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

CAMK1D Protein, Human, Recombinant (GST) is expressed in Baculovirus insect cells with GST tag. The predicted molecular weight is 69 kDa and the accession number is Q8IU85-1.

Human

Baculovirus Insect Cells

CKLiK,CaMKID,CaM-K1,calcium/calmodulin-dependent protein kinase ID

A DNA sequence encoding the human CAMK1D (NP_705718.1) (Met 1-Lys 385) was fused with the GST tag at the N-terminus. Predicted N terminal: Met

> 80 % 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.