A-kinase anchoring proteins (AKAPs) include a family of scaffolding proteins that target protein kinase A (PKA) and other signaling proteins to cellular compartments and thereby confine the activities of the associated proteins to distinct regions within cells. AKAPs bind PKA directly. The interaction is mediated by the dimerization and docking domain of regulatory subunits of PKA and the PKA-binding domain of AKAPs. Analysis of the interactions between the dimerization and docking domain and various PKA-binding domains yielded a generalized motif allowing the identification of AKAPs. Our bioinformatics and peptide array screening approaches based on this signature motif identified GSKIP (glycogen synthase kinase 3beta interaction protein) as an AKAP. GSKIP directly interacts with PKA and GSK3beta (glycogen synthase kinase 3beta). It is widely expressed and facilitates phosphorylation and thus inactivation of GSK3beta by PKA. GSKIP contains the evolutionarily conserved domain of unknown function ...
The transcription factor NF-E2-related factor 2 (Nrf2) is a master regulator of a genetic program, termed the phase 2 response, that controls redox homeostasis and participates in multiple aspects of physiology and pathology. Nrf2 protein stability is regulated by two E3 ubiquitin ligase adaptors, Keap1 and ß-TrCP, the latter of which was only recently reported. Here, two-dimensional (2D) gel electrophoresis and site-directed mutagenesis allowed us to identify two serines of Nrf2 that are phosphorylated by glycogen synthase kinase 3ß (GSK-3ß) in the sequence DSGISL. Nuclear magnetic resonance studies defined key residues of this phosphosequence involved in docking to the WD40 propeller of ß-TrCP, through electrostatic and hydrophobic interactions. We also identified three arginine residues of ß-TrCP that participate in Nrf2 docking. Intraperitoneal injection of the GSK-3 inhibitor SB216763 led to increased Nrf2 and heme oxygenase-1 levels in liver and hippocampus. Moreover, mice with ...
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Abstract Background Glycogen synthase kinase-3 (GSK-3) is a ubiquitously expressed serine/threonine (Ser/Thr) kinase comprising two isoforms, GSK-3 and GSK-3. procedures. Nevertheless, the specificity of these antibodies in immunocytochemistry offers not really been resolved in any fine detail. ResultsTaking benefit of gene silencing technology, we analyzed the specificity of many in a commercial sense obtainable anti-phosphorylated GSK-3 antibodies. We display that antibodies elevated to peptides made up of the phosphorylated Ser21/9 epitope crossreact with mysterious antigens that are extremely indicated by mitotic cells and that primarily localise to spindle poles. In addition, two antibodies elevated to peptides made up of the phosphorylated Tyr279/216 epitope recognise an mysterious proteins at focal connections, and a third antibody recognises a proteins discovered in Ki-67-positive cell nuclei. While the phosphorylated Ser9/21 GSK-3 antibodies also recognise additional protein whose ...
Several kinases implicated in multiple signaling pathways elicit conflicting responses depending on the cellular context. One such kinase is glycogen synthase kinase 3 (GSK3), a cytoplasmic serine-threonine kinase that is involved in insulin signaling and metabolic regulation, as well as in Wnt signaling and the specification of cell fates during embryonic development (3). GSK3 appears in two highly homologous and ubiquitously expressed forms, GSK3α and GSK3β (4). The insulin and Wnt signaling pathways differentially regulate GSK3α/β resulting in distinct downstream events (5), but how they accomplish this is not clear. The recent report of the crystal structure of GSK3β by Dajani and colleagues in Cell (6), together with a biochemical study of GSK3_ by Frame et al. in Molecular Cell (7), reveal how GSK3 selectively regulates different downstream targets according to which signaling pathway is activated.. GSK3 is unusual among kinases in that its normal activity in the cytoplasm is blocked ...
Of the discovery of GSK3 (glycogen synthase kinase 3) inhibitors there has been no end. I first came across it as a target it about 1997, and even then, once I
Crosstide is a peptide analog of glycogen synthase kinase α/β fusion protein sequence which is a substrate for Akt. - Mechanism of Action & Protocol.
Dysregulation of glycogen synthase kinase (GSK-3β) is implicated in the pathophysiology of many diseases, including type-2 diabetes, stroke, Alzheimers, and others. A multistage virtual screening strategy designed so as to overcome known caveats arising from the considerable flexibility of GSK-3β yielded, from among
Glycogen synthase kinase 3 beta inhibitor Chir025 reduces neuronal death resulting from oxygen-glucose deprivation, glutamate excitotoxicity, and cerebral isc
TWS119 is a glycogen synthase kinase-3β inhibitor with an IC50 of 30 nM. Find all the information about TWS119 for cell signaling research.
Glycogen synthase kinase-3 (GSK-3) exclusive position in modulating the function of the diverse group of protein in conjunction with it is association with a multitude of human disorders offers attracted significant focus on the proteins both being a therapeutic focus on and as a way to understand the molecular basis of the disorders. mobile stimulants. This paper will concentrate on the different methods to control GSK-3 activity (phosphorylation, proteins complex development, truncation, subcellular localization, etc.), the primary signalling pathways involved with its control, and its own pathological deregulation. 1. Launch Glycogen synthase kinase-3 (GSK-3) is really a CMGC serine/threonine proteins kinase initially referred to as among the kinases that phosphorylates and inhibits glycogen synthase [1]. It really is now widely recognized though that GSK-3 has an important function in various important physiological processes, such as for example development, cell routine, or apoptosis [2]. ...
Glycogen Synthase Kinase 3 (GSK-‑3) is a serine/threonine protein kinase and one of several protein kinases, which phosphorylate glycogen synthase. It is also called Factor A (F A ) for its ability to activate the MgATP-dependent form of the protein phosphatase PP1 called F C (1-4)
Active Aβ immunotherapy in Alzheimers disease (AD) induces removal of Aβ and phosphorylated tau (ptau). Glycogen Synthase Kinase (GSK)-3β is a kinase, responsible for phosphorylation of tau, activation of which can be induced by phosphorylated double-stranded RNA dependent protein kinase (pPKR). Using a post-mortem cohort of immunised AD cases, we investigated the effect of Abeta immunisation on GSK-3β expression and pPKR ...
The WNT signalling pathway controls many developmental processes and plays a key role in maintenance of intestine renewal and homeostasis. Glycogen Synthase Kinase 3 (GSK3) is an important component of the WNT pathway and is involved in regulating β-catenin stability and expression of WNT target genes. The mechanisms underpinning GSK3 regulation in this context are not completely understood, with some evidence suggesting this occurs through inhibitory N-terminal serine phosphorylation in a similar way to GSK3 inactivation in insulin signaling. To investigate this in a physiologically relevant context, we have analysed the intestinal phenotype of GSK3 knockin mice in which N-terminal serines 21/9 of GSK3α/β have been mutated to non-phosphorylatable alanine residues. We show that these knockin mutations have very little effect on overall intestinal integrity, cell lineage commitment, β-catenin localization or WNT target gene expression although a small increase in apoptosis at villi tips is ...
Recent Research Presentations (Personally presented):. Natural compounds isolated from diverse plants and their usefulness for combating fatal diseases like human oral cancer. BELMSBR, Mar 29-30, 2017 at NOU, Baripada, India. (Invited Talk). Application of Synthetic/ Natural Compounds for Combating Oral Cancer: Role of an Enzyme Glycogen Synthase Kinase 3 beta. ICFCS, Mar 16-18, 2017 at CUJ, Ranchi, India. (Invited Lecture) Awakening GSK3beta (glycogen synthase kinase 3beta), the resting conqueror, to fight against human oral epithelial cancer. World Congress on Cancer Research & Therapy on Nov 21-23, 2016 at Miami, FL, USA. (Invited Talk). Aggressiveness of human oral cancer and the role of glycogen synthase kinase 3 isoforms α/β signaling. 12th Asian Clinical Oncology Society Conference (ACOS- 2016), April 8-10, New Delhi, India. Aggressiveness of tobacco mediated human oral cancer and the role of glycogen synthase kinase 3 isoforms α/β signaling. International Conference on Environmental ...
Dive into the research topics of Staphylococcus aureus induces microglial inflammation via a glycogen synthase kinase 3β-regulated pathway. Together they form a unique fingerprint. ...
Phosphatidylinositol-3 kinase (PI3-K) and protein kinase B (Akt) activation not only stimulate NO production, but they also inhibit glycogen synthase kinase-3β (GSK3β) (8). Similarly, activation of canonical Wnt signaling inactivates GSK3β (9). Wnts are secreted glycoproteins known to regulate hematopoiesis and stem cell function (9). In the unstimulated cell, GSK3β phosphorylates and accelerates degradation of HIF-1α and β-catenin (9,10). Inhibition of GSK3β leads to cytosolic accumulation and nuclear translocation of these transcription factors in a manner that increases EPC survival, proliferation, differentiation, mobilization, and adhesion (11-13). EPCs pretreated with GSK inhibitors or EPCs that are genetically modified to overexpress VEGF or inactive GSK3β enhance vasculogenesis, augment reendothelialization, and reduce neointimal formation (11-13).. Diabetes is associated with reduced endothelial NO bioavailability and PI3-K/Akt activity, and EPCs are defective and reduced in ...
Background Glycogen synthase kinase-3 (GSK-3) is a multifunctional serine/threonine kinase that has an important function in cancers tumorigenesis and development. at both mRNA and proteins levels. Conclusion Used together, our outcomes demonstrate the fact that GSK-3 inhibitor AZD1080 suppresses ovarian cancers development and for that reason may indicate a fresh path for ovarian cancers treatment. strong course=kwd-title Keywords: ovarian cancers, GSK-3 inhibitor, AZD1080, tumorigenesis, development Introduction Ovarian cancers may be the third most common feminine reproductive system cancer tumor. The ovarian cancers mortality rate may be the highest from the gynecological malignancies because of the insufficient effective early diagnostic strategies, its chemotherapy level of resistance, and its capability to metastasize and recurrence. The 5-calendar year survival rate is certainly 30%, rendering it as a significant threat to medical and lives of females.1,2 Ovarian cancers has many ...
The graphic displays domains and Protease cut sites on the protein sequence. Drag your mouse right/left over the graphic. Use the selection boxes on the right to select which annotations to view simultaneously. Combine annotation with multiple checkmarks.. ...
IL-33 is a cytokine belonging to the IL-1 family and plays a critical role in the pathogenesis of pulmonary inflammatory diseases (7, 32). IL-33 induces IL-6 and IL-8 release in lung epithelial cells and macrophages, and increases lung endothelial permeability (7, 9). The biological effects of IL-33 are through interactions with its receptor ST2L. Therefore, understanding the regulation of cell surface expression of ST2L is important for limiting lung inflammation and injury. Ligand-induced receptor internalization and downregulation are crucial steps to control the magnitude and duration of extracellular signals in eukaryotes. Our previous studies demonstrated that ST2L is ubiquitinated and degraded in response to IL-33 in a GSK3β activation-dependent manner (5). In this study, we extend our understanding of ST2L downregulation by demonstrating a role for GSK3β in the regulation of ST2L receptor internalization. The current study indicates that FAK-activated GSK3β modulates ST2L ...
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The phosphorylation state of tau changes during neurodevelopment and highly phosphorylated tau accumulates in the paired helical filaments found in Alzheimers disease. In non-neuronal mammalian cells transiently expressed tau is predominantly not phosphorylated at sites known to be phosphorylated i …
1o6l_A mol:protein length:337 RAC-BETA SERINE/THREONINE PROTEIN KINASE KVTMNDFDYLKLLGKGTFGKVILVREKATGRYYAMKILRKEVIIAKDEVAHTVTESRVL QNTRHPFLTALKYAFQTHDRLCFVMEYANGGELFFHLSRERVFTEERARFYGAEIVSAL EYLHSRDVVYRDIKLENLMLDKDGHIKITDFGLCKEGISDGATMKTFCGTPEYLAPEVL EDNDYGRAVDWWGLGVVMYEMMCGRLPFYNQDHERLFELILMEEIRFPRTLSPEAKSLL AGLLKKDPKQRLGGGPSDAKEVMEHRFFLSINWQDVVQKKLLPPFKPQVTSEVDTRYFD DEFTAQSITITPPDRYDSLGLLELDQREEQEMFEDFDYIADW >1o6l_C mol:protein length:10 GLYCOGEN SYNTHASE KINASE-3 BETA GRPRTTSFAE >1o6l_C mol:protein length:10 GLYCOGEN SYNTHASE KINASE-3 BETA GRPRTTSFAE ...
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Glycogen synthase kinase 3 (GSK-3) in its active state complexes with APC and AXIN to suppress phosphorylation of β-catenin, which then gets degraded via the proteasome. GSK-3 becomes inactivated through the PI3K/AKT pathway when the cell receives signals like growth factors, cytokines, or insulin. WNT signaling can also inactivate GSK-3 through Dsh. Inactivation of GSK-3 leads to gene expression, cell survival, and cell proliferation.. Click on the poster below to view the interactive version.. ...
GSK3B / GSK3 Beta (C-Terminus) antibody | P49841 | Glycogen synthase kinase-3 beta, GSK-3 beta, Serine/threonine-protein kinase GSK3B, Gsk 3beta, GSK3 beta, GSK3beta
Few things can be considered to be more important to a cell than its threshold for apoptotic cell death, which can be modulated up or down, but rarely in both directions, by a single enzyme. Therefore, it came as quite a surprise to find that one enzyme, glycogen synthase kinase-3 (GSK3), has the pe …
In the prior funding period, we demonstrated that conditional elimination of the Glycogen Synthase Kinase-3s (GSK-3s), a and ?, in the embryonic nervous system...
Title: The Possible Involvement of Glycogen Synthase Kinase-3 (GSK-3) in Diabetes, Cancer and Central Nervous System Diseases. VOLUME: 17 ISSUE: 22. Author(s):Amar S., Belmaker R.H. and Agam G.. Affiliation:Beer-Sheba Mental Health Center PO Box 4600, Beer-Sheba ISRAEL.. Keywords:Glycogen synthase kinase 3-β, diabetes, cancer, CNS, bipolar disorder, schizophrenia, Wnt signaling, postmortem brain, lithium, inflammation. Abstract: Glycogen synthase kinase (GSK-3) is a key enzyme in multiple cell processes. Since many pharmacological compounds that have effects on common metabolic pathways may have uses in many different diseases, we review here the possible involvement of glycogen synthase kinase 3 in diabetes, cancer and CNS diseases. Moreover, diabetes has recently been strongly linked to CNS diseases such as schizophrenia and bipolar illness. GSK-3 is both directly and indirectly inhibited by lithium, a key compound for treatment of bipolar disorder. Several antipsychotic drugs also affect the ...
In Saccharomyces cerevisiae, nutrient levels control multiple cellular processes. Cells lacking the SNF1 gene cannot express glucose-repressible genes and do not accumulate the storage polysaccharide glycogen. The impaired glycogen synthesis is due to maintenance of glycogen synthase in a hyperphosphorylated, inactive state. In a screen for second site suppressors of the glycogen storage defect of snf1 cells, we identified a mutant gene that restored glycogen accumulation and which was allelic with PHO85, which encodes a member of the cyclin-dependent kinase family. In cells with disrupted PHO85 genes, we observed hyperaccumulation of glycogen, activation of glycogen synthase, and impaired glycogen synthase kinase activity. In snf1 cells, glycogen synthase kinase activity was elevated. Partial purification of glycogen synthase kinase activity from yeast extracts resulted in the separation of two fractions by phenyl-Sepharose chromatography, both of which phosphorylated and inactivated glycogen ...
The phosphorylation of Amyloid Precursor Protein (APP) at Thr668 plays a key role in APP metabolism that is highly relevant to AD. The c-Jun-N-terminal kinase (JNK), glycogen synthase kinase-3β (GSK-3β) and cyclin-dependent kinase 5 (Cdk5) can all be responsible for this phosphorylation. These kinases are activated by excitotoxic stimuli fundamental hallmarks of AD. The exposure of cortical neurons to a high dose of NMDA (100 μM) for 30-45 led to an increase of P-APP Thr668. During NMDA stimulation APP hyperphosphorylation has to be assigned to GSK-3β activity, since addition of L803-mts, a substrate competitive inhibitor of GSK-3β reduced APP phosphorylation induced by NMDA. On the contrary, inhibition of JNK and Cdk5 with D-JNKI1 and Roscovitine respectively did not prevent NMDA-induced P-APP increase. These data show a tight connection, in excitotoxic conditions, between APP metabolism and the GSK-3β signaling pathway.
Cytoarchitectural abnormalities have been reported in the cortex in schizophrenia. These suggest a developmental origin for this disorder. The Wnt signalling pathway is involved in the regulation of brain development; disruption of this pathway may lead to abnormal cortical development. In this study levels of three components of the Wnt signalling pathway; glycogen synthase kinase-3beta(GSK-3beta), beta-catenin and dishevelled-2 (Dvl-2) were determined in the prefrontal cortex of ten schizophrenic and ten control individuals using immunoblotting. GSK-3beta levels were significantly reduced in the schizophrenic group, while levels of beta-catenin and Dvl-2 did not differ between groups. This provides further evidence for an abnormality of the Wnt signalling pathway in schizophrenia.
The challenge for glycogen synthase kinase-3 (GSK-3) inhibitor design lies in achieving high selectivity for one isoform over the other. The therapy of certain diseases, such as acute myeloid leukemia (AML), may require α-isoform specific targeting. The scorpion shaped GSK-3 inhibitors developed by our group achieved the highest GSK-3α selectivity reported so far but suffered from insufficient aqueous solubility. This work presents the solubility-driven optimization of our isoform-selective inhibitors using a scorpion shaped lead. Among 15 novel compounds, compound 27 showed high activity against GSK-3α/β with the highest GSK-3α selectivity reported to date. Compound 27 was profiled for bioavailability and toxicity in a zebrafish embryo phenotype assay. Selective GSK-3α targeting in AML cell lines was achieved with compound 27, resulting in a strong differentiation phenotype and colony formation impairment, confirming the potential of GSK-3α inhibition in AML therapy. ...
Dive into the research topics of Dysregulation of glycogen synthase kinase-3β signaling in hepatocellular carcinoma cells. Together they form a unique fingerprint. ...
Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis, Wnt signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), CTNNB1/beta-catenin, APC and AXIN1. Requires primed phosphorylation of the majority of its substrates. Contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis. Regulates glycogen metabolism in liver, but not in muscle. May also mediate the development of insulin resistance by regulating activation of transcription factors. In Wnt signaling, regulates the level and transcriptional activity of nuclear CTNNB1/beta-catenin. Facilitates amyloid precursor protein (APP) processing and the generation of APP-derived amyloid plaques found in Alzheimer disease. May be involved in the regulation of replication in pancreatic beta-cells. Is necessary for the establishment of neuronal
Supplementary Materialsijms-20-05857-s001. = 7.4), Tf may bind two atoms of Fe3+ tightly. may be the receptor of can bind easily, and initiates Pyrithioxin dihydrochloride the clathrin-mediated endocytosis with the help of the TfR trafficking proteins [16]. Using the entry of protons, the pH in endosome filled with diferric Tf/TfR1 complicated decreases, producing a conformational alter in discharge and Tf of Fe3+ [17]. Subsequently, the apo-Tf/TfR complicated returns towards the cell surface area for another routine, whilst Fe3+ is normally decreased to Fe2+ by way of a reductase called six-transmembrane epithelial antigen from the prostate 3 ((PRV) over the hosts iron fat burning capacity [27], it really is of great importance to clarify the partnership between aquatic trojan infection as well as the iron fat burning capacity, which may donate to illuminating the antiviral iron-withholding strategies in aquatic pets and exploiting iron-related medications or feed chemicals for the avoidance ...
Recombinant Human Glycogen synthase 1/GYS1 protein is a Wheat germ Full length protein 1 to 737 aa range and validated in WB, ELISA.
4ACG: Discovery of Novel Potent and Highly Selective Glycogen Synthase Kinase-3Beta (Gsk3Beta) Inhibitors for AlzheimerS Disease: Design, Synthesis, and Characterization of Pyrazines.
Background Despite recent desire for glycogen synthase kinase-3b (GSK-3b) like a target for the treatment of mood disorders there has been very little work related to these ailments within the upstream signaling molecules that regulate this kinase as well as downstream focuses on. genes. Improved manifestation and function of Wnt2 was confirmed by secondary actions. […]. ...
Glycogen synthase kinase-3 (GSK-3) is ubiquitously expressed throughout the brain and involved in vital molecular pathways such as cell survival and synaptic reorganization and has emerged as a potential drug target for brain diseases. A causal role for GSK-3, in particular the brain-enriched GSK-3β isoform, has been demonstrated in neurodegenerative diseases such as Alzheimers and Huntingtons, and in psychiatric diseases. ...
bfu:BC1G_11987 K00693 glycogen synthase [EC:2.4.1.11] , (RefSeq) glycogen synthase (A) MSGKTNRDVKNHFLFEIATEVANRVGGIYSVIKSKAPVTTAEYGDRYTLIGPLNRQSAAV EVEALTPTNPHLAATIEAMEERGIQMVYGRWLIEGAPRVLLIDTKSAYRFLDEWKADLWN TAGIPSPPGDDETNEAVVFGYLVAWFLGEFVAHEKEKAVIAHFHEWLSGVALPLCKKRRI DVTTIFTTHATLLGRYLCAGSVDFYNNLQWFDVDAEAGKRGIYHRYCIERAATHSCDVFT TVSHITAYESEHLLKRKPDGVLPNGLNVTKFSAMHEFQNLHQQAKEKIHDFVRGHFYGHN DFDPENTLYFFTAGRYEYRNKGVDMFIESLARLNHRLKSAGSKMTVVAFIIMPAQTQSLT VEALKGQAVIKSLRDTVDVIERGVGKRIFERALKWHEGEVMPDEKDLITSQDRILLRRRL FAMKRHGLPPIVTHNMANDSEDPILNQIRRVQLFNHPSDRVKVVFHPEFLNSANPVLPMD YDEFVRGTHLGVFSSYYEPWGYTPAECTVMGVPSITTNLSGFGCYMEELIENSTDYGIYI VDRRMKGVDDSVNQLTSYMFDFAGKSRRQRINQRNRTERLSDLLDWKRMGMEYVKARQLA LRRAYPASFDGEEEDDFIPGVEQKISRPFSVPGSPRDRTGMMTPGDFASLQEGREGLSTE DYVSWKLPEEEDPDEYPFPLTLRTKKPNGSQSPYGYGGAQSPSEYAITNGNGMK ...
TY - JOUR. T1 - Inhibition of glycogen synthase kinase 3β activity with lithium in vitro attenuates sepsis-induced changes in muscle protein turnover. AU - Bertsch, Stephen. AU - Lang, Charles H.. AU - Vary, Thomas C.. N1 - Copyright: Copyright 2011 Elsevier B.V., All rights reserved.. PY - 2011/3. Y1 - 2011/3. N2 - Loss of lean body mass is a characteristic feature of the septic response, and the mechanisms responsible for this decrease and means of prevention have not been fully elucidated. The present study tested the hypothesis that in vitro treatment of skeletal muscle with lithium chloride (LiCl), a glycogen synthase kinase (GSK) 3 inhibitor, would reverse both the sepsis-induced increase in muscle protein degradation and inhibition of protein synthesis. Sepsis decreased GSK-3β phosphorylation and increased GSK-3β activity, under basal conditions. Sepsis increased muscle protein degradation, with a concomitant increase in atrogin 1 and MuRF1 mRNA and 26S proteosome activity. Incubation ...
TY - JOUR. T1 - Multiple phosphorylation of rabbit muscle glycogen synthase by glycogen synthase kinase-1. Relationship between phosphorylation state and kinetic properties. AU - Salavert, Agustí. AU - Itarte, Emilio. AU - Massaguè, Joan. AU - Guinovart, Joan J.. PY - 1979/10/15. Y1 - 1979/10/15. U2 - https://doi.org/10.1016/0014-5793(79)80514-1. DO - https://doi.org/10.1016/0014-5793(79)80514-1. M3 - Article. VL - 106. SP - 279. EP - 283. ER - ...
The cDNA for mouse brain glycogen synthase has been isolated by screening a mouse cerebral cortical astrocyte lambda ZAP II cDNA library. The mouse brain glycogen synthase cDNA is 3.5 kilobases in length and encodes a protein of 737 amino acids. The coding sequence of mouse brain glycogen synthase cDNA shares approximately 87% nucleotide identity and approximately 96% amino acid identity with the muscle isozyme, while the degree of identity is lower with the liver isozyme. The regional distribution of glycogen synthase mRNA determined by in situ hybridization in the mouse brain reveals a wide distribution throughout the central nervous system with highest densities observed in the cerebellum, hippocampus and olfactory bulb. At the cellular level the expression of brain glycogen synthase mRNA is localized both in astrocytes and neurons with, however, the higher levels observed in astrocytes. Vasoactive intestinal peptide and noradrenaline, two neurotransmitters previously shown to induce a glycogen
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
FIG. 7. Ser404 phosphorylation decreases GR function. (A and B) GR-null U-2 OS cells or those expressing WT-, S404A-, or S404D-GR were transiently transfected with pRL-Renilla and the GRE-luc (A) or MHC-luc NF-κB (B) luciferase reporters. Cells were then treated with Dex (0 to 100 nM) as indicated. After 20 h, the cells were lysed and analyzed for luciferase activity, which was normalized to the Renilla activity. Plotted are the normalized percentages of GRE transactivation or NF-κB transrepression by Dex (*, P , 0.05). (C) WT-GR-expressing U-2 OS cells were treated with the GSK-3α/β inhibitor BIO (5 μM) and Dex (100 nM) for 20 h. Cells were then lysed, analyzed by Western blotting, and probed with antibodies directed to the NF-κB regulated prosurvival genes Bcl-xL, c-IAP, and survivin. The protein band intensities were quantitated from three independent experiments and normalized to actin. (D) WT-and S404D-GR-expressing U-2 OS cells were treated with Dex for 20 h (100 nM), lysed, analyzed ...
Glycogen synthase kinase 3 has evolutionarily conserved roles in cell signaling and metabolism and is a recognized drug target in neurological pathologies, most prominently bipolar disorder. More recently it has been suggested that GSK3 may be a target for the treatment of trypanosomatid parasite infections, e.g. w
The focus of this study was to identify signaling pathways and potential therapeutic agents that would allow reproducible stimulation of DNA synthesis, cell cycle progression, and proliferation in human β-cells. We found that glucose, mTOR activity, and inhibition of GSK-3 together stimulated these regenerative processes in a highly reproducible manner in adult human β-cells regardless of sex, age, BMI, or isolation center.. Both LiCl and 1-Akp significantly enhanced DNA synthesis above that of 8 mmol/l glucose, and LiCl-mediated DNA synthesis was more sensitive to rapamycin than 1-Akp. This finding suggested that a component of 1-Akp-stimulated DNA synthesis in human islets is mTOR independent. Although lithium at higher concentrations decreased DNA synthesis in human islets, this did not appear to be due to apoptosis because cell cycle analysis (Fig. 3A and B) failed to detect a significant degree of apoptosis under similar conditions. Mussmann et al. (18) reported that lithium produces ...
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ENGLISH ABSTRACT: INTRODUCTION: Glycogen synthase kinase-3 (GSK-3) is a serine-threonine protein kinase that was first discovered as a regulator of glycogen synthase thus playing a role in glycogen synthesis (Embi et al ...
Alsterpaullone, also known as 9-Nitropaullone and NSC 705701, is a derivative of kenpaullone and an ATP-competitive inhibitor of several cyclin-dependent kinases (CDKs) as well as glycogen synthase kinase 3β (GSK3β). Alsterpaullone induces apoptosis by activation of caspase-9 due to perturbation in mitochondrial membrane potential. Alsterpaullone mediated toxicity in HeLa Cells through Apoptosis-Inducing Effect.
Kirschenbaum F, Hsu SC, Cordell B, McCarthy JV. Substitution of a glycogen synthase kinase-3beta phosphorylation site in presenilin 1 separates presenilin function from beta-catenin signaling ...
The widely used psychiatric drug lithium, and other agents that inhibit glycogen synthase kinase-3 (GSK3), have been mentioned as possible Alzheimers disease therapies for some time, primarily because GSK3 is one of several kinases known to phosphorylate tau.... ...
Glycogen Synthase antibody (glycogen synthase 1 (muscle)) for WB. Anti-Glycogen Synthase pAb (GTX50798) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.
pon:100452879 K00693 glycogen synthase [EC:2.4.1.11] , (RefSeq) GYS2; glycogen synthase 2 (A) MLRGRSLSVTSLGGLPQWEVEELPVEELLLFEVAWEVTNKVGGIYTVIQTKAKTTADEWG ENYFLIGPYFEHNMKTQVEQCEPVNDAVRRAVDAMNKHGCQVHFGRWLIEGSPYVVLFDI GYSAWNLDRWKGDLWEACSVGIPYHDREANDMLIFGSLTAWFLKEVTDHADGKHVIAQFH EWQAGIGLILSRARKLPIATIFTTHATLLGRYLCAASIDFYNHLDKFNIDKEAGERQIYH RYCMERASVHCAHVFTTVSEITAIEAEHMLKRKPDVVTPNGLNVKKFSAVHEFQNLHAMY KARIQDFVRGHFYGHLDFDLEKTLFLFIAGRYEFSNKGADIFLESLSRLNFLLRMHKSDV TVVVFFIMPAKTNNFNVETLKGQAVRKQLWDVAHSVKEKFGKKLYDALLRGEIPDMNNIL DRDDLTIMKRAIFSTQRQSLPPVTTHNMIDDSTDPILSTIRRIGLFNNRTDRVKVILHPE FLSSTSPLLPMDYEEFVRGCHLGVFPSYYEPWGYTPAECTVMGIPSVTTNLSGFGCFMQE HVADPTAYGIYIVDRRFRSPDDSCNQLTKFLYGFCKQSRRQRIIQRNRTERLSDLLDWRY LGRYYQHARHLTLSRAFPDKFHVELTSPPTTEGFKYPRPSSVPPSPSGSQASSPQSSDVE DEVEDERYDEEEEAERDRLNIKSPFSLSHIPHGKKKLHGEYKN ...