Product Description
GSK3A Antibody | 63-404 | ProSci
Host: Rabbit
Reactivity: Human
Homology: Predicted species reactivity based on immunogen sequence: Mouse, Rat
Immunogen: This GSK3A antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from amino acid residues surrounding S21 of human GSK3A.
Research Area: Cell Cycle, Neuroscience, Signal Transduction
Tested Application: WB
Application: For WB starting dilution is: 1:1000
Specificiy: N/A
Positive Control 1: N/A
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: 51 kDa
Validation: N/A
Isoform: N/A
Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.
Clonality: Polyclonal
Clone: N/A
Isotype: Rabbit Ig
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.
Concentration: batch dependent
Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Alternate Name: Glycogen synthase kinase-3 alpha, GSK-3 alpha, Serine/threonine-protein kinase GSK3A, GSK3A
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: Glycogen synthase kinase 3-alpha (GSK3A) is a multifunctional protein serine kinase implicated in the control of several regulatory proteins including glycogen synthase and transcription factors. It also plays a role in the WNT and PI3K signaling pathways. Under resting conditions GSK3A and its homologs are highly phosphorylated at tyr279 in the phosphorylation loop. Constitutive phosphorylation of this tyrosine is important for kinase activity. Dephosphorylation of tyr279 after mitogen activation is accompanied by kinase inactivation. PKA as well as PI3K-activated PKB inactivate GSK3A by phosphorylation at ser21. Lysophosphatidic acid primarily utilizes a PKC-dependent pathway to modulate GSK3 and certain growth factors (e.g., PDGFB) , which control GSK3 mainly through PIK3-PKB, are able to regulate GSK3 through an alternative, redundant PKC pathway. In mice expressing familial AD-associated mutations in APP and PSEN1, lithium reduced the levels of beta-amyloid peptides GSK3A also phosphorylates the tau protein, the principal component of neurofibrillary tangles in AD, and suggested that inhibition of GSK3A may offer a new therapeutic approach to AD.