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Facts about Glycogen synthase kinase-3 alpha.
Contributes to insulin regulation of glycogen synthesis by phosphorylating and inhibiting GYS1 activity and hence metabolic synthesis. May also mediate the progression of insulin resistance by regulating activation of transcription factors.
Human | |
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Gene Name: | GSK3A |
Uniprot: | P49840 |
Entrez: | 2931 |
Belongs to: |
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protein kinase superfamily |
DKFZp686D0638; EC 2.7.11; EC 2.7.11.26; glycogen synthase kinase 3 alpha; glycogen synthase kinase-3 alpha; GSK3 alpha; GSK-3 alpha; GSK3A
Mass (kDA):
50.981 kDA
Human | |
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Location: | 19q13.2 |
Sequence: | 19; NC_000019.10 (42230186..42243330, complement) |
High-affinity primary antibodies are ideal for a wide variety of applications, including immunohistochemistry, Western blotting, and ELISA. Boster offers antibodies that have been validated on multiple platforms, including Western Blotting and Immunohistochemistry. Boster antibodies have been thoroughly validated for research and education. They are available for both human and murine applications.
The high-affinity primary antibodies were generated using a GSK3A marker and a well-coated 50 ml phosphoS9 peptide. These antibodies show clear parenchymal and somatodendritic staining. Scale bars = 50 mm. These antibodies can also be used to identify phosphoS9GSK3b protein within cell cultures.
GSK3b immunoprecipitation requires high-affinity antibody. These antibodies include 12B2 & 15C2. These primary antibodies recognize npS9 GSK3b and npS21. They immunoprecipitate GSK3b a/b protein. The phospho-S9 and 15C2 antibodies bind to both peptides, which make them suitable for western blotting.
Two high-affinity primary antibody beads were used to conjugate the two high-affinity primary antibodies. Ms IgG served as the non-immune control. The non-immune mouse IgG did not immunoprecipitate GSK3a and b. The two antibodies were then diluted in 2% goat sera and incubated overnight at 40°C. The second step involved the addition of goat anti-mouse HRP conjugated antibody at a 1:5,000 dilution. After incubating at 4°C for 2 h and allowing to dry, the final step involved DAPI anti-mouse counterstaining the membrane.
The two primary antibodies used to detect GSK3b/a are 12B2 and 15C2, both of which stain npS9/21 recombinant proteins. These antibodies stained npS9/21 rat brain tissue sections. Both antibodies were highly specific and showed high levels of specificity for their targets. However the 12B2 antibody produced a stronger staining signal and more specific staining.
The Ser9-phosphorylated GSK-3b was used to produce the antibody. Additionally, the antibodies were used to identify GSK-3b in a high affinity IB assay. Chemicon supplied the latter. It was combined with secondary antibodies to visualize the immunoreactive proteins in the membrane. These results were then compared to those obtained by conventional antibodies using other methods.
High-affinity antibodies against the GSK3A mark are extremely useful in identifying phosphorylated cells in tissue and cell culture. These antibodies are also able to detect a wide range of proteins that play crucial roles in the brain, including the one associated with Alzheimer's. GSK-3 modulators have also been shown to be effective in treating central nervous system diseases. GSK-3 kinase inhibitors can inhibit the phosphorylation and growth of certain proteins in the brain.
GSK3A is a transcription factor that regulates many developmental processes in the brain including neurogenesis, migration and synaptic plasticity. Signaling pathways controlling GSK3 activity include wingless (Wnt) proteins and GPCRs, which activate the b-arrestin receptor. These signaling pathways could be useful in helping researchers identify the causes of diseases.
Healthy individuals have neurons that express the GSK3A protein. Its overactivity is associated with the destabilization of the MT in dendrites and axons. It may also affect the rate of microtubules, a key component of the major cellular compartments of neurons. This gene is involved in both LTP (low-level) and LTD (high-level) development of neuronal cells.
GSK3 regulation is proposed by two forms. However, the exact roles of GSK3a and GSK3b remain unknown. While these markers are useful for education, researchers still don't understand which endogenous targets of differential control. The GSK3A genes are still not well understood. This may explain why it is not widely utilized.
This gene is attractive for translational research because of its potential to target neural defect by inhibiting GSK3. It is crucial for both basic and translational science to identify the major mediator of neural defects. GSK3 inhibitor has been shown to be a potential treatment for a variety neurologic conditions. Its high level in complexity and wide regulatory coverage make it an ideal candidate of translational research.
This gene is a substrate of the GSK3 protein MT-associated protein 1B. CLASP regulates MT dynamics and configuration within the growth cone. GSK3 may coordinate MT dynamic and configuration with CLASP. MT-associated genes may act as a signaling device. Molecular interactions between GSK3 and CLASP may help in identifying diseases that involve this protein. Regulating axon development is facilitated by the GSK3 - CLASP-MT triad.
It is unknown which gene is the primary target for Alzheimer's. GSK3 beta has been identified as a possible treatment target for FRAXA by many research groups. GSK3 Alpha is less toxic than GSK3 beta and may have fewer adverse effects. Some researchers believe that lithium could be a promising inhibitor to the GSK3A markers. The enzyme is necessary to promote efficient axon proliferation.
PMID: 10868943 by Nikoulina S.E., et al. Potential role of glycogen synthase kinase-3 in skeletal muscle insulin resistance of type 2 diabetes.
PMID: 12761548 by Phiel C.J., et al. GSK-3alpha regulates production of Alzheimer's disease amyloid-beta peptides.
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