Anti-CaMKII antibody [EPR6685(B)] - BSA and Azide free

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

CaMKII also known as calcium/calmodulin-dependent protein kinase II is an enzyme functioning critically in cellular signaling. It consists of multiple isoforms including alpha beta gamma and delta with the delta isoform Delta 1829 frequently highlighted for its specific roles. The molecular weight of CaMKII is approximately 50 to 60 kDa varying slightly between isoforms. CaMKII is widely expressed in the brain but is also present in the heart skeletal muscle and other tissues. Its structure includes a catalytic domain regulatory segment and association domain which allows auto-regulation and interaction with other molecules.

Biological function summary

CaMKII plays a vital role in cellular processes such as learning memory and muscle contraction. It can form a complex structure involving multiple subunits which allows for its unique ability to signal in response to calcium influx and calmodulin binding. This causes autophosphorylation of CaMKII allowing it to remain active even when calcium levels diminish. This property makes CaMKII essential for long-term potentiation (LTP) in neuron synapses influencing cognitive functions deeply.

Pathways

CaMKII is an important component of both the calcium signaling and synaptic plasticity pathways. In the calcium signaling pathway CaMKII interacts with calmodulin and other kinases to modulate calcium entry and signaling. In synaptic plasticity CaMKII works closely with proteins like NMDA receptors which regulate synaptic strength and modulation essential for encoding learning and memory. These interactions highlight its significance as a mediator between signaling cascades and cellular responses.

Associated diseases and disorders

Abnormal regulation or expression of CaMKII links to Alzheimer's disease and cardiac arrhythmias. In Alzheimer's the dysregulation of CaMKII affects synaptic integrity and memory formation involving interaction with beta-amyloid plaques. In cardiac arrhythmias CaMKII dysfunction leads to improper cardiac muscle contractions often linked to the protein phospholamban. These associations highlight the clinical relevance of CaMKII in addressing and understanding mechanisms underpinning these diseases.