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Glycogen synthase kinase 3 alpha

GSK-3alpha, glycogen synthase kinase 3alpha
This gene encodes a multifunctional Ser/Thr protein kinase that is implicated in the control of several regulatory proteins including glycogen synthase, and transcription factors, such as JUN. It also plays a role in the WNT and PI3K signaling pathways, as well as regulates the production of beta-amyloid peptides associated with Alzheimer's disease. [provided by RefSeq, Oct 2011] (from NCBI)
Top mentioned proteins: AML1, Akt, Insulin, CAN, ACID
Papers on GSK-3alpha
Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice.
Kim et al., Omaha, United States. In Mol Neurobiol, Aug 2015
To examine the role of GSK-3 in astrocytes, we generated a conditional knockout mouse using a glial fibrillary acidic protein (GFAP)-cre driver, in which the GSK-3 alpha and beta genes are deleted in astrocytes.
AR-A 014418 Used against GSK3beta Downregulates Expression of hnRNPA1 and SF2/ASF Splicing Factors.
Taneja et al., Delhi, India. In J Oncol, 2013
AR-A 014418, 48 hrs posttreatment, caused dose (25-100  μ M) dependent inhibition in U373 and U87 cell viability with also inhibition in activating tyrosine phosphorylation of GSK3alpha (Tyr 279) and beta (Tyr 216).
Regulation of glycogen synthase kinase-3 by thymosin beta-4 is associated with gastric cancer cell migration.
Moon et al., Seoul, South Korea. In Int J Cancer, 2012
investigated whether GSK-3 activity is regulated by thymosin beta-4 (Tbeta4) and associated with Tbeta4-mediated migration in gastric cancer cells; expression of GSK-3alpha, beta-catenin and E-cadherin could be negatively regulated by Tbeta4 induced ERK phosphorylation; suggests that Tbeta4 could be a novel regulator to control Wnt signal pathway
GSK-3α and GSK-3β proteins are involved in early stages of chondrocyte differentiation with functional redundancy through RelA protein phosphorylation.
Kawaguchi et al., Tokyo, Japan. In J Biol Chem, 2012
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.
Selectively silencing GSK-3 isoforms reduces plaques and tangles in mouse models of Alzheimer's disease.
Lee et al., Philadelphia, United States. In J Neurosci, 2012
data from both approaches suggest that GSK-3alpha contributes to both SP and NFT pathogenesis while GSK-3beta only modulates NFT formation.
GSK3-TIP60-ULK1 signaling pathway links growth factor deprivation to autophagy.
Lin et al., Xiamen, China. In Science, 2012
glycogen synthase kinase-3 (GSK3), when deinhibited by default in cells deprived of growth factors, activates acetyltransferase TIP60 through phosphorylating TIP60-Ser86, which acetylates and stimulates the protein kinase ULK1, which is required for autophagy
GSK3 inhibitor-BIO regulates proliferation of immortalized pancreatic mesenchymal stem cells (iPMSCs).
Hua et al., China. In Plos One, 2011
GSK3 inhibitor-BIO regulates proliferation of immortalized pancreatic mesenchymal stem cells
Constitutive glycogen synthase kinase-3alpha/beta activity protects against chronic beta-adrenergic remodelling of the heart.
Marber et al., London, United Kingdom. In Cardiovasc Res, 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.
Glycogen Synthase Kinase 3 (GSK-3) influences epithelial barrier function by regulating occludin, claudin-1 and E-cadherin expression.
Nusrat et al., Atlanta, United States. In Biochem Biophys Res Commun, 2010
Reduction of GSK-3 activity, either by small molecule inhibitors or siRNA targeting GSK-3 alpha and beta mRNA, resulted in increased permeability to both ions and bulk solutes.
GSK-3alpha directly regulates beta-adrenergic signaling and the response of the heart to hemodynamic stress in mice.
Force et al., Philadelphia, United States. In J Clin Invest, 2010
Herein, we present what we believe to be the first studies defining the role of GSK-3alpha in the mouse heart using gene targeting.
Disruption of AMPKalpha1 signaling prevents AICAR-induced inhibition of AS160/TBC1D4 phosphorylation and glucose uptake in primary rat adipocytes.
Ceddia et al., Toronto, Canada. In Mol Endocrinol, 2010
Phosphorylation of Akt substrates glycogen synthase kinase 3alpha and -beta were unaltered by AICAR, indicating that the AMPK-regulatory effects were specific to the AS160/TBC1D4 signaling pathway.
Abrogation of de novo lipogenesis by stearoyl-CoA desaturase 1 inhibition interferes with oncogenic signaling and blocks prostate cancer progression in mice.
Fajas et al., Montpellier, France. In Mol Cancer Ther, 2010
Increased de novo fatty acid (FA) synthesis is one hallmark of tumor cells, including prostate cancer.
Glycogen synthase kinase-3 plays a central role in mediating glucocorticoid-induced apoptosis.
Sionov et al., Jerusalem, Israel. In Mol Endocrinol, 2010
Glycogen synthase kinase (GSK3) plays a central role in promoting glucocorticoid-induced apoptosis.
TEAD-1 overexpression in the mouse heart promotes an age-dependent heart dysfunction.
Ji et al., Columbia, United States. In J Biol Chem, 2010
Western blot analyses revealed decreases in p-phospholamban, SERCA2a, p-CX43, p-GSK-3alpha/beta, nuclear beta-catenin, GATA4, NFATc3/c4, and increased NCX1, nuclear DYKR1A, and Pur alpha/beta protein.
Cyr61 mediates hepatocyte growth factor-dependent tumor cell growth, migration, and Akt activation.
Laterra et al., Baltimore, United States. In Cancer Res, 2010
Cyr61 siRNA inhibited a second phase of Akt phosphorylation measured 12 hours after cell stimulation with HGF and also inhibited HGF-induced phosphorylation of the Akt target glycogen synthase kinase 3alpha.
Hyperactivity and enhanced curiosity of mice expressing PKB/SGK-resistant glycogen synthase kinase-3 (GSK-3).
Lang et al., Tübingen, Germany. In Cell Physiol Biochem, 2009
METHODS: Gene-targeted knockin mice with mutated and thus PKB/SGK-resistant GSK-3alpha, beta (gsk-3(KI)) were compared to corresponding wild type mice (gsk-3(WT)).
Angiotensin II inhibits insulin-stimulated GLUT4 translocation and Akt activation through tyrosine nitration-dependent mechanisms.
Bottari et al., Grenoble, France. In Plos One, 2009
The inhibitory effect of nitration on Akt activity was confirmed by the ability of SIN-1 to completely block GSK3alpha phosphorylation in vitro.
GSK3 influences social preference and anxiety-related behaviors during social interaction in a mouse model of fragile X syndrome and autism.
Jope et al., Birmingham, United States. In Plos One, 2009
impaired inhibitory regulation of GSK3 in Fmr1 knockout mice may contribute to some socialization deficits
Glycogen synthase kinase 3alpha-specific regulation of murine hepatic glycogen metabolism.
Woodgett et al., Toronto, Canada. In Cell Metab, 2007
GSK-3alpha knockout (GSK-3alpha KO) animals are viable but display enhanced glucose and insulin sensitivity accompanied by reduced fat mass.
GSK-3alpha regulates production of Alzheimer's disease amyloid-beta peptides.
Klein et al., Philadelphia, United States. In Nature, 2003
Paper shows that GSK-3 isoforms are not functionally equivalent in regulating the production of Abeta peptides. siRNA used to knockdown endogenous GSK-3 isoforms in cultured cells.
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