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Validated All-in-One™ qPCR Primer for GSK3B(NM_002093.3) Search again
Product ID:
HQP054075
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
-
Gene Description:
glycogen synthase kinase 3 beta
Target Gene Accession:
NM_002093.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
Glycogen synthase kinase-3 (GSK3) is a proline-directed serine-threonine kinase that was initially identified as a phosphorylating and inactivating glycogen synthase (see GYS1, MIM 138570). Two isoforms, alpha (GSK3A; MIM 606784) and beta, show a high degree of amino acid homology (Stambolic and Woodgett, 1994 [PubMed 7980435]). GSK3B is involved in energy metabolism, neuronal cell development, and body pattern formation (Plyte et al., 1992 [PubMed 1333807]).[supplied by OMIM].
Gene References into function
- The intracellular distribution of GSK-3 beta is dynamically regulated by signaling cascades, and apoptotic stimuli cause increased nuclear levels of GSK-3 beta, which facilitates interactions with nuclear substrates.
- Protein kinase A enhances, whereas glycogen synthase kinase-3 beta inhibits, the activity of the exon 2-encoded transactivator domain of heterogeneous nuclear ribonucleoprotein D in a hierarchical fashion.
- Arg(96) mutant has a dominant-negative effect on GSK-3beta-dependent phosphorylation of beta-catenin and targeting of beta-catenin for degradation requires prior priming through phosphorylation of Ser(45)
- signaling systems determining cell fate appear to be important targets of mood stabilizers, and these may include signaling pathways encompassing GSK3beta, including transcription factors regulated by GSK3beta(REVIEW)
- reacts with p53 protein after dna damage
- Human serum and glucocorticoid-inducible kinase-like kinase (SGKL) phosphorylates glycogen syntheses kinase 3 beta (GSK-3beta) at serine-9 through direct interaction
- improves insulin action and glucose metabolism in skeletal muscle
- GSK3b binds to and phosphorylates serine493 in glutamate E segment of NEFH
- A-kinase anchoring protein AKAP220 binds to this enzyme and mediates protein kinase A-dependent inhibition of GSK-3beta
- GSK3beta functions at the nodal point of converging signaling pathways in endothelial cells to regulate vessel growth through its control of vascular cell migration and survival.
- Glycogen synthase kinase 3 beta influenced post-natal maturation and differentiation of neurons in vivo in transgenic mice that overexpress a constitutively active GSK-3beta.
- Data show that endoplasmic reticulum stress induced by thapsigargin not only activated the apoptosis effector caspase-3 but also caused a large and prolonged increase in the activity of glycogen synthase kinase-3beta.
- GSK-3 beta is inhibited by endothelial cell costimulation, allowing nuclear accumulation of NFAT and prolonging IL-2 synthesis in the presence of cyclosporin A.
- inhibition of GSK3beta activity appears to trigger nuclear accumulation of cyclin D1 and cell cycle progression
- GSK3b expresion is regulated by reelin
- Fresh lymphocytes from schizophrenic patients showed no difference in GSK-3 alpha and GSK-3beta mRNA levels, GSK-3beta protein levels, or total GSK-3 (alpha+beta) enzyme activity compared with findings in control subjects.
- role in phosphorylating tau protein
- Data report the crystal structure of glycogen synthase kinase 3beta (GSK3beta) in complex with a minimal GSK3beta-binding segment of axin, at 2.4 A resolution.
- plays a role in Alzheimer disease and other CNS disorders (REVIEW)
- GSK3 beta functions as a natural activator of MEKK1
- Messenger RNA of beta-catenin and Tcf-4, but not GSK-3beta, was found to be overexpressed in HCC(hepatocellular carcinoma).
- role in mouse hepatic carcinogenesis
- first demonstration that glycogen synthase kinase-3beta associates with type 1 protein phosphatase/inhibitor-2 (PP1C/I-2) complex and phosphorylates I-2 at T72 in intact cells
- Cell adhesion to the extracellular matrix protein fibronectin modulates radiation-dependent G2 phase arrest and involve this enzyme in vitro.
- GSK-3 regulates its own phosphorylation status
- manipulation of GSK-3beta activity may be a mechanism by which HHV-8 latency-associated nuclear antigen (LANA) may modify transcriptional activity and contribute to the phenotype of HHV-8 primary effusion lymphoma.
- molecular cross-talk between glycogen synthase kinase-3 beta (GSK-3 beta) and the p105 precursor of the NF-kappa B p50 subunit
- glycogen synthase kinase-3beta is suppressed by Akt in prostate cancer cells which leads to the phosphorylation of cAMP-response element-binding protein
- Overexpression of phospho-GSK-3beta is associated with hepatocellular carcinoma
- possible role of GSK-3 beta, a pro-apoptotic factor participating in signal transduction involved in cell survival, is discussed in relation to schizophrenia
- Increased expression of glycogen synthase kinase 3 is associated with ovarian epithelial cell transformation and in tumour progression
- role in binding to and promoting action of p53
- multisite phosphorylation by Cdk2 and GSK3 controls cyclin E degradation
- GSK3beta is a potential regulator of platelet function
- activation of Csk and GSK-3beta by Galphaq may contribute to the physiological and pathological effects of Gq-coupled receptors
- a mechanism involving GSK-3beta activation may be responsible for tumor necrosis factor-related apoptosis-inducing ligand resistance in prostate cancer cells
- TSH/cAMP-stimulated p70S6 kinase activity and cell proliferation is regulated by Rap1GAP in thyroid cells
- CF101 inhibits human colon carcinoma growth in mice via modulation of GSK3B.
- GSK3B regulates the cytoskeleton and translocation of Rac1 in keratinocyte lamellipodia.
- No association was detected between GSK3-beta -50 T/C SNP and the presence of bipolar illness. Homozygotes for the wild variant (T/T) showed an earlier age at onset than carriers of the mutant allele (F=5.53, d.f.=2,182, P=0.0047).
- ER stress induces GSK-3beta binding to p53 in the nucleus and enhances the cytoplasmic localization of the tumor suppressor.
- glycogen synthase kinase-3 beta phosphorylates the androgen receptor, thereby inhibiting androgen receptor-driven transcription
- Clozapine appears to regulate the phosphorylation of GSK3B through Wnt signal pathways involving Dvl upstream but not through the P13K-Akt pathway in human neuroblastoma cells.
- Most importantly, knocking down GSK-3beta expression via a small interference RNA-mediated gene silencing approach also reduced R1881-stimulated gene expression, demonstrating the specificity of GSK-3beta involvement.
- APC/GSK-3beta, through beta-catenin, may crossregulate NF-kappaB signaling pathway
- Glycogen synthase kinase-3beta is tyrosine-phosphorylated by mitogen-activated protein kinase kinase 1 in fibroblasts.
- These results suggest that short-term exposure to TNF-alpha augments insulin effects through protein kinase B-alpha and glycogen synthase kinase-3 beta, whereas long-term exposure causes insulin resistance in HepG2 cells.
- GSK3beta is connected to tau by 14-3-3 and Ser(9)-phosphorylated GSK3beta phosphorylates tau
- 6-OHDA inhibited phosphorylation of GSK3beta at Ser9, & induced hyperphosphorylation of Tyr216 with little effect on expression. GSK3beta is a critical intermediate in pro-apoptotic signaling cascades that are associated with neurodegenerative diseases.
- GSK3 beta may function as a repressor to suppress AR-mediated transactivation and cell growth
- GSK-3beta has a role in cAMP-induced degradation of cyclin D3
- the reduction in brain GSK-3beta is reflected in CSF of schizophrenia patients
- A glycogen synthase kinase 3-beta promoter gene single nucleotide polymorphism is associated with age at onset and response to total sleep deprivation in bipolar depression.
- overexpression of human GSK-3beta in skeletal muscle of male mice resulted in impaired glucose tolerance despite raised insulin levels
- A portion of the p53 that is activated in senescent cells is modulated by its association with GSK3beta in the nucleus.
- Results propose a new mechanism by which lithium indirectly inhibits glycogen synthase kinase-3beta via phosphatidylinositol 3 kinase-dependent activation of protein kinase C alpha.
- In transgenic mice, GSK3betaS9A resulted in hyperphosphorylation of tau and morphology reminiscent of pretangle-like neurons in cortex and hippocampus.
- FRAT-2 enhances GSK3 beta-mediated phosphorylation of a primed substrate to a greater extent than an unprimed substrate
- Total GSK-3 protein was increased in both Alzheimer's disease and in mild cognitive impairment without a compensatory decrease in activity
- GSK3 and PKB/Akt have roles in the integrin-mediated regulation of PTHrP, IL-6 and IL-8 in pancreatic cancer
- Data show that the activity of glycogen synthase kinase-3 (GSK-3) is necessary for the maintenance of the epithelial architecture, and that GSK-3 inhibition stimulates the transcription of Snail.
- Results indicate that GSK3B may not play a major role in Japanese schizophrenia.
- In kinase assay, we also showed that CABYR variants act as an ideal substrate for GSK3beta within the extensin-like domain and phosphorylation sites on CABYR were mapped.
- KCl-induced depolarization causes undulating GSK-3beta phosphorylation/dephosphorylation, which is regulated for the most part by phosphatidylinositol 3-kinase and Akt (phosphorylation) and PP2A and PP2B (dephosphorylation), respectively
- a unique cooperative interaction possible between 2 critical oncogenic pathways in colorectal tumorigenesis, and pivotal role of GSK-3beta suggested
- GSK-3beta reactivation is involved in the process through which LY294002 sensitizes hepatoma cells to chemotherapy-induced apoptosis via death receptor and mitochondria signalling pathways
- These data indicate that 14-3-3zeta may not be directly interacting with GSK3beta and tau in the brain, but may indirectly facilitate the interactions by binding to other proteins.
- No significant genetic alterations were found.
- These findings suggest that glycogen synthase kinase-3beta is involved in hydrogen peroxide-mediated inhibition of Tcf/Lef-dependent transcriptional activity.
- GSK3 has a role in modulating the inflammatory response and toll-like receptor-mediated cytokine production
- Our findings demonstrate an unrecognized role of GSK3beta in tumor cell survival and proliferation other than its predicted role as a tumor suppressor.
- GSK3-dependent phosphorylation of Mdm2 regulates p53 abundance
- GSK-3 interacts with and phosphorylates ESRalpha and is involved in the regulation of receptor activity
- multiple kinases, including CK2 and GSK3beta, participate in PTEN phosphorylation and GSK3beta may provide feedback regulation of PTEN
- GSK3beta modulates synphilin-1 ubiquitylation and cellular inclusion formation by SIAH
- findings suggest the ERK/MAPK and PI3K pathways may regulate VEGF expression in part through regulating the action of these repressor proteins
- These results identify glycogen synthase kinase 3beta and FBW7 as potential cancer therapeutic targets and MYC as a critical substrate in the GSK3beta survival-signaling pathway.
- GSK-3beta directly phosphorylates and activates MARK2/PAR-1
- GSK-3, acting through PKCdelta, is a negative regulator of ERK1/2
- GSK3B polymorphisms alter transcription and splicing and interact with Tau haplotypes to modify disease risk in Parkinson disease
- GSK-3 is a specific in vivo modulator of hematopoietic stem cell activity
- a direct interaction between LRP6 and GSK3 results in an attenuation of GSK3 activity
- inhibition of GSK-3beta stimulates COX-2 expression in gastric cancer cells
- A trend was found towards an association for the C allele in the whole group of schizophrenic patients and for the heterozygous T/C genotype of bipolar patients.
- Our results demonstrate that the flow cytometry-based method is a convenient tool to analyze the effect of GSK-3beta inhibitors on Tau phosphorylation. This
- GSK3beta is not only a critical regulator of proproliferative signalling but also a promiscuous one as PI3K/Akt pools of GSK3beta are, at least in part, functionally interchangeable with those of the Wnt/beta-catenin pathway
- GSK-3 and h-prune cooperatively regulate the disassembly of focal adhesions to promote cell migration and that h-prune is useful as a marker for tumor aggressiveness.
- Cytokine-dependent GSK-3 phosphorylation in hemopoietic cells proceeds primarily through Protein Kinase B independent pathways.
- The results demonstrate that the control of MCL-1 stability by GSK-3 is an important mechanism for the regulation of apoptosis by growth factors, PI3K, and AKT.
- GSK3beta inhibits the xenobiotic and antioxidant cell response by direct phosphorylation and nuclear exclusion of the transcription factor Nrf2
- protection of beta-catenin from ubiquitination and proteasomal degradation induced by glycogen synthase kinase (GSK)-3beta inhibition
- GSK-3beta selectively regulates NFkappaB-mediated inflammatory gene expression of IL-1beta and TNF-alpha by controlling the flow of NFkappaB activity between transcription of inflammatory and survival genes
- GSK3 alters phosphorylation of CRMP-1, -2, and -4 isoforms
- findings show an increase in the immunoreactivities for the nuclear C-terminal fragments of APLP2 and for GSK-3beta in the brains of Alzheimer disease patients
- Multisite glycogen synthase kinase 3beta (GSK3beta) phosphorylation and ubiquitination by SCFbetaTrCP are required for Gli3 processing.
- there is tissue specificity for the regulation of GSK-3 in humans; in skeletal muscle GSK-3 plays a role in control of metabolism and insulin action, whereas the function in adipose tissue is less clear
- Hypertonic conditions induced with NaCl and other osmolytes were used to stimulate several tumor cell lines, Glycogen Synthase Kinase 3beta (GSK3beta) was rapidly dephosphorylated at serine 9 and its kinase activity was increased.
- Results suggest that glycogen synthase kinase-3beta activity is important for the proliferation of ovarian cancer cells, implicating this kinase as a potential therapeutic target in ovarian cancer.
- Cyclic expression of GSK-3beta's active and inactive forms in the endometrium suggests that sex hormones regulate its expression. In vitro experiments demonstrate that progesterone induces phosphorylation of endometrial GSK-3beta.
- substrate recognition involves interactions with GSK-3beta residues: Phe67, Gln89, and Asn95, which confer a common basis for substrate binding and selectivity, yet allow for substrate diversity
- analysis of critical variations in the function and regulation of GSK-3alpha and GSK-3beta
- We demonstrate, for the first time in human skeletal muscle, that the regulation of Akt and its downstream signalling pathways GSK-3beta, mTOR and Foxo1 are associated with both the skeletal muscle hypertrophy and atrophy processes.
- These results suggest i) an essential role of PI3K/Akt/GSK-3alpha/beta signaling for a successful replication of VZV and ii) a key function of VZV kinases pORFs 47 and 66 to activate this pathway.
- GSK3 activity has little influence over cyclin D1 expression levels during any cell cycle phase.
- The GSK-3beta nuclear accumulation as a hallmark of poorly differentiated pancreatic adenocarcinoma, and provide new insight into the mechanism by which GSK-3beta regulates NF-kappaB activity in pancreatic cancer.
- GSKIP is a naturally occurring protein that is homologous with the GSK3beta interaction domain of Axin and is able to negatively regulate GSK3beta of the Wnt signaling pathway.
- this study provides, for the first time, insights into the involvement of MRP2 in neurite outgrowth, which occurs in a GSK3beta-dependent manner.
- NT uses PKC-dependent pathways to modulate GSK-3, which may play a role in the NT regulation of intestinal cell growth
- This study fails to support reduced signaling of the AKT-GSK3beta molecular cascade in schizophrenia.
- These results indicate that the protein phosphatase-1/inhibitor-2 complex differentially regulates GSK3 dephosphorylation induced by KCl and that GSK3 activity regulates SERCA2 levels.
- Hypersensitivity of medulloblastoma cells in anchorage-independence is linked to GSK-3beta activity.
- GSK-3B is the missing link between the amyloid and tau-pathology, and position GSK-3B as prominent player in the pathogenesis in Alheimer disease.
- GSK-3beta but also DYRK1B modulates cyclin D1 subcellular localization by the phosphorylation of Thr(288). These results suggest that DIF-3 induces degradation of cyclin D1 through the GSK-3beta- and DYRK1B-mediated threonine phosphorylation in HeLa cell
- offer a new mechanism of regulation of E2F transcription factor 1 by direct binding of GSK3beta to its transactivation domain
- S6K1 regulates GSK3 under conditions of mTOR-dependent feedback inhibition of Akt
- The identification of a beta-catenin-T-cell factor-regulated Axin2-GSK3beta-Snail1 axis provides new mechanistic insights into cancer-associated epithelial-mesenchymal transition programmes.
- The current data suggest that, following exposure to zinc, the sequential activation of Akt and GSK-3beta plays an important role directing hippocampal neural precursor cell death.
- R-Ras and ILK have roles upstream of GSK-3beta in the regulation of neuronal polarity
- These results imply that GSK-3beta may function in transporting centrosomal proteins to the centrosome by stabilizing the BICD1 and dynein complex, resulting in the regulation of a focused microtubule organization.
- We conclude that hCSCs exhibit mesenchymal features and that Akt/GSK-3beta may be crucial modulators for hCSC maintenance in human heart.
- Of special interest was the rapid decrease in expression of MITF in melanocytes treated with DKK1, which is concurrent with the decreased activities of beta-catenin and of glucose-synthase kinase 3beta
- GSK3beta-dependent protein degradation was switched between Hath1 and beta-catenin by Wnt signaling, leading to the dramatic alteration of cell status between proliferation and differentiation in colon cancer
- IL-6, via the PI3-kinase/Akt pathway leads to inhibition of the repressive kinases MAPK/pERK and GSK3beta, and this converts inactive HSF-1 to an intermediate DNA-binding form augmenting transcriptional activation in the presence of a second stressor.
- This is the first demonstration of GSK-3beta as the missing link between UV-induced ATR activation and p21 degradation.
- direct regulation of hypoxia-inducible factor 1 alpha subunit stability by GSK-3 may influence physiological processes or pathophysiological situations such as metabolic diseases or tumors
- GSK3beta may be involved in Bipolar Disorder susceptibility in some individuals.
- Our results fail to replicate the association of the GSK-3 beta gene with susceptibility to schizophrenia in the Chinese population.
- Results indicate that the turnover of Mcl-1 by beta-TrCP is an essential mechanism for GSK-3beta-induced apoptosis and contributes to GSK-3beta-mediated tumor suppression and chemosensitization.
- abnormal activation of glycogen synthase kinase 3beta can reduce neuronal viability and synaptic plasticity via modulating Presenilin 1/N-cadherin/beta-catenin interaction and thus have important implications in the pathophysiology of Alzheimer disease.
- Our results imply that phosphorylation of serine 256 in ataxin-3 by GSK 3beta regulates ataxin-3 aggregation.
- antiapoptotic effect of GSK3beta in tumor necrosis factor-induced apoptosis is mediated by cytosolic, not nuclear, GSK3beta
- Unrestrained glycogen synthase kinase 3 beta is responsible for growth factor withdrawal induced activated T cell death.
- GSK-3beta was dephosphosphorylated at Ser9 & its enzymatic activity increased in palmitate-treated human umbilical vein endothelial cells. GSK-3beta inhibitors & transduction with a catalytically inactive GSK-3beta protected the cells from apoptosis.
- cyclin D2 expression in normal and malignant hematopoietic cells is regulated by ubiquitin/proteasome-dependent degradation triggered by Thr280 phosphorylation by GSK3beta or p38, which is induced by inhibition of the PI3K pathway
- 3,3'-diindolylmethane -induced cell growth inhibition and apoptosis induction are partly mediated through the regulation of Akt/FOXO3a/GSK-3beta/beta-catenin/AR signaling
- phosphorylation sites in tau from Alzheimer brain show that casein kinase 1delta may have a role, together with glycogen synthase kinase-3beta, in the pathogenesis of Alzheimer disea
- GSK3beta facilitates the association of T4 and T4C3, and the presence of caspase-cleaved tau is necessary for the evolution of tau oligomers into Sarkosyl-insoluble inclusions even though it is not extensively phosphorylated
- We demonstrated that treatment with EGCG reduced the A beta levels by enhancing endogenous APP nonamyloidogenic proteolytic processing.
- GSK-3 is required for E2-induced ERalpha phosphorylation at Ser-118 and full transcriptional activity of the receptor upon E2 stimulation.
- Single nucleotide polymorphisms are not asociated with bipolar disorder.
- Ajuba promoted GSK-3beta-mediated phosphorylation of beta-catenin by reinforcing the association between beta-catenin and GSK-3beta.
- pGSK-3beta-ser-9 may confer the cisplatin resistance of ovarian carcinomas through the stabilization of p53 expression
- analysis of phosphorylation and regulation of human CTPS1 in human cells shows that GSK3 is a novel regulator of CTPS activity
- observations indicate a role for GSK-3 in accurate chromosome segregation
- a direct link between GSK-3beta and MLK3 activation in a neuronal cell death pathway and identify MLK3 as a direct downstream target of GSK-3beta.
- GnRH treatment mediates the inactivation of glycogen synthase kinase-3, a protein serine/threonine kinase that regulates beta-catenin degradation within the Wnt signaling pathway
- This indicates that if the majority of tau is phosphorylated at S396/S404, in combination with increased GSK3beta activity, tau aggregation is favored. T
- glycogen synthase kinase-3beta (GSK-3beta) was found to regulate NF kappa B activation and the proliferation and survival of pancreatic cancer cells.[review]
- modulation of phosphatidylinositol 3-kinase/Akt/GSK3beta signaling cascades can be beneficial for protecting or facilitating recovery from cellular LeTx intoxication in cells that depend on basal MEK1 activity for proliferation.
- Phosphorylated-GSK3beta-ser9 and EGFR are involved in the histogenesis of different lung carcinomas.
- Association between GSJ-3beta-50T/C polymorphism and personality and psychotic symptoms in mood disorders.
- cAMP/PKA signaling activates the canonical Wnt pathway through the inactivation of GSK-3beta, whereas Wnt signaling might inhibit bone resorption through a negative impact on RANKL expression in osteoblasts.
- GSK3B protects melanoma cells from the apoptotic effects sorafenib, providing a survival signal that minimizes cellular injury.
- GSK3beta interacts with and phosphorylates the spindle-associated protein Astrin, resulting in targeting Astrin to the spindle microtubules and kinetochores.
- HSP105 appears to chaperone the responses to endoplasmic reticulum (ER) stress through its interactions with GRP78 and GSK3, and without HSP105 cell death following ER stress proceeds by a non-caspase-3-dependent process.
- sFRP-1 can interact with Wnt receptors Frizzled 4 and 7 on endothelial cells to transduce downstream to cellular machineries requiring Rac-1 activity in cooperation with GSK-3beta
- Glycogen synthase kinase-3beta (GSK-3beta) phosphorylates Cdc25A to promote its proteolysis in early cell-cycle phases.
- Abnormal GSK3beta regulation is a potential mechanism for the insulin resistance that is seen in some women with polycystic ovary syndrome.
- phosphorylation of Ser-468 was indispensable for the physical interaction between RelA/p65 and GSK3beta.
- GSK3beta acts as a negative regulator of platelet function in vitro and in vivo.
- When transfected into mice, beta cells have reduced mass and proliferation.
- GSK3beta expression is upregulated in frontal and temporal cortex in ALS with cognitive impairment.
- GSK-3beta enters the nucleus, forms a complex with beta-catenin and lowers the levels of beta-catenin/TCF-dependent transcription in a mechanism that involves GSK-3beta-Axin binding
- Ionizing radiation-induced GSK-3beta phosphorylation could contribute to the transcriptional transactivation of NF-kappaB in an ATM-independent manner.
- that inhibition of the GSK-3beta/eIF2Bepsilon translational control pathway contributes to airway smooth muscle hypertrophy in vitro and in vivo.
- The formation of an ERK.GSK3beta complex retained pERK1/2 in the cytoplasm.
- GSK-3beta regulates the localization of gamma-tubulin ring complex, including GCP5, to the spindle poles, thereby controlling the formation of proper mitotic spindles
- GSK3 beta is a bona fide PRLr kinase that phosphorylates PRLr on Ser(349) and is required for the recognition of PRLr by beta Trcp, as well as for PRLr ubiquitination and degradation
- GSK-3beta modulates the early mitotic Aurora-A level through binding and phosphorylating AIP.
- the functional regulation of p53 by triptolide was mediated by an intranuclear association of p53 with glycogen synthase kinase-3beta (GSK3beta), which was inactivated by protein kinase C (PKC).
- Results suggest that GSK-3 regulates nuclear p27 Kip1 expression through downregulation of Skp2 expression and regulates p27 Kip1 assembly with CDK2, playing a critical role in the G0/G1 arrest associated with intestinal cell differentiation.
- tetrandrine induces G(1) arrest and apoptosis through PI3K/kip1/AKT/GSK3beta pathway
- Activin A may mediate ovarian oncogenesis by activating Akt and repressing GSK to stimulate cellular proliferation.
- p38 mitogen-activated protein kinase (MAPK) also inactivates GSK3beta by direct phosphorylation at its C terminus, and this inactivation can lead to an accumulation of beta-catenin
- Our results suggest that GSK3beta polymorphisms might be involved in schizophrenia risk
- findings suggest that hepatitis B virus X protein (HBx) negatively regulated proliferation of CCL13-HBx-stable cells via the GSK-3beta/beta-catenin cascade
- We conclude that the phosphorylation of tau by GSK-3beta either prior to or following polymerization promotes polymer/polymer interactions that result in stable clusters of tau filaments.
- These results demonstrated that GSK3beta is implicated in the regulation of melanogenesis.
- review of the roles of GSK3beta in tumorigenesis and cancer chemotherapy [review]
- inhibition of GSK-3beta by lithium chloride elicited a stimulatory effect on DeltaNp63 promoter activity
- GSK-3beta signaling is a key regulator of radiation-induced damage in hippocampal neurons
- isoflavone-induced inhibition of cell proliferation and induction of apoptosis are partly mediated through the regulation of the Akt/FOXO3a/GSK-3beta/AR signaling network.
- Tissue kallikrein decreased GSK-3beta activity via the phosphatidylinositol 3-kinase-Akt pathway and enhanced VEGF and VEGFR-2 expression in endothelial cells.
- Inhibition of PI3-K/Akt induces a 40% decrease of cyclin D1 half-life as a result of accumulation of the dephosphorylated/active form of GSK-3beta within the nucleus, where it can phosphorylate cyclin D1 on Thr286 thereby promoting its nuclear export.
- As the downstream of Akt activation, H. pylori infection inactivated the inactivation of glycogen synthase kinase 3beta at Ser 9 by its phosphorylation.
- GSK3B is a novel marker and modulator of inflammatory injury in chronic renal allograft disease.
- 33 (52%) of 64 mantle cell lymphoma tumors showed nuclear localization of beta-catenin, which significantly correlated with the expression of the phosphorylated/inactive form of GSK3beta
- Reduced CREB phosphorylation (Ser-129) associated with inactivation of GSK3beta by Ser-9 phosphorylation may be the major mechanism underlying PEPCK-C gene suppression by AMPK-activating agents such as biguanide
- Glycogen synthase kinase 3 beta is phosphorylated and inhibited by Thrombopoietin-induced Proto-Oncogene Proteins c-akt, promoting survival and proliferation in megakaryocytic cells through a pathway that does not involve beta-catenin
- pharmacological, physiological and genetic studies that demonstrate an oncogenic requirement for GSK3 in the maintenance of a specific subtype of poor prognosis human leukaemia, genetically defined by mutations of the MLL proto-oncogene
- GSK-3 and IKK as potential therapeutic targets for pancreatic cancer.
- Results describe a convergence point of the GSK-3beta and the glucocorticoid receptor pathways, and suggest a mechanism by which GSK-3beta activity can dictate how cells will ultimately respond to glucocorticoids.
- The fat-1 gene expression inhibited prostate cancer cell proliferation via reduction of GSK-3beta phosphorylation and subsequent down-regulation of both beta-catenin and cyclin D1.
- To our knowledge, this is the first evidence that a gene known to be involved in tau phosphorylation, GSK3B, is associated with risk for primary neurodegenerative dementias.
- Novel regulation of vascular endothelial growth factor-A (VEGF-A) by transforming growth factor (beta)1: requirement for Smads, (beta)-CATENIN, AND GSK3(beta).
- Lys85 is important to GSK-3beta activity; the mutation of this residue could inhibit the activity of GSK-3beta.
- This review concentrates on the role of protein kinase glycogen synthase kinase 3 in the different types of Alzheimers' disease.
- VacA activates the PI3K/Akt signaling pathway, resulting in phosphorylation and inhibition of GSK3beta, and subsequent translocation ofbeta-catenin to the nucleus, consistent with effects of VacA on beta-catenin-regulated transcriptional activity.
- Our results suggest that GSK-3beta plays a role in the pathogenesis of Parkinson Disease but not in that of Multiple System Atrophy.
- glycogen synthase kinase 3beta protein is expressed in normal colon epithelium and aberrantly distributed in colorectal cancer
- GSK3beta regulates the magnitude of IL-10 production by memory CD4-positive T cells; repression of GSK3beta activity enhances the productivity and frequency of IL-10-producing memory CD4+ T cells.
- small molecule inhibitors of glycogen synthase kinase 3 (GSK-3) consistently caused a strong short period phenotype in contrast to the well-known period lengthening by lithium, another presumed GSK-3 inhibitor.
- Phosphorylated LRP6/5 both recruits and directly inhibits GSK3beta using two distinct portions of its cytoplasmic sequence.
- ligation of ApoER2 by APC signals via Dab1 phosphorylation and subsequent activation of PI3K and Akt and inactivation of GSK3beta, thereby contributing to APC's beneficial effects on cells.
- Results describe a novel function of chaperonin 10 as a general differentiation factor, not limited to erythroid cells, and show how this biological effect is mediated by GSK-3alpha/beta.
- CD16 cross-linking activated PI3K and that active PI3K limited TNF-alpha production by inhibiting GSK-3beta activity, that blocked the action of NF-kappaB.
- Galectin-3 mediates Wnt signaling acts by regulationg GSK3B phosphorylation and thus, the degradation of beta-catenin in colon cancer cells.
- Missplicing of GSK3beta represents a unique mechanism for the emergence of blast crisis chronic myeloid leukemia stem cells.