CAMKI Protein, Human, Recombinant

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.

Pack Size	Availability	Price/USD	Quantity
50 μg	5 days	$ 398.00

Description

Species	Human
Expression System	E. coli
Tag	Tag Free
Accession Number	B0YIY3
Synonyms	calcium/calmodulin-dependent protein kinase I, CAMKI
Construction	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.
Protein Purity	> 85 % as determined by SDS-PAGE
Molecular Weight	41.5 kDa (predicted)

Endotoxin	Please contact us for more information.
Formulation	Supplied as sterile 50mM Tirs, 150mM NaCl, 10% glycerol, pH 7.5. Please contact us for any concerns or special requirements. Please refer to the specific buffer information in the hard copy of CoA.
Reconstitution	A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.
Stability & Storage	Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Shipping	Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice. Shipment made at ambient temperature may seriously affect the activity of the ordered products.
Research Background	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.