DATASHEET
Host:
Rabbit
Target Protein:
GSK3 Alpha Ser21
Specificity:
This phosphorylation site is homologous to that of Ser21 in Mouse and Rat.
Modification Site:
Ser21
Clonality:
Polyclonal
Isotype:
IgG
Entrez Gene:
2931
Swiss Prot:
P49840
Source:
KLH conjugated synthetic phosphopeptide derived from human GSK3 Alpha around the phosphorylation site of Ser21
Purification:
Purified by Protein A.
Storage Buffer:
Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
Storage:
Store at -20°C for 12 months.
Background:
Constitutively active protein kinase that acts as a negative regulator in the hormonal control of glucose homeostasis, Wnt signaling and regulation of transcription factors and microtubules, by phosphorylating and inactivating glycogen synthase (GYS1 or GYS2), CTNNB1/beta-catenin, APC and AXIN1. Requires primed phosphorylation of the majority of its substrates. Contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence glycogen synthesis. Regulates glycogen metabolism in liver, but not in muscle. May also mediate the development of insulin resistance by regulating activation of transcription factors. In Wnt signaling, regulates the level and transcriptional activity of nuclear CTNNB1/beta-catenin. Facilitates amyloid precursor protein (APP) processing and the generation of APP-derived amyloid plaques found in Alzheimer disease. May be involved in the regulation of replication in pancreatic beta-cells. Is necessary for the establishment of neuronal polarity and axon outgrowth. Through phosphorylation of the anti-apoptotic protein MCL1, may control cell apoptosis in response to growth factors deprivation.
Conjugation:
Biotin
Excitation/ Emission:
N/A
Size:
100ul
Concentration:
1ug/ul
Applications:
WB(1:300-5000)
ELISA(1:500-1000)
IHC-P(1:200-400)
IHC-F(1:100-500)
54
Mouse
Rat
Predicted Cross Reactive Species:
Human
Dog
Pig
Horse
Chicken
For research use only. Not intended for diagnostic or therapeutic use.