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C9869

Sigma-Aldrich

CAMK2α, active, GST tagged human

PRECISIO® Kinase, recombinant, expressed in baculovirus infected Sf9 cells, ≥70% (SDS-PAGE), buffered aqueous glycerol solution

Synonym(s):

CAMKA, KIAA0968

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About This Item

UNSPSC Code:
12352200
NACRES:
NA.32

recombinant

expressed in baculovirus infected Sf9 cells

Quality Level

200

product line

PRECISIO® Kinase

assay

≥70% (SDS-PAGE)

form

buffered aqueous glycerol solution

specific activity

218-294 nmol/min·mg

mol wt

~74 kDa

UniProt accession no.

Q9UQM7

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... CAMK2A(815)

Biochem/physiol Actions

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.

Physical form

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.

Legal Information

PRECISIO is a registered trademark of Merck KGaA, Darmstadt, Germany

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)

Certificates of Analysis (COA)

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Tara C Thiagarajan et al.
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
A J Silva et al.
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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