Calcium/calmodulin-dependent protein kinase II beta
CAMK2B Protein, Recombinant
|Molecule||Species||Description //For Detailed Info. and Price------CLICK!||Cat. No|
|CAMK2B||Human||CAMK2B Protein, Recombinant, with GST Tag||11738-H20B|
CAMK2B Related Areas
Signal Transduction>>Protein Kinase>>Intracellular Kinase>>CAMK2B
CAMK2B Alternative Names
CAMK2B, CAM2, CAMK2, CAMKB, MGC29528 [Homo sapiens]
Camk2b, RP23-340E18.5, Camk2d, MGC90738 [Mus musculus]
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.
CAMK2B Related Studies
- Hiestand DM, et al. (1992)Calcium/calmodulin dependent protein kinase II mRNA in the gerbil brain after cerebral ischemia. Neurosci Lett. 144(1-2): 75-8.
- Shackelford DA, et al. (1995) Effect of cerebral ischemia on calcium/calmodulin-dependent protein kinase II activity and phosphorylation. J Cereb Blood Flow Metab. 15(3): 450-61.
- Walikonis R S, et al. (2001) Densin-180 forms a ternary complex with the (alpha)-subunit of Ca2+/calmodulin-dependent protein kinase II and (alpha)-actinin. J. Neurosci. (United States). 21 (2): 423-33.
- Shimazaki A, et al. (2006) Calcium/calmodulin-dependent protein kinase II in human articular chondrocytes. Biorheology. 43(3-4): 223-33.
- Novak G, et al. (2006) Increased expression of calcium/calmodulin-dependent protein kinase IIbeta in frontal cortex in schizophrenia and depression. Synapse. 59(1): 61-8.
- Rokhlin OW, et al. (2007) Calcium/calmodulin-dependent kinase II plays an important role in prostate cancer cell survival. Cancer Biol Ther. 6(5): 732-42.
- Liu X, et al. (2008) CaMKII promotes TLR-triggered proinflammatory cytokine and type I interferon production by directly binding and activating TAK1 and IRF3 in macrophages. Blood. 112(13): 4961-70.
- van Woerden GM, et al. (2009) betaCaMKII controls the direction of plasticity at parallel fiber-Purkinje cell synapses. Nat Neurosci. 2009 Jul;12(7): 823-5. .