GSK-3 alpha/beta Antibody (1H8) Summary
| Immunogen |
Recombinant Xenopus GSK3 alpha/beta (1H8)
|
| Specificity |
GSK3 alpha/beta Antibody (1H8)
|
| Isotype |
IgG2b
|
| Clonality |
Monoclonal
|
| Host |
Mouse
|
| Gene |
GSK3A
|
| Purity |
Protein G purified
|
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|
Applications/Dilutions
| Dilutions |
|
| Application Notes |
Western Blot, Immunohistochemistry-Paraffin. May be useful in Immunocytochemistry.
|
Reactivity Notes
May cross react with Hamster. Please note that this antibody is reactive to Mouse and derived from the same host, Mouse. Additional Mouse on Mouse blocking steps may be required for IHC and ICC experiments. Please contact Technical Support for more information.
Packaging, Storage & Formulations
| Storage |
Store at -20C. Avoid freeze-thaw cycles.
|
| Buffer |
PBS (pH 7.2) and 50% Glycerol
|
| Preservative |
0.09% Sodium Azide
|
| Purity |
Protein G purified
|
Alternate Names for GSK-3 alpha/beta Antibody (1H8)
- DKFZp686D0638
- EC 2.7.11
- EC 2.7.11.26
- glycogen synthase kinase 3 alpha
- glycogen synthase kinase-3 alpha
- GSK-3 alpha
- GSK-3 alpha/beta
Background
Glycogen Synthase Kinase 3beta (GSK-3beta) is a unique serine/threonine kinase that is inactivated by phosphorylation. In response to insulin binding, PKB/AKT phosphorylates GSK-3beta on serine 9, which prevents GSK-3beta from phosphorylating glycogen synthase. Unphosphorylated glycogen synthase is active and able to synthesize glycogen. GSK-3beta 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-3beta. The phosphorylated serine binds to the GSK-3beta priming phosphate position and prevents binding of alternative substrates. In addition to insulin signaling, GSK-3beta 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-3beta is unable to phosphorylate beta-catenin, which leads to stabilization of beta-catenin. The Wnt pathway inactivates GSK-3beta via the proteins, Dishevelled and FRAT, which disrupt the interaction of GSK-3beta with axin, beta-catenin, and APC. Clinically, there is considerable interest in GSK-3beta inhibitors because they may mimic the effect of insulin or reduce the hyperphosphorylation of Tau that is observed in Alzheimers Disease.