Aliases for CAMK2G Gene
External Ids for CAMK2G Gene
Previous HGNC Symbols for CAMK2G Gene
Previous GeneCards Identifiers for CAMK2G Gene
The product of this gene is one of the four subunits of an enzyme which belongs to the serine/threonine protein kinase family, and to the Ca(2+)/calmodulin-dependent protein kinase subfamily. Calcium signaling is crucial for several aspects of plasticity at glutamatergic synapses. In mammalian cells the enzyme is composed of four different chains: alpha, beta, gamma, and delta. The product of this gene is a gamma chain. Many alternatively spliced transcripts encoding different isoforms have been described but the full-length nature of all the variants has not been determined.[provided by RefSeq, Mar 2011]
GeneCards Summary for CAMK2G Gene
CAMK2G (Calcium/Calmodulin-Dependent Protein Kinase II Gamma) is a Protein Coding gene. Diseases associated with CAMK2G include occlusion precerebral artery and usher syndrome, type 1f. Among its related pathways are Immune System and Signaling by GPCR. GO annotations related to this gene include protein homodimerization activity and protein kinase activity. An important paralog of this gene is DCX.
UniProtKB/Swiss-Prot for CAMK2G Gene
Calcium/calmodulin-dependent protein kinase that functions autonomously after Ca(2+)/calmodulin-binding and autophosphorylation, and is involved in sarcoplsamic reticulum Ca(2+) transport in skeletal muscle and may function in dendritic spine and synapse formation and neuronal plasticity. In slow-twitch muscles, is involved in regulation of sarcoplasmic reticulum (SR) Ca(2+) transport and in fast-twitch muscle participates in the control of Ca(2+) release from the SR through phosphorylation of the ryanodine receptor-coupling factor triadin. In neurons, may participate in the promotion of dendritic spine and synapse formation and maintenance of synaptic plasticity which enables long-term potentiation (LTP) and hippocampus-dependent learning.
Calmodulin-dependent kinases (CaMK) are a family of serine/threonine kinases that mediate many of the second messenger effects of Ca2+. At basal Ca2+ levels, CaMKs are maintained in a dormant state through autoinhibition, which can be relieved by increases in Ca2+ levels.