Anti-phospho-CAMK2A/2B (Thr286)(C11-65R)
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Description :Rabbit Polyclonal Antibody
Species :Rabbit
Tag :
Expression System:
Sequence :
Specificity :Recognizes the CAM2KA/2B protein phosphorylated at threonine 286
Cited Applications :WB
Cross Reactivity :Human, Mouse, Rat and Xenopus
Host :Rabbit, IgG
Immunogen :Synthetic phospho-peptide corresponding to amino acid residues surrounding Thr286 conjugated to KLH
Purification :Affinity Chromatography
Stability :Store at 4oC (add 0.1% NaN3) for several months, and at -20oC for longer periods. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Sample Data :Western blot of rat brain lysate showing specific immunolabeling of the ~50kDa CAMK2A and the ~60kDa CAMK2B phosphorylated at Thr286 (Control). The phosphospecificity of this labeling is shown in the second lane (lambda-phosphatase: lambda-Ptase). The blot is identical to the control except that it was incubated in lambda-Ptase (1200 units for 30 min) before being exposed to the Anti-phospho-CAMK2A/2B (Thr286). The immunolabeling is completely eliminated by treatment with lambda-Ptase.
Scientific Background :Ca2+/calmodulin-dependent protein kinase II (CAMK2) is a multi-functional calcium and calmodulin-dependent serine/threonine kinase that mediates cellular responses to a wide variety of intercellular signals (1). CAMK2 is abundant in the brain and has been shown to regulate diverse cellular functions including synaptic plasticity, neurotransmitter synthesis and release, gene expression, ion channel function, carbohydrate metabolism, cytoskeletal function, and Ca2+-homeostasis (2,3). Phosphorylation of Thr286 produces an autonomously active form of CAMK2 (4). Autophosphorylation of Thr305 inhibits the activity CAMK2, which leads to reduced localization to the postsynaptic density and consequently reduced neuronal plasticity and capacity for learning (5).
References :
1. Kennedy, M B.: Signal transduction molecules at the glutamatergic postsynaptic membrane. 1998 Brain Res Rev 1998 26:243-257.
2. Gleason, M R. et al: Translocation of CaM kinase II to synaptic sites in vivo. Nature Neurosci 2003 6:217-218.
3. Hudmon, A. et al: Neuronal Ca2+/calmodulin-dependent protein kinase II: The role of structure and autoregulation in cellular function. Annu Rev Biochem 2002 71:473-510.
4. Meng, F J. et al: Autophosphorylated calcium/calmodulin-dependent protein kinase IIa (CaMKIIa) reversibly targets to and phosphorylates N-methyl-D-aspartate receptor subunit 2B (NR2B) in cerebral ischemia and reperfusion in hippocampus of rats. Brain Res 2003 967:161-169.
5. Elgersma, Y. et al: Inhibitory autophosphorylation of CaMKII controls PSD association, plasticity, and learning. Neuron 200236:493-505.
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Research Areas :Cardiovascular Disease, ERK/MAPK Pathway, Neurobiology, PKA/PKC Pathway, Ser/Thr Kinases, Neurobiology, Cardiovascular Disease, ERK/MAPK Pathway, PKA/PKC Pathway, Ser/Thr Kinases