C9869
CAMK2α, active, GST tagged human
PRECISIO® Kinase, recombinant, expressed in baculovirus infected Sf9 cells, ≥70% (SDS-PAGE), buffered aqueous glycerol solution
Sinônimo(s):
CAMKA, KIAA0968
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About This Item
recombinante
expressed in baculovirus infected Sf9 cells
Nível de qualidade
linha de produto
PRECISIO® Kinase
Ensaio
≥70% (SDS-PAGE)
Formulário
buffered aqueous glycerol solution
atividade específica
218-294 nmol/min·mg
peso molecular
~74 kDa
nº de adesão UniProt
Condições de expedição
dry ice
temperatura de armazenamento
−70°C
Informações sobre genes
human ... CAMK2A(815)
Ações bioquímicas/fisiológicas
CAMK2α is a ser/thr protein kinase that is a member of the Ca2+/calmodulin-dependent protein kinase family. CAMK2α is abundant in the brain as a major constituent of the postsynaptic density and is required for hippocampal long-term potentiation (LTP) and spatial learning. In addition to its CaCa2+/calmodulin-dependent activity, CAMK2α can undergo autophosphorylation, resulting in Ca2+/calmodulin-independent activity. The protein level of CAMK2α fluctuates during neuronal activity in cultured rat pup hippocampal neurons. The levels of CAMK2α increased with heightened neuronal activity.
forma física
Supplied in 50 mM Tris-HCl, pH 7.5, with 150 mM NaCl, 0.2 5mM DTT, 0.1 mM EGTA, 0.1 mM EDTA, 0.1 mM PMSF, and 25% glycerol.
Informações legais
PRECISIO is a registered trademark of Merck KGaA, Darmstadt, Germany
Código de classe de armazenamento
10 - Combustible liquids
Classe de risco de água (WGK)
WGK 1
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
Equipamento de proteção individual
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
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Neuron, 36(6), 1103-1114 (2002-12-24)
We show that alpha and betaCaMKII are inversely regulated by activity in hippocampal neurons in culture: the alpha/beta ratio shifts toward alpha during increased activity and beta during decreased activity. The swing in ratio is approximately 5-fold and may help
Science (New York, N.Y.), 257(5067), 206-211 (1992-07-10)
Although long-term potentiation (LTP) has been studied as the mechanism for hippocampus-dependent learning and memory, evidence for this hypothesis is still incomplete. The mice with a mutation in the alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII), a synaptic protein enriched in the hippocampus
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