Abcam, ab94251, CaMKII alpha overexpression 293T lysate (whole cell)

Size: 100µL
CaMKII alpha overexpression 293T lysate (whole cell) suitable for WB. View our extensive range of validated lysates from normal and diseased human, mouse and rat tissue.
Key facts
Species or organism:Human,
Form:LiquidSee storage information

Product details:
ab94251 is a 293T cell transfected lysate in which Human CaMKII alpha has been transiently over-expressed using a pCMV-CaMKII alpha plasmid. The lysate is provided in 1X Sample Buffer.

Properties and Storage Information:
Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
CaMKII alpha also known as CAMK2A is an enzyme belonging to the CaMK kinase family. This protein is a calcium/calmodulin-dependent protein kinase and exhibits a molecular weight of approximately 50 to 60 kDa. CaMKII alpha is primarily expressed in the brain specifically in the hippocampus and other regions involved in synaptic activity. Due to its role as a serine/threonine kinase CaMKII alpha is significant in phosphorylating various substrates as part of cellular signaling.
Biological function summary
CaMKII alpha plays an important role in synaptic plasticity a process vital for learning and memory. The protein acts as an important component of the postsynaptic density complex where it interacts with other proteins to regulate synaptic strength. When calcium levels rise CaMKII alpha is activated through phosphorylation altering its conformation and allowing interactions with downstream substrates. This regulatory mechanism highlights its role in modulating neurotransmission synaptic potentiation and memory consolidation.
Pathways
CaMKII alpha functions within the calcium signaling pathway contributing to long-term potentiation (LTP) and long-term depression (LTD). It interacts with proteins such as NMDA receptors to facilitate changes in synaptic strength alongside other kinases. This pathway's activation leads to memory formation and synaptic plasticity in the central nervous system. Additionally CaMKII alpha connects with the MAPK signaling pathway integrating signals from various neurotransmitter systems which help coordinate neuronal response to stimuli.
Alterations in CaMKII alpha have been linked to neurological conditions such as Alzheimer's disease and schizophrenia. In Alzheimer's discourse in CaMKII alpha phosphorylation correlates with impaired memory and cognitive function. The protein also interfaces with tau another key protein related to neurofibrillary tangles in Alzheimer's. In schizophrenia abnormalities in CaMKII alpha expression and activity suggest its role in synaptic dysfunction and neurodevelopmental irregularities. Targeting CaMKII alpha may provide therapeutic opportunities for managing these and related neurological disorders.