Alternative Name: | Glycogen synthase kinase-3α/β |
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Clone: | 6D3 |
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Host: | Mouse |
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Isotype: | IgG1 |
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Immunogen: | Synthetic peptide corresponding to a portion of mouse GSK phosphorylated at Tyr216/279. |
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UniProt ID: | Q2NL51 (GSK3A), Q9WV60 (GSK3B) |
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Species reactivity: | Human, Mouse
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Applications: | WB
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Purity Detail: | Thiophilic adsorption and size exclusion chromatography purified. |
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Formulation: | Lyophilized from 1ml of 2x PBS containing 0.09% sodium azide, PEG, and sucrose. |
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Reconstitution: | Reconstitute with 1ml water (15 minutes at room temperature). |
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Use/Stability: | Stable at -80°C up to 1 year, at 4°C up to 3 months. |
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Handling: | Avoid freeze/thaw cycles. After reconstitution, prepare aliquots and store at -80°C. |
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Shipping: | Shipped on Blue Ice |
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Long Term Storage: | -20°C |
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Scientific Background: | Glycogen Synthase Kinase 3β (GSK-3β) is a unique serine/threonine kinase that is inactivated by phosphorylation. In response to insulin binding, PKB/AKT phosphorylates GSK-3β on serine 9, which prevents GSK-3β from phosphorylating glycogen synthase. Unphosphorylated glycogen synthase is active and able to synthesize glycogen. GSK-3β is also unique in that it requires a substrate that has been phosphorylated by a distinct kinase before it can phosphorylate the substrate. This phosphate priming mechanism explains why phosphorylation of serine 9 inactivates GSK-3β. The phosphorylated serine binds to the GSK-3β priming phosphate position and prevents binding of alternative substrates. In addition to insulin signaling, GSK-3β participates in the Wnt signaling pathway, where it forms a complex with axin, beta-catenin and adenomatous polyposis coli (APC) protein. In the presence of Wnts, GSK-3β is unable to phosphorylate beta-catenin, which leads to stabilization of beta-catenin. The Wnt pathway inactivates GSK-3β via the proteins, Dishevelled and FRAT, which disrupt the interaction of GSK-3β with axin, beta-catenin, and APC. Clinically, there is considerable interest in GSK-3β inhibitors because they may mimic the effect of insulin or reduce the hyperphosphorylation of Tau that is observed in Alzheimer's Disease. |
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Regulatory Status: | RUO - Research Use Only |
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Western blot analysis of serum starved cancer cells: HeLa (1), HepG2 (2), HEK293 (3), SH-SY5Y (4), MDCK (5), PC12 (6), CMT 93 (7), Neuro 2A (8), and NIH-3T3 (9), with GSK3 α/β (phospho-Tyr215/278) mAb (6D3).