The specific activity was determined to be ＞70 nmol/min/mg using Autocamtide-2 synthetic peptide (KKALRRQETVDAL-amide) as substrate.

CAMKI Protein, Human, Recombinant is expressed in E. coli expression system. The predicted molecular weight is 41.5 kDa and the accession number is B0YIY3.

Human

E. coli

CAMKI,calcium/calmodulin-dependent protein kinase I

A DNA sequence encoding the human CAMK1 (NP_003647.1) (Leu 2-Leu 370) was expressed and purified, with two additional amino acids (Gly & Pro) at the N-terminus. Predicted N terminal: Gly

> 85 % as determined by SDS-PAGE

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store the product under sterile conditions at -20°C to -80°C. Samples are stable for up to 12 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

Calcium/calmodulin-dependent protein kinase orCaM kinases are serine/threonine-specific protein kinasesthat are primarily regulated by the Calcium/calmodulin complex. These kinases show a memory effect on activation. CaM kinases activity can outlast the intracellular calcium transient that is needed to activate it. Inneurons, this property is important for the induction of synaptic plasticity. Pharmacological inhibition of CaM kinases II blocks the induction oflong-term potentiation. Upon activation, CaM kinases II phosphorylates postsynaptic glutamate receptors and changes the electrical properties of the synapse. Calcium/calmodulin-dependent protein kinase type 1D, also known as CaM kinase I delta, CaM kinase ID, CaMKI-like protein kinase, CKLiK and CAMK1D, is a member of theprotein kinase superfamily and CaMK subfamily. It contains oneprotein kinase domain. CAMK1D is broadly expressed. It is highly and mostly expressed in polymorphonuclear leukocytes (neutrophilic and eosinophilic granulocytes) while little or no expression is observed in monocytes and lymphocytes. Engineered overexpression of CAMK1D in non-tumorigenic breast epithelial cells led to increased cell proliferation, and molecular and phenotypic alterations indicative of epithelial-mesenchymal transition (EMT), including loss of cell-cell adhesions and increased cell migration and invasion. CAMK1D is a potential therapeutic target with particular relevance to clinically unfavorable basal-like tumors.