Research Highlights: In Brief...

Exploring CAMKII associations with calcium L-type channels to regulate physiological changes in tissues

SA Abiria, RJ Colbran (2010). CaMKII associates with CaV1.2 L-type calcium channels via selected beta subunits to enhance regulatory phosphorylation. J Neurochem. 112 (1): 150-61.

Voltage activated L-type calcium channels (LTCCs) are known to generate Ca2+ signals important for numerous physiological process such as muscle contraction, neurotransmitters, neuronal plasticity and others. In particular the calcium/calmodulin dependant kinase II (CaMKII) protein has been shown to augment the Ca2+ signals in response to growth factors or hormones. Excessive Cav1.2LTCC activity can produce a variety of pathological symptoms including cardiac arrhythmias, multi-organ human genetic disorder and cases of parkinsons disease in animal models. While CAMKII facilitates LTCC activity physiologically, the molecular basis of CAMKII interactions and its modulation of LTCCs is yet to be understood. The authors of this paper transfected HEK293 cells from the forebrain of 7-8week old rats to explore the role of β subunits in targeting CAMKII to LTCC α1 subunits. They found that CAMKII co-immunoprecipitates with forebrain LTCCs that contain Cav1.2α1 and β1 or β2 subunits, but not LTCC complexes containing b4 subunits. These targeted mechanistic interactions between CAMKII and LTCCs will be crucial in providing insights into our understanding of physiological and pathological process in different tissues.