How does CaMKII contribute to long-term potentiation?
CaMKII subsequently translocates to the synapse, where it binds to NMDA-type glutamate receptors and produces potentiation by phosphorylating principal and auxiliary subunits of AMPA-type glutamate receptors. These processes are all localized to stimulated spines and account for the synapse-specificity of LTP.
What does CaM kinase II do?
Multifunctional CaM kinases, also collectively called CaM kinase II, which play a role in neurotransmitter secretion, transcription factor regulation, and glycogen metabolism.
Where is CaMKII located?
CAMKII Structure and Mechanism of Activation The enzyme is expressed mainly in the brain, but also in the rest of the tissues. In some regions of the brain, such as the hippocampus, the protein levels reach up to 2% of total proteins (Erondu and Kennedy, 1985; Hudmon and Schulman, 2002).
What is CaMKII learning and memory?
Calcium/calmodulin-dependent protein kinase II (CaMKII) is a key protein kinase in neural plasticity and memory, as have been shown in several studies since the first evidence in long-term potentiation (LTP) 30 years ago.
What is camk2 and what does it do?
Unsurprisingly, CaMK2 has been demonstrated to be implicated in the regulation of cell proliferation, migration, and metastasis in a variety of cancer types by a series of experimental studies (Table (Table22). Table 2
Is camk2β downregulated in brain tumors?
Their results showed that CaMK2β was strongly downregulated in tumors compared to that in normal brain tissue.
What is the prognosis of camk2af/f mice injected with CAG-creesr?
All injected Camk2af/f; Camk2bf/f; CAG-CreESR mice died within 24–53 d, with a median survival of 37 d ( Fig. 2 c ). These mice did not show any obvious alterations in behavior until their last 24 h, during which they would stop moving, eating, and drinking. Importantly, Camk2af/f; Camk2bf/f mice without CAG-CreESR (control group) all survived.
How is activity of camk2 governed by multiple phosphorylation sites?
Activity of CAMK2 is governed by multiple phosphorylation sites, of which the Thr286 (Thr287 in CAMK2B) is important for Ca 2+ -independent activity ( Fig. 1 d, bottom) and Thr305/Thr306 (Thr306/Thr307 in CAMK2B) for the Ca 2+ -dependent activity ( Fig. 1 d, middle), because they are located within the Ca 2+ /calmodulin binding site on CAMK2.