Mouse Anti-GSK-3α-UNLB

Cat. No.
10900-01  
Size
0.1 mg  
Price (USD)
$315.00 
Clone SBGSK3a1
Isotype Mouse (BALB/c) IgG2aκ
Isotype Control Mouse IgG2a-UNLB
Immunogen Recombinant N-terminal GSK-3α
Specificity Human/Mouse GSK-3α
Alternalte Name(s) Glycogen synthase kinase-3 alpha
Description Glycogen synthase kinase-3 (GSK-3) is a protein serine kinase that phosphorylates glycogen synthase and thereby inactivates it. Insulin stimulates the dephosphorylation of glycogen synthase at the sites phosphorylated by GSK-3 and subsequently inhibits GSK-3 acutely leading to the stimulation of glycogen synthesis. GSK-3 signaling is performed by two isoforms, GSK-3α and GSK-3β. The two isoforms share 97% sequence similarity within their catalytic domains. GSK-3 has also been shown to play a role in protein synthesis, cell adhesion, cell proliferation, cell differentiation, microtubule dynamics, and cell motility.
Format/Conjugate UNLB (Unconjugated)
Buffer Formulation Borate buffered saline, pH 8.2
Concentration 0.5 mg/mL
Volume 0.2 mL
Storage & Handling 2-8°C
Please refer to product specific SDS
Applications
Applications for relevant formats of this clone include -
Western Blot – Quality tested 1
Recommended Dilutions Please refer to product specific Technical Bulletin
RRID AB_2794515
  • Total cell lysates from Jurkat cells were resolved by electrophoresis, transferred to PVDF membrane, and probed with Mouse Anti-GSK-3α-UNLB (SB Cat. No. 10900-01). Proteins were visualized using Goat Anti-Mouse IgG, Human ads-HRP (SB Cat. No. 1030-05) secondary antibody and chemiluminescent detection.

Total cell lysates from Jurkat cells were resolved by electrophoresis, transferred to PVDF membrane, and probed with Mouse Anti-GSK-3α-UNLB (SB Cat. No. 10900-01). Proteins were visualized using Goat Anti-Mouse IgG, Human ads-HRP (SB Cat. No. 1030-05) secondary antibody and chemiluminescent detection.
 
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References
1. Sun M, Song L, Li Y, Zhou T, Jope RS. Identification of an antiapoptotic protein complex at death receptors. Cell Death Differ. 2008;15:1887-1900. (WB)