CAMKII beta/CAMK2B Protein, Human, Recombinant (His)

Representative specific activity data for CAMK2β were obtained using different assay formats: - 5700 nmol/min/mg, determined by radioactive kinase assay - 2109 nmol/min/mg, determined by ADP-Glo kinase assay, corresponding to 5000 nmol/min/mg in the radioactive kinase assay Different lots may be tested using different assay methods; therefore, values obtained using different assay formats are not directly comparable.

CAMKII beta/CAMK2B Protein, Human, Recombinant (His) is expressed in Baculovirus-Insect Cells. The accession number is Q13554.

Human

Baculovirus-Insect Cells

>70% as determined by SDS-PAGE.

Calcium/calmodulin-dependent protein kinase II beta (CAMK2B) is a member of the serine/threonine protein kinase family and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. CaMKII is an important player in prostate cancer cells ability to escape apoptosis under androgen ablation and facilitate the progression of prostate cancer cells to an androgen independent state. As a multifunctional protein kinase, the loss of activity may play a critical role in initiating the changes leading to ischemia-induced cell death. CaMKII are found to be important for the functions of immune cells. CaMKII can be activated by TLR ligands, and in turn promotes both myeloid differentiating factor 88 and Toll/IL-1 receptor domain-containing adaptor protein-inducing IFN-beta-dependent inflammatory responses by directly activating TAK1 and IRF3. CAMKII has four subunit isoforms (alpha, beta, gamma, delta). It is possible that distinct isoforms of this chain have different cellular localizations and interact differently with calmodulin. The alpha- and beta-isoforms have narrow distributions restricted mainly to neuronal tissues, but the gamma- and delta-isoforms are ubiquitously expressed within neuronal and non-neuronal tissues. CAMK2B is important for controlling the direction of plasticity at the parallel fiber-Purkinje cell synapse. CaMK2 is involved in neuronal survival through the reorganization of the neuroarchitecture and that the regulation of this role is controlled at the level of gene expression. Because CaMK2B influences the expression of many neuroreceptors and influences neural outgrowth and pruning, its altered expression in the cerebral cortex in schizophrenia or depression may contribute to schizophrenia and depression.