Cell Signaling Technology

Product Pathways - PI3K / Akt Signaling

GSK-3α Antibody #9338

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk Endogenous 51 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

GSK-3alpha Antibody detects endogenous levels of total GSK-3alpha protein. It does not cross-react with recombinant GSK-3beta.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the sequence of human GSK-3alpha. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, transfected with 100 nM SignalSilence® Control siRNA (Fluorescein Conjugate) #6201 (-), SignalSilence® GSK-3α siRNA II (+) or SignalSilence® GSK-3α siRNA I #6312 (+), using GSK-3α Antibody #9338 and β-Actin (13E5) Rabbit mAb #4970. GSK-3α Antibody confirms silencing of GSK-3α expression and β-Actin (13E5) Rabbit mAb is used to control for loading and specificity of GSK-3α siRNA.

Western Blotting

Western Blotting

Western blot analysis of recombinant GST-GSK-3beta protein (76kD), and extracts from HeLa and PC3 cells, using GSK-3alpha Antibody (left) and GSK-3beta Antibody (right).

Background

Glycogen synthase kinase-3 (GSK-3) was initially identified as an enzyme that regulates glycogen synthesis in response to insulin (1). GSK-3 is a ubiquitously expressed serine/threonine protein kinase that phosphorylates and inactivates glycogen synthase. GSK-3 is a critical downstream element of the PI3K/Akt cell survival pathway whose activity can be inhibited by Akt-mediated phosphorylation at Ser21 of GSK-3α and Ser9 of GSK-3β (2,3). GSK-3 has been implicated in the regulation of cell fate in Dictyostelium and is a component of the Wnt signaling pathway required for Drosophila, Xenopus, and mammalian development (4). GSK-3 has been shown to regulate cyclin D1 proteolysis and subcellular localization (5).

GSK-3alpha regulates the production of amyloid-beta peptides, a major component of the plaques that accumulate with progression of Alzheimer's disease. Administration of therapeutic concentrations of lithium, a GSK-3 inhibitor, attenuates amyloid-beta production by specifically inhibiting the cleavage of amyloid precursor protein (APP) by gamma secretase, blocking accumulation of amyloid-beta peptides in the brains of mice that overproduce APP (6).

  1. Welsh, G.I. et al. (1996) Trends Cell. Biol. 6, 274-279.
  2. Srivastava, A.K. and Pandey, S.K. (1998) Mol. Cell. Biochem. 182, 135-141.
  3. Cross, D.A. et al. (1995) Nature 378, 785-789.
  4. Nusse, R. (1997) Cell 89, 321-323.
  5. Diehl, J.A. et al. (1998) Genes Dev. 12, 3499-3511.
  6. Phiel, C.J. et al. (2003) Nature 423, 435-9.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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