Article
The CaMKII D135N mutation blocks kinase activity and reduces GluN2B binding.
Molecular pharmacology - 1 Jan 2026
Larsen Matthew E, Barker C Madison, Vargas Raul Satoshi, Coultrap Steven J, Bayer K Ulrich
Abstract excerpt
Three recent studies claimed that induction of long-term potentiation of synaptic strength requires structural rather than enzymatic functions of the Ca2+/calmodulin-dependent protein kinase II (CaMKII). One study used the CaMKII D135N mutation, which was claimed to abolish enzymatic activity without affecting the structural function, that is, binding to GluN2B. We found here that the D135N mutant indeed...
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