MBP Antibodies) and tau protein.
cAMP/PKA regulation of GSK3beta/beta-catenin (show CTNNB1 Antibodies) 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