GSK3 beta (phospho-Ser9) rabbit polyclonal antibody

Brand: Stressgen Print Page
Description Size Catalog# Price Quantity  
GSK-3beta (phospho-Ser9) Polyclonal Antibody  100 µL KAP-ST011E $325.00  
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 Alzheimer's Disease.

Table of Abbreviations

Conjugate

Applications
EIA, WB

Isotype
not applicable

Purification
Peptide Affinity

Immunogen
Synthetic phospho-peptide derived from the sequence of human GSK3 ¦Â

Host
Rabbit

Clone Number
not applicable

Species Reactivity
H, M, R, HA

For research use only, not for diagnostic or therapeutic use.

Documentation
TechSpec

Product Manual

Product Name Catalog # Manual
GSK-3beta (phospho-Ser9) Polyclonal Antibody KAP-ST011E  

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Citations
Launch Citation Database

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