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CAMK1G/CLICK III/CaMKIgamma  Protein

All CAMK1G Reagents

Expression host: Baculovirus-Insect Cells  
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CAMK1G/CLICK III/CaMKIgamma Summary & Protein Information

CAMK1G/CLICK III/CaMKIgamma Background

Gene Summary: This gene encodes a protein similar to calcium/calmodulin dependent protein kinase, however, its exact function is not known.
General information above from NCBI
Catalytic activity: ATP + a protein = ADP + a phosphoprotein.
Enzyme regulation: Activated by Ca(2+)/calmodulin. Binding of calmodulin is thought to result in a conformational change and leads to activation through phosphorylation by CAMKK1 (By similarity).
Domain: The autoinhibitory domain overlaps with the calmodulin binding region and interacts in the inactive folded state with the catalytic domain as a pseudosubstrate (By similarity).
Subcellular location: Cytoplasm (By similarity). Golgi apparatus membrane; Peripheral membrane protein (By similarity). Cell membrane; Peripheral membrane protein (By similarity).
Tissue specificity: Mainly expressed in brain with small amounts in skeletal muscles, kidney, spleen and liver. Strongly expressed in forebrain neocortex, striatum and limbic system.
Post-translational: May be prenylated on Cys-473 (By similarity).
Sequence similarity: Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. CaMK subfamily.
Contains 1 protein kinase domain.
General information above from UniProt

Calmodulin-Dependent Protein Kinase (CaM Kinase) is a kind of protein phosphorylate multiple downstream targets. Concentration of cytosolic calcium functions as a second messenger that mediates a wide range of cellular responses. Calcium binds to calcium binding proteins (calmodulin/CaM) and stimulates the activity of a variety of enzymes, including CaM kinases referred to as CaM-kinases (CaMKs), such as CaMKI, CaMKII, CaMKIV and CaMKK. Calmodulin-dependent protein kinase CL3/CaMKIγ is a memberane-anchored CaMK belonging to the CaM kinase family. Its C-terminal region is uniquely modified by two sequential lipidification steps: prenylation followed by a kinase-activity-regulated palmitoylation. These modifications are essential for CaMKIγ membrane anchoring and targeting into detergent-resistant lipid microdomains in the dendrites. It has been found that CaMKIγ critically contributed to BDNF-stimulated dendritic growth. Raft insertion of CaMKIγ specifically promoted dendritogenesis of cortical neurons by acting upstream of RacGEF STEF and Rac, both present in lipid rafts. Thus, CaMKIγ may represent a key element in the Ca2+-dependent and lipid-raft-delineated switch that turns on extrinsic activity-regulated dendrite formation in developing cortical neurons. 

CAMK1G/CLICK III/CaMKIgamma Alternative Name

CAMK1G/CLICK III/CaMKIgamma Related Studies

  • Davare MA, et al. (2009) Transient receptor potential canonical 5 channels activate Ca2+ / calmodulin kinase Igamma to promote axon formation in hippocampal neurons. J Neurosci. 29 (31): 9794-808.
  • Takemoto-Kimura S, et al. (2007) Regulation of dendritogenesis via a lipid-raft-associated Ca2+ / calmodulin - dependent protein kinase CLICK-III / CaMKIgamma. Neuron. 54 (5): 755-70.
  • Harrill JA, et al. (2010) Splice variant specific increase in Ca2+ / calmodulin-dependent protein kinase 1-gamma mRNA expression in response to acute pyrethroid exposure. J Biochem Mol Toxicol. 24 (3): 174-86.