CAMK1D (Protein|Antibody|cDNA Clone|ELISA Kit)

All CAMK1D reagents are produced in house and quality controlled, including 15 CAMK1D Gene, 1 CAMK1D Lysate, 1 CAMK1D Protein, 1 CAMK1D qPCR. All CAMK1D reagents are ready to use.

Recombinant CAMK1D proteins are expressed by Baculovirus-Insect Cells with fusion tags as N-GST.

CAMK1D cDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each CAMK1D of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.

CAMK1D Protein (1)


CAMK1D Protein, Human, Recombinant (GST Tag)


Expression host: Baculovirus-Insect Cells

Human CAMK1D/CKLiK Protein 9068

CAMK1D cDNA Clone (15)


CAMK1D qPCR Primer (1)

CAMK1D Lysate (1)

Calcium/calmodulin-dependent protein kinase or CaM kinases are serine/threonine-specific protein kinases that 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. In neurons, this property is important for the induction of synaptic plasticity. Pharmacological inhibition of CaM kinases II blocks the induction of long-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 the protein kinase superfamily and CaMK subfamily. It contains one protein 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.