Interaction with the NMDA receptor locks CaMKII in an active conformation

By K. Bayer, P. De Koninck, A. Leonard, J. Hell, H. Schulman, Arturo Gomez, Patrick William Gutschow, Michael Wageih Hanna, L. F. Harp, Hisami Sarah Hayashi and 3 more. Nature, 2001

762 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2b293f1a6ebf4098505d2caed8c2876f81c5fc34

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Citations in the corpus

Differential Roles of NR2A and NR2B-Containing NMDA Receptors in Cortical Long-Term Potentiation and Long-Term Depression (2004, background): “…signaling cascades remain to be determined, data suggesting that NR2A and NR2B subunits couple variously to different intracellular substrates (Bayer et al., 2002; Li et al., 2002) may provide clues as to how extrasynaptic NR2B receptors may produce one form of plasticity and synaptic NR2A…”
Glutamate Receptor Ion Channels: Structure, Regulation, and Function (2010, background): “…NMDA receptors can be modified rapidly upon Ca2 influx associated with NMDA receptor activation and in this sense may represent the prototype of a kinase activated by its target (Bayer et al., 2001), but the functional consequences of this modification have not been directly addressed.”
Regulatory mechanisms of AMPA receptors in synaptic plasticity (2007, background): “, and this interaction is crucial for the generation of both sustained kinase activity and LT”
Long-term potentiation and memory. (2004, background): “It seems that binding to the NR2B subunit occurs and that this leads to increased association of calmodulin with CaMKII and, subsequently, an increased association with the postsynaptic density (48).”
Mechanisms of CaMKII action in long-term potentiation (2012, background): “The region near S1303 in NR2B binds activated CaMKII in a way that does not require T286 phosphorylation; a second binding site in NR2B between amino acids 839 and 1120 does require T286 phosphorylatio”
The Role of N-Methyl-d-Aspartate (NMDA) Receptors in Pain: A Review (2003, background): “By interfering with autoinhibitory interactions within CaMKII, binding to NR2B locks CaMKII in an activated state that cannot be reversed by phosphatases (50).”
Making memories last: the synaptic tagging and capture hypothesis (2010, background): “, closer to many of its targets, where it becomes less accessible to inhibitory phosphatase”
Regulation of NMDA Receptor Subunit Expression and Its Implications for LTD, LTP, and Metaplasticity (2008, background): “Activated CaMKII binds strongly to NR2B (Strack and Colbran, 1998), allowing CaMKII to remain active even after dissociating from Ca2þ/calmodulin (Bayer et al., 2001).”
AMPA receptor trafficking and synaptic plasticity. (2002, background): “Such a stimulus can also recruit CaMKII to synapses (Liao et al. 2001, Shen & Meyer 1999), where it may bind to NMDA receptors (Bayer et al. 2001, Leonard et al. 1999, Strack & Colbran 1998, Strack et al. 2000).”
NMDA receptor subunit composition controls synaptic plasticity by regulating binding to CaMKII. (2005, neutral): “, 1989), a peptide homologous to the interacting site of endogenous NR2B (Bayer et al., 2001).”
Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear (2010, neutral): “Interaction with NMDA receptors, particularly the NR2B subunit, can lock the molecule in this active form (23).”