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Validated All-in-One™ qPCR Primer for CAMK2G(NM_172170.5) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The product of this gene belongs to the Serine/Threonine protein kinase family, and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses. In mammalian cells the enzyme is composed of four different chains: alpha, beta, gamma, and delta. The product of this gene is a gamma chain. Six alternatively spliced variants that encode six different isoforms have been characterized to date. Additional alternative splice variants that encode different isoforms have been described, but their full-length nature has not been determined. [provided by RefSeq].
Gene References into function
- role in cell communication
- cloning, genomic structure and detection of variants in subjects with Type II diabetes
- measured differences in CaMKII binding affinities for CaM play a minor role in the autophosphorylation of the enzyme, largely dictated by autophosphorylation rate for alpha, beta, gamma and delta isoforms
- CaMKIIgamma is necessary to suppress MCAK depolymerase activity in vivo.
- A transgenic, constitutively active, Ca2+-independent form of CaMKgamma reduces positive selection of T cells by maintaining association of SHP-2 with the T cell receptor (TCR) complex, and halting TCR signaling.
- Amphetamine in a cell line induces a robust increase in cytosolic Ca2+ and concomitant activation of calcium/calmodulin-dependent protein kinase II (CaMKII).
- Significant cross-talk between calcium and retinoic acid signaling pathways regulates the differentiation of myeloid leukemia cells.
- insulin in the presence of Angiotensin II inhibits protein phosphatase-2A (PP-2A) and stimulates autonomous CaM kinase II activities and thus vascular smooth muscle migration
- study observed that CaMKIIgamma is the CaMK that is predominantly expressed in myeloid cells; this enzyme localizes to the promoter of RAR target genes, physically interacts with and phosphorylates RARalpha and inhibits RAR transcriptional activity
- CaMKIIgamma is a critical regulator of multiple signaling networks regulating the proliferation of myeloid leukemia cells
- In Turner yndrome, loss of voltage-dependent inactivation is an upstream initiating event for arrhythmia phenotypes that are ultimately dependent on CaMKII activation.
