GSK3A (phospho S21) polyclonal antibody
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Western Blot (Cell lysate)
Western blot using GSK3A (phospho S21) polyclonal antibody (Cat # PAB10054) shows detection of a 52 KDa band corresponding to human GSK3A in various human derived 293T cell extracts.
Cells were serum starved for 24 h.
Lane 1 : control, Lane 2: treated with IGF-1 (100 ng/mL) for 20 min, Lane 3 : pre-treated with 10 uM PI3K inhibitor and treated with IGF-1 (100 ng/mL) for 20 min.
Lane 1 shows some baseline GSK3A reactivity that is intensified upon stimulation (lane2) and diminished when aninhibitor is added (Lane 3).
Approximately 20 ug of lysate was run on a SDS-PAGE and transferred onto nitrocel followed by reaction with a 1:1,000 dilution of anti-GSK3A antibody.
Signal was detected using standard techniques.
Personal communication, Angela Carter, Experimental Therapeutics, Ontario Cancer Inst, Toronto, Canada.
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Specification
Product Description
Rabbit polyclonal antibody raised against synthetic phosphopeptide of GSK3A.
Immunogen
Synthetic phosphopeptide corresponding to residues surrounding S21 of human GSK3A.
Host
Rabbit
Reactivity
Chimpanzee, Human, Rat
Specificity
This phospho specific polyclonal antibody reacts with phosphorylated pS21 of human GSK3A. Reactivity with non-phosphorylated human GSK3A is minimal.
Form
Liquid
Quality Control Testing
Antibody Reactive Against Synthetic Peptide.
Recommend Usage
ELISA (1:2000-1:10000)
Western Blot (1:500-1:3000)
The optimal working dilution should be determined by the end user.Storage Buffer
In 20 mM KH2PO4, 150 mM NaCl, pH 7.2 (0.01% sodium azide)
Storage Instruction
Store at 4°C. For long term storage store at -20°C.
Aliquot to avoid repeated freezing and thawing.Note
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
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Applications
Western Blot (Cell lysate)
Western blot using GSK3A (phospho S21) polyclonal antibody (Cat # PAB10054) shows detection of a 52 KDa band corresponding to human GSK3A in various human derived 293T cell extracts.
Cells were serum starved for 24 h.
Lane 1 : control, Lane 2: treated with IGF-1 (100 ng/mL) for 20 min, Lane 3 : pre-treated with 10 uM PI3K inhibitor and treated with IGF-1 (100 ng/mL) for 20 min.
Lane 1 shows some baseline GSK3A reactivity that is intensified upon stimulation (lane2) and diminished when aninhibitor is added (Lane 3).
Approximately 20 ug of lysate was run on a SDS-PAGE and transferred onto nitrocel followed by reaction with a 1:1,000 dilution of anti-GSK3A antibody.
Signal was detected using standard techniques.
Personal communication, Angela Carter, Experimental Therapeutics, Ontario Cancer Inst, Toronto, Canada.Immunofluorescence
Enzyme-linked Immunoabsorbent Assay
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Gene Info — GSK3A
Entrez GeneID
2931Protein Accession#
P49840;NP_063937Gene Name
GSK3A
Gene Alias
DKFZp686D0638
Gene Description
glycogen synthase kinase 3 alpha
Omim ID
606784Gene Ontology
HyperlinkGene Summary
Glycogen synthase kinase 3-alpha (GSK3A; EC {2.7.1.37}) is a multifunctional protein serine kinase, homologous to Drosophila 'shaggy' (zeste-white3) and implicated in the control of several regulatory proteins including glycogen synthase (see GYS1, {138570}) and transcription factors (e.g., JUN, {165160}). It also plays a role in the WNT ({164820}) and PI3K (see PIK3CG, {601232}) signaling pathways (see review by {1:Ali et al. (2001)}).[supplied by OMIM
Other Designations
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Publication Reference
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The primary defect in glycogen synthase activity is not based on increased glycogen synthase kinase-3alpha activity in diabetic myotubes.
Gaster M, Brusgaard K, Handberg A, Højlund K, Wojtaszewski JF, Beck-Nielsen H.
Biochemical and Biophysical Research Communications 2004 Jul; 319(4):1235.
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Regulation of glycogen synthase kinase 3 in human platelets: a possible role in platelet function?
Barry FA, Graham GJ, Fry MJ, Gibbins JM.
FEBS Letters 2003 Oct; 553(1-2):173.
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Inhibition of glycogen synthase kinase 3 improves insulin action and glucose metabolism in human skeletal muscle.
Nikoulina SE, Ciaraldi TP, Mudaliar S, Carter L, Johnson K, Henry RR.
Diabetes 2002 Jul; 51(7):2190.
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The primary defect in glycogen synthase activity is not based on increased glycogen synthase kinase-3alpha activity in diabetic myotubes.
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