CAMK1G, Active recombinant protein
CAMK1g, Calcium/calmodulin-dependent protein kinase type I gamma
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q96NX5 |
---|---|
Concentration | 0.1 |
Calculated MW | 60.0 kDa |
Gene ID | 57172 |
---|---|
Gene Symbol | CAMK1G |
Other Names | CAMK1g, Calcium/calmodulin-dependent protein kinase type I gamma, CaMK-like CREB kinase III |
Source | Baculovirus (Sf9 insect cells) |
Assay&Purity | SDS-PAGE; ≥90% |
Assay2&Purity2 | HPLC; |
Recombinant | Yes |
Format | Liquid |
Storage | -80°C; Recombinant protein in storage buffer (50 mM Tris-HCl, pH 7.5, 150 mM NaCl, 0.25 mM DTT, 0.1 mM EGTA, 0.1 mM EDTA, 0.1 mM PMSF, 25% glycerol). |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
info@abcepta.com, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
Background
CLICK-III/CaMKIG is a novel membrane-anchored neuronal Ca2+/calmodulin-dependent protein kinase (CaMK), an isoform of the CaMKI family with an extended C-terminal domain ending with CAAX motif (where AA is aliphatic acid). As expected from the similarity of its kinase domain with the other CaMKI isoforms, full activation of CLICK-III/CaMKIG required both Ca(2+)/CaM and phosphorylation by CaMKK. Ca(2+)/cAMP-response element-binding protein (CREB) was a good substrate for CLICK-III/CaMKIG, at least in vitro. Interestingly enough, CLICK-III/CaMKIG transcripts were most abundant in neurons, with the highest levels in limited nuclei such as the central nucleus of the amygdala (CeA) and the ventromedial hypothalamus. Consistent with the presence of the CAAX motif, CLICK-III/CaMKIG was found to be anchored to various membrane compartments, especially to Golgi and plasma membranes. Both point mutation in the CAAX motif and treatment with compactin, a HMG-CoA reductase inhibitor, disrupted such membrane localization, suggesting that membrane localization of CLICK-III/CaMKIG occurred in a prenylation-dependent way. These findings provide a novel mechanism by which neuronal CaMK activity could be targeted to specific membrane compartments.
If you have used an Abcepta product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at tech@abcepta.com.